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[post_title] => USE OF YKL-40 AS A BIOMARKER FOR ASSESSING FUNCTIONAL OUTCOME IN ACUTE ISCHEMIC STROKE PATIENTS TREATED WITH ENDOVASCULAR THERAPY
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-ykl-40-as-a-biomarker-for-assessing-functional-outcome-in-acute-ischemic-stroke-patients-treated-with-endovascular-therapy/
[post_content] => Today, more than 40% of acute ischemic stroke (AIS) patients treated with endovascular therapy (EVT) will remain severely disabled at 3 months. The inventors hypothesized that acute microglial inflammation plays a pivotal role in post-AIS brain changes leading to poor functional outcome. Glycoprotein YKL-40 is a biomarker of astrocytic and microglial activation. The inventors thus conducted a monocentric prospective study including 120 patients treated with EVT, for whom 3 blood samples (before, within 1-h, 24-h post-EVT) were drawn to measure plasma YKL-40 concentrations. The inventors found that 3-month functional outcome was significantly and independently associated with acute plasma YKL-40 levels. the present invention relates to the use of YKL-40 as a biomarker for assessing functional outcome in AIS patients treated with EVT.
[post_date] => 2024-10-24 17:10:02
[post_modified] => 2024-10-24 17:10:02
[ID] => 8130
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[date_application] => 2023-10-17
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO22401-D1
[keywords] => acute ischemic stroke (AIS), YKL-40, Prognosis, ELISA
[pub_scient_inv_dispo] => Eur Stroke J, 2024 Jun 6:23969873241256813., Boutelier et al., Acute astrocytic reaction is associated with 3-month functional outcome after stroke treated with endovascular therapy, doi: 10.1177/23969873241256813. Online ahead of print.
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[rare_disease] => 0
[second_indication] => 0
[inventors] => MAIER Benjamin; DESILLES Jean-Philippe; PAQUET Claire; DELVOYE François; MAZIGHI Mikhael; BOUTELIER Ada
[number_application] => EP23 306 815.4 on 17/10/23 and PCT/EP2024/079157on 16/10/2024
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
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[taxonomie] => Acute ischemic stroke, Biomarker, Central Nervous System, Immunoassay, Pre-Analytic Validation
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Acute ischemic stroke,
Biomarker,
Central Nervous System,
Immunoassay,
Pre-Analytic Validation
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[post_title] => METHODS OF PROGNOSIS AND TREATMENT OF PATIENTS SUFFERING FROM CANCER
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-of-prognosis-and-treatment-of-patients-suffering-from-cancer/
[post_content] => Lung fibroblast play an important role in lung cancer tumor microenvironment (TME). Senescence is involved in the pathophysiology of tumorogenesis. analyze how sPLA2 influenced lung cancer cell malignant properties. The inventors show that secreted PLA2 XIIA (sPLA2 XIIA) play a key role in lung cancer cell malignant properties. They demonstrate that sPLA2 XIIA increases the proliferation, the migration and organoid growth of both lung cancer cell lines (NCI and A549). Indeed, they shows that sPLA2 XIIA induces notably the epithelial mesenchymal transition (EMT), which is involved in the invasion of cancer cells and in the formation of metastasis. They also demonstrate that the effect of sPLA2 XIIA is mediated in particular by syndecan 1 and 4. Taken altogether, these data define sPLA2 XIIA as a circulating biomarker of poor prognosis in lung cancer and establish a requirement for sPLA2 XIIA inhibition for the treatment or prevention of cancer, especially lung cancer in the COPD patients.
[post_date] => 2024-10-24 16:55:01
[post_modified] => 2024-10-24 16:55:01
[ID] => 8129
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[date_application] => 2023-10-12
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO19258-D1
[keywords] => Lung Cancer, COPD, Prognosis, Treatment response prediction, sPLA2, Q-PCR
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[rare_disease] => 0
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[inventors] => HERATH Danushki; BOCZKOWSKI Jorge Bernardo; ORANGER Mathilde
[number_application] => EP23 306 700.8 on 03/10/23 and PCT/EP2024/077748 on 02/10/2024
[technology_engineering] =>
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[technological_platform] => transcriptomics
[post_categoryname] => Diagnostic
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[taxonomie] => Biomarker, Biomarker, In vitro poc, Lung cancer, Method, Oncology, Target, Transcriptomics
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Biomarker,
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In vitro poc,
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Method,
Oncology,
Target,
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[post_title] => METHODS FOR THE DIAGNOSIS, TREATMENT AND ANALYSIS OFNLRP3-ASSOCIATED AUTOINFLAMMATORY DISEASES
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-the-diagnosis-treatment-and-analysis-ofnlrp3-associated-autoinflammatory-diseases-2/
[post_content] => Using NLRP3-deficient U937 cells reconstituted with doxycycline-inducible NLRP3 variants in response to NLRP3 induction, the present inventors have developed a novel functional cell-based assay to screen for NLRP3 variants that uncouples NLRP3 induction, priming and activation. The inventors studied and characterized 38 NLRP3 variants by assessing pyroptosis and IL-1u03b2/18 secretion in, priming and/or activation. The results were confirmed in primary monocytes from patients carrying different variants. The present invention pertains to a method for characterizing NLRP3 mutations that allows discriminating gain-of-function mutants from polymorphism without any impact on NLRP3 activity. The invention also relates to methods for the diagnosis of NLRP3-associated autoinflammatory diseases and for predicting a response to NLRP3 inhibitors based on the detection of specific NLRP3 mutations in a sample obtained from a patient. The invention also relates to new NLRP3 inhibitors.
[post_date] => 2024-10-24 16:05:01
[post_modified] => 2024-10-24 18:10:02
[ID] => 8128
)
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[idSugar] => 4551d172-921f-11ef-b929-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 2023-09-04
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO23231-D1
[keywords] => NLRP3, mutation, Autoinflammatory diseases, Cryopyrin-associated autoinflammatory syndromes (CAPS), prognosis, sequencing
[pub_scient_inv_dispo] => J Exp Med, 2024 May 6;221(5):e20231200., Cosson et al., Functional diversity of NLRP3 gain-of-function mutants associated with CAPS autoinflammation; doi: 10.1084/jem.20231200. Epub 2024 Mar 26.
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => PY Bénédicte
[number_application] => EP23 306 463.3 on 04/09/23 and PCT/EP2024/074525 on 03/09/2024
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => sequencing
[post_categoryname] => Diagnostic
[parent_category] => 195
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[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 2
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Human POC, Immunology, Method, Other Immunological Disorders, Sequencing
[taxonomieurl] =>
Biomarker,
Biomarker,
Human POC,
Immunology,
Method,
Other Immunological Disorders,
Sequencing
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[post_title] => METHODS AND KITS FOR DIAGNOSING CAUSE OF NEPHROTIC SYNDROME AND GUIDING THERAPY
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-kits-for-diagnosing-cause-of-nephrotic-syndrome-and-guiding-therapy/
[post_content] => The present invention describes the identification of a soluble glomerular permeability factor, anti-Vasorin (or anti-VASN) autoantibodies synthesized by immune system cells, which opens up new perspectives for pathophysiological understanding, monitoring, and therapy of nephrotic syndrome. Clinical applications can include strategies for preventing the action of autoantibodies against said podocyte protein, inhibiting the production of antibodies against this protein, or eliminating these autoantibodies. Although the exact role of anti-VASN autoantibodies and VASN in nephrotic syndrome is still not well understood, the presence of circulating autoantibodies against VASN is highly specific to nephrotic syndrome. Up to now, no anti-VASN autoantibodies have been described in healthy individuals.Thus, the present invention relates to methods and kits for determining whether a subject has or is at risk of having a nephrotic syndrome associated with anti-VASN auto-antibodies or not.
[post_date] => 2024-10-24 15:10:01
[post_modified] => 2024-10-24 15:10:01
[ID] => 8127
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[idSugar] => 09dc850e-9217-11ef-a18e-506b8df7f2c7
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[date_application] => 2023-07-24
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO23308-D1
[keywords] => anti-VASN autoantibodies, nephrotic syndrome, Diagnosis, Prognosis, Prevention, Treatment response prediction, ELISA
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => GHIGGERI Gian Marco; BRUSCHI Maurizio; LENOIR Olivia; D/u2019IZARNY-GARGAS Thibaut; THARAUX Pierre-Louis
[number_application] => EP23 306 270.2 on 24/07/23 and PCT/EP2024/073960 on 27/08/2024
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 3
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Genito Urinary System, Glomerulonephritis, Immunoassay, Method, Pre-Analytic Validation
[taxonomieurl] =>
Biomarker,
Biomarker,
Genito Urinary System,
Glomerulonephritis,
Immunoassay,
Method,
Pre-Analytic Validation
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[post] => stdClass Object
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[post_title] => METHODS FOR PREDICTING COGNITIVE DECLINE IN A SUBJECT
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-predicting-cognitive-decline-in-a-subject/
[post_content] => Alzheimer/u2019s disease is strongly linked to biological aging and bioenergetic abnormalities. Systemic dysregulation of metabolism is a hallmark of the physiological decline of tissues with age. We aimed to explore untargeted metabolomic profiling of blood samples from amyloid-positive people to distinguish individuals who progressed to cognitive decline from those who remained cognitively intact despite having amyloid deposits in the brain. A minimal signature of 9 metabolites identified decliners and non-decliners of cognitive function in participants with an amyloid load. These findings are of clinical importance as they suggest that a metabolic fingerprint may help to predict patients who will develop cognitive decline. Due to the high prevalence of brain amyloid-positivity in older adults, identifying adults who will have cognitive decline will enable the development of personalized and early interventions. The present invention relates to an in vitro method for predicting cognitive decline in a subject comprising the step of determining the level of at least one metabolite selected in the group consisting of 3-hydroxybutyrate, acetone, triglyceride 48:3, glucose, citrate, succinate, methionine, serine, sphingomyelin d18:1/C26:0 in a biological sample obtained from the subject.
[post_date] => 2024-10-24 14:25:01
[post_modified] => 2024-10-24 14:25:01
[ID] => 8126
)
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[idSugar] => 800c0e8a-9211-11ef-ba87-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 2023-08-18
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO23195-D1
[keywords] => Alzheimer, Prognosis, Metabolite Signature, Mass Spectrometry
[pub_scient_inv_dispo] => J Gerontol A Biol Sci Med Sci, 2024 May 1;79(5):glae077., Tremblay-Franco et al., Integrative Multimodal Metabolomics to Early Predict Cognitive Decline Among Amyloid Positive Community-Dwelling Older Adults, doi: 10.1093/gerona/glae077.
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => ADER-PERARNAU Isabelle; VELLAS Bruno; TREMBLAY-FRANCO Marie
[number_application] => EP23 306 392.4 on 18/08/23 and PCT/EP2024/073060 on 16/08/2024
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => mass_spectrometry
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
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[first_name] => Inserm
[last_name] => Transfert
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[author] => 1
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[wp_user_level] => 2
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 4
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Central Nervous System, Human POC, Mass spectrometry, Method
[taxonomieurl] =>
Biomarker,
Biomarker,
Central Nervous System,
Human POC,
Mass spectrometry,
Method
)
[5] => stdClass Object
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[post] => stdClass Object
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[post_title] => NEW PROGNOSTIC METHOD OF KIDNEY FAILURE
[guid] => https://technology-offers.inserm-transfert.com/offer
ew-prognostic-method-of-kidney-failure/
[post_content] => The present invention relates to the prediction of kidney injury. In this study, the inventors studied the transcriptomic landscape in AAV-GN to find biomarkers for refining diagnosis and/or prognosis, which would help stratify patient risk and tailor therapeutic management. The objectives of this study were to investigate the potential prognostic value and/or pathogenic role of the most relevant genes associated with kidney survival. They identified a 4-gene signature (XRCC6, PRKCD, TEK, and CLU) that predicted kidney survival better than histological-based classifications. Thus, the invention relates to a method for predicting the development of a kidney failure in a patient suffering from an ANCA-associated vasculitis-associated GN (AAV-GN).
[post_date] => 2024-10-24 13:55:02
[post_modified] => 2024-10-24 13:55:02
[ID] => 8125
)
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[application] =>
[idSugar] => 77b5e656-920d-11ef-aceb-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 2023-08-02
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO22461-D1
[keywords] => Kidney Failure, Prognosis, XRCC6, PRKCD, TEK, CLU, Q-PCR, RNA-Seq
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => DELNESTE Yves; COPIN Marie-christine; AUGUSTO Jean-François
[number_application] => EP23 306 324.7 on 02/08/23 and PCT/EP2024/071795 on 01/08/2024
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => transcriptomics
[post_categoryname] => Diagnostic
[parent_category] => 195
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[tags_order_view] => stdClass Object
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[type_of_patent] => Type of patent
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[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 5
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Analytic validation, Biomarker, Biomarker, Genito Urinary System, Glomerulonephritis, Transcriptomics
[taxonomieurl] =>
Analytic validation,
Biomarker,
Biomarker,
Genito Urinary System,
Glomerulonephritis,
Transcriptomics
)
[6] => stdClass Object
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[post] => stdClass Object
(
[post_title] => METHODS OF DETERMINING WHETHER A SUBJECT SUFFERING FROM LUPUS NEPHRITIS (LN) WILL ACHIEVE A RESPONSE WITH AN INDUCTION THERAPY
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-of-determining-whether-a-subject-suffering-from-lupus-nephritis-ln-will-achieve-a-response-with-an-induction-therapy/
[post_content] => Systemic lupus erythematosus (SLE) is an autoimmune disease in which circulating immune complexes can cause different types of glomerulonephritis, according to immune deposits and to the type of glomerular cell injury. Proliferative lesions represent the most severe form of lupus nephritis (LN) and often lead to kidney failure and death. Mucosal-associated invariant T (MAIT) are a subset of innate-like T cells that recognize microbial-derived ligands from the riboflavin synthesis pathway. Now the inventors analyzed the phenotype and function of peripheral blood MAIT cells by flow cytometry in 26 patients with LN and in a control group of 16 healthy volunteers. The inventors found that MAIT cell frequencies are markedly reduced in blood of LN patients. More particularly, among LN patients, baseline MAIT cell frequency, Ki-67 expression evaluating proliferative activity and granzyme B production measuring cytotoxicity represent promising prognostic factors of renal response one year after induction therapy. In conclusion, the inventors showed that baseline frequency and cytotoxic profile of MAIT cells may represent a promising prognostic factor of renal remission one year after induction therapy.
[post_date] => 2024-10-24 13:20:02
[post_modified] => 2024-10-24 13:20:02
[ID] => 8124
)
[post_meta] => stdClass Object
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[object] =>
[application] =>
[idSugar] => 6a31e3fe-9208-11ef-bb62-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 2023-07-24
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO23304-D1
[keywords] => Lupus Nephritis, Systemic lupus erythematosus, MAIT Cells, Flow Cytometry, Diagnosis, Treatment response prediction
[pub_scient_inv_dispo] => Front Immunol, 2023 Oct 10:14:1205405, Litvinova et al., MAIT cells altered phenotype and cytotoxicity in lupus patients are linked to renal disease severity and outcome, . doi: 10.3389/fimmu.2023.1205405. eCollection 2023.
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => FLAMENT Héloïse; MONTEIRO Renato; LEHUEN-MONTEIRO Agnès
[number_application] => EP23 306 270.2 on 24/07/23 and PCT/EP2024/070803
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 6
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Human POC, Immunoassay, Immunology, Method, Systemic Lupus Erythematosus
[taxonomieurl] =>
Biomarker,
Human POC,
Immunoassay,
Immunology,
Method,
Systemic Lupus Erythematosus
)
[7] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => CD1A AS A BIOMARKER AND BIOTARGET IN CUTANEOUS T-CELL LYMPHOMAS
[guid] => https://technology-offers.inserm-transfert.com/offer/cd1a-as-a-biomarker-and-biotarget-in-cutaneous-t-cell-lymphomas/
[post_content] => The present study of the regulatory T phenotype of Sézary cells led to the discovery of the expression of CD1a by Sézary cells. CD1a therefore appears as a diagnostic marker for monitoring Sézary syndrome and as a therapeutic target. Accordingly, the present invention relates to methods for the diagnosis and treatment of cutaneous T cell-lymphomas.
[post_date] => 2024-10-24 10:05:02
[post_modified] => 2024-10-24 10:05:02
[ID] => 8123
)
[post_meta] => stdClass Object
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[application] =>
[idSugar] => 40a9931c-91ed-11ef-81de-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 2023-07-17
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO23255-D1
[keywords] => Sézary Syndrome, cutaneous T cell lymphomas, Diagnosis, Treatment response Prediction, CD1a, ELISA
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => BENSUSSAN Armand; GIUSTINIANI Jérôme; DE MASSON Adele
[number_application] => EP23 306 229.8 on 17/07/23
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
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[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 7
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Human POC, Immunoassay, Lymphoma, Oncology, Sezary syndrome, Target
[taxonomieurl] =>
Biomarker,
Biomarker,
Human POC,
Immunoassay,
Lymphoma,
Oncology,
Sezary syndrome,
Target
)
[8] => stdClass Object
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[post_title] => METHODS AND COMPOSITIONS FOR DISCRIMINATING AND TREATING STROKE
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-compositions-for-discriminating-and-treating-stroke/
[post_content] => Stroke is the second cause of death and the first cause of adult disability in industrialized countries. The goal of emergency therapy for acute ischemic stroke is prompt restoration of blood flow to regions of brain that are ischemic but not yet infarcted. Based on this, the inventors compare the plasma concentration of total tPA (antigenic: active + PAI-1 bound) in patients with acute ischemic stroke before any treatment with those in a healthy control group, to evaluate the interest of tPA as a potential diagnostic biomarker in the acute phase of ischemic stroke.In particular, the present invention relates to method for discriminating at early stage an hemorrhagic stroke from an ischemic stroke or a mimic stroke in a subject in need thereof, comprising the steps of i) determining in a blood sample obtained from the said subject the level of tissue-type plasminogen activator (tPA), ii) comparing the level determined in step i) with a reference value and iii) concluding when the level of tissue-type plasminogen activator (tPA) determined at step i) is higher than the reference value is predictive of a risk of having or developing an ischemic stroke or a mimic stroke or concluding when the level of tissue-type plasminogen activator (tPA) determined at step i) is lower than the reference value is predictive of a risk of having or developing a hemorrhagic stroke
[post_date] => 2024-10-24 09:50:02
[post_modified] => 2024-10-24 09:50:02
[ID] => 8122
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[date_application] => 2023-05-23
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO23212-D1
[keywords] => Stroke, Differential diagnostic, Ischemic stroke, Hemorrhagic stroke, tPA, ELISA
[pub_scient_inv_dispo] => Ann Clin Transl Neurol, 2024 Sep 10, Jauquet et al., Endogenous tPA levels: A biomarker for discriminating hemorrhagic stroke from ischemic stroke and stroke mimics, doi: 10.1002/acn3.52197. Online ahead of print.
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => ROUSSEL Benoît; VIVIEN Denis
[number_application] => European Procedure (Patents) (EPA) - 23 Mai 2023 - 23 305 817.1 and PCT/EP2024/064107 on 22/05/2024
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
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[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 8
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Central Nervous System, Immunoassay, Method, Pre-Analytic Validation, Stroke
[taxonomieurl] =>
Biomarker,
Central Nervous System,
Immunoassay,
Method,
Pre-Analytic Validation,
Stroke
)
[9] => stdClass Object
(
[post] => stdClass Object
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[post_title] => STRATIFICATE AND METHOD TO TREAT A PATIENT SUFFERING FROM A CANCER
[guid] => https://technology-offers.inserm-transfert.com/offer/stratificate-and-method-to-treat-a-patient-suffering-from-a-cancer/
[post_content] => The present invention relates the stratification and treatment of patient suffering from a cancer. In this study, the inventors analyzed the adenosine methylation level of miR-125a-5p (m6A-miR-125a-5p) using RNA immunoprecipitation with an anti-methyl-base-antibody followed by qPCR. CLIP and ELISA were used to study the effect of m6A-miR-125a-5p on its ability to be recruited on GW182 and impact PD-1 expression, respectively. They showed that the METTL3-mediated m6A-miR-125a-5p regulates the expression of IGSF11/VSIG3 which acts as a molecular determinant of the immunogenicity of tumor cells. Observations in two lung cancer patients treated with anti-PD-1 therapy show that the m6A-miR-125a-5p level is analyzable from EVs/exosomes from longitudinal blood samples. These data provide that m6A-miR-125a-5p level can be used as a biomarker and therapeutic solutions (anti-IGSF11 antibody and METTL3 inhibitor) could potentially address the anti-PD1 therapy failure in a context of precision and personalized medicine intended for the right patient, at the right time, with the right therapy. Thus the invention relates to a method of identifying a patient having or at risk of having or developing a resistance to anti-PD-1 therapy based on the expression level of the extracellular vesicles adenosine methylated miR-125a-5p (m6A-miR-125a-5p).
[post_date] => 2024-10-23 16:10:02
[post_modified] => 2024-10-23 16:10:02
[ID] => 8121
)
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[application] =>
[idSugar] => d6523172-9156-11ef-924d-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 2023-05-17
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO21448-D1
[keywords] => Lung Cancer, miRNA, treatment response prediction, immunotherapy
[pub_scient_inv_dispo] => Cancers (Basel). 2023 Jun 14;15(12):3188., Bougras-Cartion et al., Adenosine Methylation Level of miR-125a-5p Promotes Anti-PD-1 Therapy Escape through the Regulation of IGSF11/VSIG3 Expression, doi: 10.3390/cancers15123188.
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => CARTRON Pierre-François; NADARADJANE Arulraj; BOUGRAS-CARTRON Gwenola
[number_application] => European Procedure (Patents) (EPA) - 17 Mai 2023 - 23 305 796.7 and PCT/EP2024/063568 on 16/05/2024
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => transcriptomics
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
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[thera_area] => Therapy Area
[type_of_patent] => Type of patent
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[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 9
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Human POC, Lung cancer, Method, Oncology, Transcriptomics
[taxonomieurl] =>
Biomarker,
Human POC,
Lung cancer,
Method,
Oncology,
Transcriptomics
)
[10] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => BIALLELIC GENE MUTATIONS FOR THE DIAGNOSIS OF NEONATAL SYSTEMIC HYPERTENSION
[guid] => https://technology-offers.inserm-transfert.com/offer/biallelic-gene-mutations-for-the-diagnosis-of-neonatal-systemic-hypertension/
[post_content] => The present invention relates to a method and kit for identifying a subject having or at risk of having or developing an isolated neonatal systemic hypertension (NSH) and/or NSH associated cardiogenic shock, comprising determining, in a sample obtained from said subject, the presence or absence of bi-allelic nucleotide variants (NV) located in NPR1 gene, said NV predicted to be pathogenic and being associated with NPR1 loss of function. The present inventors have established a statistical link between specific predicted pathogenic variants located in the NPR1 gene and neonatal systemic hypertension (NSH) in a cohort of NSH disease families. More precisely, the present inventors have established a link between specific predicted biallelic pathogenic variants contained in NPR1 in patients with NSH and/or cardiogenic shock (in multiplex and consanguineous families) associated sometime with increased Nuchal Translucency (NT). Another object of the invention relates to a method for treating neonatal systemic hypertension (NSH) and/or NSH associated cardiogenic shock.
[post_date] => 2024-10-23 15:45:02
[post_modified] => 2024-10-23 17:50:02
[ID] => 8120
)
[post_meta] => stdClass Object
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[application] =>
[idSugar] => 63651e02-9153-11ef-8699-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 2023-04-24
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO23100-D1
[keywords] => neonatal systemic hypertension (NSH), NPR1, Diagnosis, mutation, sequencing, transcriptomics
[pub_scient_inv_dispo] => J Med Genet, 2023 Apr 20, Capri et al, Biallelic NPR1 loss of function variants are responsible for neonatal systemic hypertension, doi: 10.1136/jmg-2023-109176. Online ahead of print.
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => MELKI Judith,CAPRI Yline
[number_application] => European Procedure (Patents) (EPA) - 24 Avr. 2023 - 23 315 100.0 and PCT/EP2024/060551 on 18/04/2024
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => sequencing,transcriptomics
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
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[type_of_patent] => Type of patent
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[last_name] => Transfert
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 10
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Cardiovascular Diseases, Human POC, Hypertension/Pulmonary Arterial Hypertension, Method, Sequencing, Transcriptomics
[taxonomieurl] =>
Biomarker,
Biomarker,
Cardiovascular Diseases,
Human POC,
Hypertension/Pulmonary Arterial Hypertension,
Method,
Sequencing,
Transcriptomics
)
[11] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHOD FOR DISCRIMINATING MONO-IMMUNOTHERAPY FROM COMBINED IMMUNOTHERAPY IN CANCERS
[guid] => https://technology-offers.inserm-transfert.com/offer/method-for-discriminating-mono-immunotherapy-from-combined-immunotherapy-in-cancers/
[post_content] => Combination therapy with anti-PD-1 and anti-CTLA-4 is now indicated in many cancers. It appears to be more effective than anti-PD-1 monotherapy, but more toxic. This work has shown that plasma levels of soluble CD27 are inversely correlated with survival in melanoma patients treated with anti-PD-1. This result was validated in 2 independent cohorts of patients representing 180 patients in total. Interestingly, this predicting role of sCD27 in anti-PD-1 treated melanoma patients was found both with an optimal cut-off defined by the Youden test, but also with the same cut-off previously defined in kidney cancer. This suggests some analytical robustness of this marker. Inventors have also shown that plasma sCD27 levels prior to anti-PD-1 treatment are inversely correlated with progression free survival (PFS). On the contrary, in patients with metastatic melanoma treated with anti-PD-1 and anti-CTLA-4, plasma sCD27 levels are not statistically significantly associated with patient survival or progression-free survival. They therefore find a discrepancy between the predictive impact of sCD27 on survival of patients treated with anti-PD-1 immunotherapy alone or with combined anti-PD-1 and anti-CTLA-4 immunotherapy. Plasma sCD27 concentrations represents a new type of biomarker to help in the management of these patients.
[post_date] => 2024-10-23 15:15:02
[post_modified] => 2024-10-23 15:15:02
[ID] => 8119
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => 2fb0a8a0-914f-11ef-9ef7-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 2023-03-28
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO23133-D1
[keywords] => Melanoma, Kidney Cancer, Treatment response prediction, Prognosis, Combinatory treatment, sCD27
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => TARTOUR Eric,OUDARD Stephane,SAM Ikuan,LEBBÉ Céleste,BEN HAMOUDA Nadine
[number_application] => European Procedure (Patents) (EPA) - 28 Mars 2023 - 23 305 423.8 and EP23 305 423.8 on 28/03/23 and PCT/EP2024/058363 on 27/03/2024
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
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[first_name] => Inserm
[last_name] => Transfert
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(
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)
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 11
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Analytic validation, Biomarker, Biomarker, Immunoassay, Melanoma, Oncology
[taxonomieurl] =>
Analytic validation,
Biomarker,
Biomarker,
Immunoassay,
Melanoma,
Oncology
)
[12] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => A GENE SIGNATURE FOR DIAGNOSING STIMULATOR OF INTERFERON GENES (STING)-ASSOCIATED VASCULOPATHY WITH ONSET IN INFANCY (SAVI)
[guid] => https://technology-offers.inserm-transfert.com/offer/a-gene-signature-for-diagnosing-stimulator-of-interferon-genes-sting-associated-vasculopathy-with-onset-in-infancy-savi/
[post_content] => Gain-of-function mutations in STING1, that codes for the Stimulator of Interferon Gene (STING), result in a severe autoinflammatory disease termed STING-associated vasculopathy with onset in infancy (SAVI). Although elevated type I interferon (IFN) production is thought to be the leading cause of the symptoms observed in patients, STING can induce a set of pathways, and their role in the onset and severity of SAVI remains to be elucidated. To address this point, the inventors compared a single-cell RNA sequencing (scRNA-seq) dataset of peripheral blood mononuclear cells (PBMCs) from SAVI patients to a dataset of healthy PBMCs treated with recombinant IFN-u03b2. In particular, scRNA-seq clustering identified a patient-specific subset of monocytes, highly inflammatory and expressing a strong integrated stress response (ISR). Even more particularly, the inventors have identified at the transcriptomic level a STING-associated signature of 21 genes that is driven by STING activation, independently of type I IFN. This signature is therefore suitable to better distinguish SAVI from other type I interferonopathy.
[post_date] => 2024-10-23 14:40:01
[post_modified] => 2024-10-23 16:50:02
[ID] => 8118
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => a53b5eee-914a-11ef-9cd5-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 2023-03-27
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO23085-D1
[keywords] => STING-associated vasculopathy with onset in infancy (SAVI), RNA Signature, Diagnostic, Prognosis, Treatment response prediction
[pub_scient_inv_dispo] => Cell Rep Med, 2023 Dec 19;4(12):101333., De Cevins et al. , Single-cell RNA-sequencing of PBMCs from SAVI patients reveals disease-associated monocytes with elevated integrated stress response, doi: 10.1016/j.xcrm.2023.101333.
[access_to_detailed_offer] =>
[rare_disease] => 1
[second_indication] => 0
[inventors] => MENAGER Mickaël; RIEUX-LAUCAT Frédéric
[number_application] => International Procedure (PCT) - 27 Mars 2023 - PCT/IB2023/000159
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => transcriptomics
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
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[first_name] => Inserm
[last_name] => Transfert
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(
[author] => 1
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)
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[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 12
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Cardiovascular Diseases, Human POC, Method, Transcriptomics, Vasculitis
[taxonomieurl] =>
Biomarker,
Biomarker,
Cardiovascular Diseases,
Human POC,
Method,
Transcriptomics,
Vasculitis
)
[13] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => THE CIRCULAR RNA CIRCLTBP2 AS A BIOMARKER AND BIOTARGET IN INTRAHEPATIC CHOLANGIOCARCINOMAS
[guid] => https://technology-offers.inserm-transfert.com/offer/the-circular-rna-circltbp2-as-a-biomarker-and-biotarget-in-intrahepatic-cholangiocarcinomas/
[post_content] => Intrahepatic cholangiocarcinoma (iCCA) is a deadly cancer worldwide with an increasing incidence and limited therapeutic options. Therefore, there is an urgent need to open the field to new concepts for identifying clinically relevant therapeutic targets and biomarkers. Here, the inventors explored the role and the clinical relevance of circular RNA circLTBP2 in iCCA. In particular, CircLTBP2 (hsa_circ_0032603) was identified as a novel TGFu03b2-induced circRNA in several CCA cell lines. CircLTBP2 promotes tumor cell proliferation, migration and resistance to gemcitabine-induced apoptosis in vitro and tumor growth in vivo. Mechanistically, circLTBP2 acts as a competitive RNA regulating notably the activity of the tumor suppressor microRNA miR-338-3p, leading to the overexpression of its pro-metastatic targets. The restoration of miR-338-3p levels in iCCA cells reversed the pro-tumorigenic effects driven by circLTBP2, including the resistance to gemcitabine-induced apoptosis. In addition, circLTBP2 expression predicted a reduced survival, as detected in tumor tissues but also in serum exosomes isolated from patients with iCCA. In conclusion, CircLTBP2 is a novel effector of the pro-tumorigenic arm of TGFu03b2 and a clinically relevant biomarker easily detected from liquid biopsies in iCCA. Thus, the present invention relates to the circulating RNA circLTBP2 as a biomarker and biotarget in intrahepatic cholangiocarcinomas.
[post_date] => 2024-10-23 10:10:01
[post_modified] => 2024-10-23 10:10:01
[ID] => 8117
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => d7ee2b76-9124-11ef-886f-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 2023-03-14
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO21460-D1
[keywords] => Intrahepatic cholangiocarcinoma (iCCA), dignosis, prognosis, treatment response prediction, CircLTBP2, transcriptomic
[pub_scient_inv_dispo] => JHEP Rep, 2023 Sep 5;5(12):100900., Louis C et al., TGFu03b2-induced circLTBP2 predicts a poor prognosis in intrahepatic cholangiocarcinoma and mediates gemcitabine resistance by sponging miR-338-3p, doi: 10.1016/j.jhepr.2023.100900. eCollection 2023 Dec.
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => COULOUARN Cédric,EDELINE Julien,LOUIS Corentin,DESOTEUX Matthis
[number_application] => European Procedure (Patents) (EPA) - 14 Mars 2023 - 23 305 343.8 and PCT/EP2024/056634 on 13/03/2024
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => transcriptomics
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
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(
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[first_name] => Inserm
[last_name] => Transfert
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(
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[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 13
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Liver Cancer, Method, Oncology, Pre-Analytic Validation, Transcriptomics
[taxonomieurl] =>
Biomarker,
Biomarker,
Liver Cancer,
Method,
Oncology,
Pre-Analytic Validation,
Transcriptomics
)
[14] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => INDOLE-3-PROPIONIC ACID AS AN IMPORTANT CONTRIBUTOR TO VIRAL INFECTION OUTCOMES AND A BIOMARKER OF VIRAL INFECTION SEVERITY
[guid] => https://technology-offers.inserm-transfert.com/offer/indole-3-propionic-acid-as-an-important-contributor-to-viral-infection-outcomes-and-a-biomarker-of-viral-infection-severity/
[post_content] => The gut-to-lung axis is critical during respiratory infections, including influenza A virus (IAV) infection. In the present study, the inventors used high-resolution shotgun metagenomics and targeted metabolomics analyses to characterize influenza-associated changes in the mouse gut microbiota/u2019s composition and metabolism. Quantitative targeted metabolomics analysis of serum revealed changes in specific classes of gut microbiota metabolites, including SCFAs, indole-containing tryptophan metabolites, trimethylamine, and polyamines. The changes in microbiota-associated metabolites were correlated with changes in taxon abundances and levels of disease markers. For instance, the tryptophan metabolite indole-3-propionic acid (IPA) was correlated positively with some Bacillota species but negatively with Bacteroidales bacteria M7, the viral load, and inflammation markers. Given its marked fall during infection, the inventors tested the effects of IPA supplementation in diseased animals. This supplementation was associated with a lower viral load and lower levels of local (lung) and systemic inflammation during influenza. Taken as a whole, the results highlighted IPA as both an important metabolic modulator to disease severity and a potential biomarker of influenza outcomes.
[post_date] => 2024-10-23 09:35:05
[post_modified] => 2024-10-23 09:35:05
[ID] => 8116
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[date_application] => 2023-02-24
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
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[reference_online] => BIO23038-D1
[keywords] => Influenza, prognosis, Mass spectrometry, metabolite, indole-3-propionic acid (IPA)
[pub_scient_inv_dispo] => Gut Microbes, 2024 Jan-Dec;16(1):2325067., Heumel et al., Shotgun metagenomics and systemic targeted metabolomics highlight indole-3-propionic acid as a protective gut microbial metabolite against influenza infection, doi: 10.1080/19490976.2024.2325067. Epub 2024 Mar 6.
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[rare_disease] => 0
[second_indication] => 0
[inventors] => TROTTEIN François,VINOLO Marco Aurélio Ramirez,SENCIO Valentin,RODRIGUEZ Patricia Brio,RODOVALHO Vinicius de Rezende,HEUMEL Séverine
[number_application] => European Procedure (Patents) (EPA) - 24 Févr. 2023 - 23 305 245.5 and PCT/EP2024/054616 on 23/02/2024
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => mass_spectrometry
[post_categoryname] => Diagnostic
[parent_category] => 195
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[0] => Diagnostic
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[taxonomie] => Animal POC, Biomarker, Biomarker, Infectious Diseases, Influenza, Mass spectrometry, Target
[taxonomieurl] =>
Animal POC,
Biomarker,
Biomarker,
Infectious Diseases,
Influenza,
Mass spectrometry,
Target
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[post_title] => VASORIN AS A BIOMARKER AND BIOTARGET IN NEPHROLOGY
[guid] => https://technology-offers.inserm-transfert.com/offer/vasorin-as-a-biomarker-and-biotarget-in-nephrology/
[post_content] => Aiming to identify factors underlying podocytes loss, the inventors revealed a markedly decreased expression of Vasorin (VASN) using comparative deep RNA sequencing of microdissected glomeruli from controls and patients diagnosed with FSGS or crescentic glomerulonephritis (CGN), that they further confirmed by in situ hybridization and immunohistochemistry. In particular, the inventors found that VASN is mainly expressed in podocytes during health. Furthermore, the inventors found that the level of glomerular or podocyte expression of the VASN gene depends on the kind of glomerular disease considered, suggesting this could be a helpful biomarker for differential diagnosis or outcome prediction.Of specific interest, 1/ the expression of VASN is significantly less in kidneys from patients suffering from secondary FSGS or anti-neutrophil cytoplasmic antibodies (ANCA) associated crescentic glomerulonephritis than in control normal kidneys or minimal change disease (MN), suggesting that low VASN abundance would predict poor outcome. 2/ Podocyte expression of the VASN gene is significantly less in secondary FSGS than in primary FSGS. 3/ Podocyte expression of the VASN gene is significantly less in FSGS (primary and secondary) than in MCD cases. 4/ Podocyte or glomerular expression of the VASN gene is increased substantially in kidneys biopsies diagnosed with membranous nephropathy (MN), minimal change disease (MCD), and lupus nephritis (LN) as compared with controls and FSGS, suggesting that this could be used to discriminate disease types, causes, outcome, or response to therapy.Accordingly, the present invention relates to the use of VASN as a biomarker and a biotarget for kidney diseases.
[post_date] => 2024-10-22 17:30:01
[post_modified] => 2024-10-22 17:30:01
[ID] => 8115
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[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO22440-D1
[keywords] => Chronic Kidney Disease, Differential diagnostic, primary focal segmental glomerulosclerosis, secondary focal segmental glomerulosclerosis, Vasorin
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => KRAUTZBERGER Anja Michaela; MAHTAL Nassim; SCHREWE Heinrich; SIEGERIST Florian; ENDLICH Nicole; THARAUX Pierre-Louis
[number_application] => European Procedure (Patents) (EPA) - 17 Janv. 2023 - 23 305 057.4 and PCT/EP2024/050919 on 16/01/2024
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => imaging,transcriptomics
[post_categoryname] => Diagnostic
[parent_category] => 195
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[comteur] => 15
[terms] => Array
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[0] => Diagnostic
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[taxonomie] => Biomarker, Biomarker, Genito Urinary System, Glomerulonephritis, Human POC, Imaging, Target, Transcriptomics
[taxonomieurl] =>
Biomarker,
Biomarker,
Genito Urinary System,
Glomerulonephritis,
Human POC,
Imaging,
Target,
Transcriptomics
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[16] => stdClass Object
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[post_title] => METHODS FOR PROGNOSIS AND MONITORING PULMONARYHYPERTENSION
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-prognosis-and-monitoring-pulmonaryhypertension/
[post_content] => In the present invention, in Pulmonary Arterial Hypertension (PAH) patient/u2019s blood samples (EFFORT cohort), inventors results indicate that activinu2013Smad2/3 signaling is overactive, as reflected by the overabundance of inhibin-u03b2A, inhibin-u03b2B, activin type-I and type-II receptors, and phospho-Smad2/3 in PAH vascular endothelial and smooth muscle cells and by the fact that elevated levels of activin A and follistatin-like 3 (FSTL3) level in serum predict adverse outcome. With an independent external PAH cohort, inventors confirmed that both activin A and FSTL3 are prognostic biomarkers in PAH. Thereafter, this approach allows to identify a BMP/TGF ligands combinations that represent a reliable biomarker of PAH severity and/or mortality, validated in a second independent cohorts of PAH patient (Imperial College of London, UK study) 2-biomarker panel composed of activin A and follistatin-like 3 (FSTL3) that was independently associated with prognosis both at the time of PAH diagnosis and at the first follow-up after PAH therapy initiation. More specifically present invention relates to methods for prognosis and/or monitoring of the severe form of Pulmonary Hypertension (PH) and PAH through comparison of specific markers combinations in PH or PAH patient.
[post_date] => 2024-10-22 17:00:01
[post_modified] => 2024-10-22 17:00:01
[ID] => 8114
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[date_application] => 2022-12-21
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO22307-D1
[keywords] => Pulmonary Arterial Hypertension (PAH), Pulmonary Hypertension (PH), Prognosis, ELISA, Biomarker, follistatin-like 3 (FSTL3)
[pub_scient_inv_dispo] => Circulation, 2023 Jun 13;147(24):1809-1822., Guignabert et al, Serum and Pulmonary Expression Profiles of the Activin Signaling System in Pulmonary Arterial Hypertension, doi: 10.1161/CIRCULATIONAHA.122.061501. Epub 2023 Apr 25.
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => GUIGNABERT Christophe,SITBON Olivier,BOUCLY Athénaïs,TU Ly,HUMBERT Marc,SAVALE Laurent
[number_application] => European Procedure (Patents) (EPA) - 21 Déc. 2022 - 22 306 977.4 and EP22 306 977.4 on 21/12/22 and PCT/EP2023/086809 on 20/12/2023
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
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[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 16
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Cardiovascular Diseases, Human POC, Hypertension/Pulmonary Arterial Hypertension, Immunoassay, Method
[taxonomieurl] =>
Biomarker,
Biomarker,
Cardiovascular Diseases,
Human POC,
Hypertension/Pulmonary Arterial Hypertension,
Immunoassay,
Method
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[post_title] => Non-invasive diagnosis of steatohepatitis based on cytokeratin 18 in asymptomatic patients hospitalized for alcohol withdrawal
[guid] => https://technology-offers.inserm-transfert.com/offer
on-invasive-diagnosis-of-steatohepatitis-based-on-cytokeratin-18-in-asymptomatic-patients-hospitalized-for-alcohol-withdrawal/
[post_content] => The invention relates to the field of diagnosing steatohepatitis, in particular alcoholic steatohepatitis. By following studies on a cohort of nearly 200 patients, the inventors showed that four or five specific, readily available markers, when combined in a function, make it possible, by themselves, to highly accurately diagnose steatohepatitis at the early stages of the disease, when the subject is still asymptomatic. In particular, the invention relates to a non-invasive, highly performant method of diagnosing steatohepatitis in a subject, which combines in a function the values of the age, the blood concentration of cytokeratin 18 and at least two of: the body mass index, the blood concentration of a-2-macroglobulin and a data representative of liver stiffness as obtained by an ex vivo imaging technique. The method of the invention makes it possible to identify asymptomatic patients that may then benefit from potential therapeutics and/or be motivated to reduce alcohol consumption.
[post_date] => 2024-10-22 16:30:02
[post_modified] => 2024-10-22 16:30:02
[ID] => 8113
)
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[application] =>
[idSugar] => f5de2b5c-9090-11ef-b93e-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 2022-11-17
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO21437-D1
[keywords] => Steatohepatitis, CK18, signature, biomarqueur, prevention, diagnosis, prognosisi, treatment response prediction, biomarker
[pub_scient_inv_dispo] => Aliment Pharmacol Ther. 2023 Jul;58(1):80-88. doi: 10.1111/apt.17515. Epub 2023 Apr 20.
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => SAMSON Michel,MOIRAND Romain,CHALIN Arnaud
[number_application] => European Procedure (Patents) (EPA) - 17 Nov. 2022 - 22 306 690.3 and PCT/EP2023/082033 on 16/11/2023
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 17
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Gastrointestinal Diseases, Immunoassay, Liver Disease, Non-Alcoholic Steatohepatitis, Pre-Analytic Validation
[taxonomieurl] =>
Biomarker,
Gastrointestinal Diseases,
Immunoassay,
Liver Disease,
Non-Alcoholic Steatohepatitis,
Pre-Analytic Validation
)
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[post_title] => USE OF THE POPULATION OF SLAMF4+ CCR5+ EFFECTOR MEMORY CD4+ T CELLS AS A BIOMARKER IN RHEUMATOID ARTHRITIS
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-the-population-of-slamf4-ccr5-effector-memory-cd4-t-cells-as-a-biomarker-in-rheumatoid-arthritis/
[post_content] => CD4+ Foxp3- conventional T cells (Tconv) play a key role in the inflammatory process involved in rheumatoid arthritis (RA). It is now becoming increasingly clear that in RA, chronic Tconv stimulation does not induce a sufficient level of exhaustion to inhibit their pathological response. The inventors/u2019 objectives were to determine whether SLAMF receptors are involved in the establishment of the Tconv pro-inflammatory response and whether these receptors represent a protection against Tconv exhaustion. Thus the inventors immunophenotyped blood T cells from RA patients (n=64) and from healthy donors (HD) (n=14) using a 13-marker flow cytometry panel. The expression of SLAMF receptors was determine among four Tconv subpopulations with different activation status (naive, central memory, effector memory and terminally differentiated effector CD4+ T cells). To assess the inflammatory tropism and functionality of different Tconv subpopulations, CCR5 expression was studied. Only the frequency of SLAMF4+ cells among effector memory T cells (Tem; CCR7-, CD45RA-) was correlated with disease activity. More particularly, the inventors showed that only SLAMF4+ Tem expressing CCR5 were linked to RA activity. The inventors revealed that SLAMF4+ CCR5+ Tem represent a distinct Tconv subpopulation resistant to PD-1 mediated inhibition and strongly linked to RA activity.
[post_date] => 2024-10-22 14:45:01
[post_modified] => 2024-10-22 16:45:05
[ID] => 8112
)
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[idSugar] => b82a1e06-9081-11ef-8e81-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 2022-11-14
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO22284-D1
[keywords] => rheumatoid arthritis (RA), Biomarker, Prognosis, Flow Cytometry, SLAMF4
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => BITON Jérôme,BOUZIDI Houda Ghozlane,BESSIS Natacha,LACAUD Mégane,BOISSIER Marie-Christophe
[number_application] => International Procedure (PCT) - 14 Nov. 2022 - PCT/EP2022/081802
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
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[thera_area] => Therapy Area
[type_of_patent] => Type of patent
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[last_name] => Transfert
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[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 18
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Human POC, Immunoassay, Immunology, Method, Rheumatoid Arthritis
[taxonomieurl] =>
Biomarker,
Biomarker,
Human POC,
Immunoassay,
Immunology,
Method,
Rheumatoid Arthritis
)
[19] => stdClass Object
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[post] => stdClass Object
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[post_title] => METHOD FOR DETERMINING THE RELATIVE AGE OF RED BLOOD CELLS
[guid] => https://technology-offers.inserm-transfert.com/offer/method-for-determining-the-relative-age-of-red-blood-cells/
[post_content] => Glycated Hb was measured and compared between five healthy donors (AA), seven non-diabetic and non-transfused homozygous SCD patients (SS) and five non-diabetic, transfused SS patients. The single cell glycation was assessed by flow cytometry using mouse anti-human HbA1c antibody. The inventors demonstrated that glycated Hb was significantly lower in SS patients than in healthy donors (glycated HbS =3.7%, glycated HbA =5.3%, p=0.0025 by DCA and HPLC respectively, and by flow cytometry p=0.0061). In transfused SS patients, results showed that glycated Hb was lower in autologous SS-RBCs than in AA-RBCs by a factor of four (P= 0.008), thus confirming the characterized reduced lifespan of SS RBCs. Glycated Hb levels were measured in RBC sub-populations based on their HbF level (high HbF or low HbF subfractions) in non-transfused SS patients. Single cell glycated Hb assessed by flow cytometry allows to simultaneously estimate the relative age of different RBC sub-populations. This new tool is noninvasive and requires only one single time point measurement.The present invention relates to a method for in vitro determination of the relative age evaluation of subpopulation of red blood cells by using intracellular glycated hemoglobin measurement by flow cytometry.
[post_date] => 2024-10-22 14:20:02
[post_modified] => 2024-10-22 14:20:02
[ID] => 8111
)
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[idSugar] => 70925dc2-907e-11ef-afb9-506b8df7f2c7
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[date_application] => 2022-11-22
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO22218-D1
[keywords] => Diagnostic, Biomarker, Glycated Hb, sickle cell disease (SCD), Flow Cytometry
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => BARTOLUCCI Pablo,DJOUDER Nassima,HEBERT Nicolas
[number_application] => European Procedure (Patents) (EPA) - 03 Nov. 2022 - 22 306 656.4 and PCT/EP2023/080678 on 03/11/2023
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
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[thera_area] => Therapy Area
[type_of_patent] => Type of patent
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[first_name] => Inserm
[last_name] => Transfert
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 19
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Anemia, Biomarker, Biomarker, Hematological Disorders, Human POC, Immunoassay, Method, Sickle Cell Disease
[taxonomieurl] =>
Anemia,
Biomarker,
Biomarker,
Hematological Disorders,
Human POC,
Immunoassay,
Method,
Sickle Cell Disease
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[20] => stdClass Object
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[post] => stdClass Object
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[post_title] => METHOD AND COMPOSITION FOR DETERMINING THE LEVEL OF OGLCNACYLATION IN HORSES
[guid] => https://technology-offers.inserm-transfert.com/offer/method-and-composition-for-determining-the-level-of-oglcnacylation-in-horses/
[post_content] => Inventors have used three cohorts of horses: a cohort consisting of healthy horses (n=20), a cohort consisting of horses hospitalized for colic without signs of sepsis until discharge (n=17) and horses hospitalized for colic with signs of sepsis (n=20). They performed western blot analysis and confirmed the presence of O-GlcNAc in the blood of the horses and showed that, that the O-GlcNAc levels in septic horses tended to decrease between admission and the first day (D1) after admission. This decrease became significant from the second day (D2) of hospitalization. Accordingly, the invention relates to a method for diagnosing whether a horse is at risk of or is susceptible to have a risk of sepsis comprising following steps:i) quantifying the expression level of O-GlcNAcylation in a biological sample obtained from the horse; ii) comparing the expression level quantified at step i) with its predetermined reference value; andiii) concluding that the horse is at risk of or is susceptible to have a risk of sepsis when the expression level of O-GlcNAcylation quantified at step i) is lower than its predetermined reference value.
[post_date] => 2024-10-22 13:55:01
[post_modified] => 2024-10-22 13:55:01
[ID] => 8110
)
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[idSugar] => f339d6b4-907a-11ef-9757-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 2022-10-18
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO22254-R1
[keywords] => Sepsis, O-GlcNacylation, biomarker, Horse, veterinary
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => LAUZIER Benjamin,LEROUX Aurélia,BLANGY-LETHEULE Angélique,DUPAS Thomas
[number_application] => European Procedure (Patents) (EPA) - 18 Oct. 2022 - 22 306 576.4
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Research
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
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[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 20
[terms] => Array
(
[0] => Research
)
[taxonomie] => Infectious Diseases, Research tool, Sepsis / Septic Shock
[taxonomieurl] =>
Infectious Diseases,
Research tool,
Sepsis / Septic Shock
)
[21] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => CD81 AS A BIOMARKER AND BIOTARGET IN T-CELL MALIGNANCIES
[guid] => https://technology-offers.inserm-transfert.com/offer/cd81-as-a-biomarker-and-biotarget-in-t-cell-malignancies/
[post_content] => The present study of the regulatory T phenotype of Sézary cells led to the discovery of the overexpression of CD81 by Sézary cells. CD81 has also been shown to be a relevant therapeutic target in the treatment of Sézary syndrome, NK/T lymphoma, hepatosplenic T-cell lymphoma and acute T cell leukemia. CD81 therefore appears as a diagnostic marker and as a therapeutic target in T-cell malignancies. Accordingly, the present invention relates CD81 as a biomarker and biotarget in T-cell malignancies.
[post_date] => 2024-10-22 13:35:02
[post_modified] => 2024-10-22 13:35:02
[ID] => 8109
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => 97885af4-9078-11ef-ae6c-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 2022-10-12
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO22403-D1
[keywords] => CD81, Flow Cytometry, Sezary syndrome, Cutaneous T cell Lymphoma
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => BENSUSSAN Armand,ORTONNE Nicolas,GIUSTINIANI Jérôme,DE MASSON Adele
[number_application] => European Procedure (Patents) (EPA) - 12 Oct. 2022 - 22 306 545.9 and PCT/EP2023/078198 11/11/2023
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
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[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 21
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Immunoassay, In vitro poc, Lymphoma, Method, Oncology, Sezary syndrome, Target
[taxonomieurl] =>
Biomarker,
Biomarker,
Immunoassay,
In vitro poc,
Lymphoma,
Method,
Oncology,
Sezary syndrome,
Target
)
[22] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => USE OF ALBUMIN ISOFORMS PROFILES FOR THE CHARACTERIZATION OF THE ETIOLOGY AND SEVERITY OF LIVER INJURIES
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-albumin-isoforms-profiles-for-the-characterization-of-the-etiology-and-severity-of-liver-injuries/
[post_content] => The inventors hypothesized that each type of liver injury can be revealed by a specific profile of HSA posttranslational modifications. Therefore, the aim of inventors was to study the pattern of albumin isoforms in rats intoxicated with acetaminophen (APAP), ethanol, and CCl4. The second objective was to explore the potential of these isoforms as biomarkers of liver specific injuries. The results demonstrate that albumin posttranslational modifications (Alb-PTM) occur very early during the course of liver injuries induced by hepatotoxic substances. In 3 animal models, native albumin started to decrease in favor of other isoforms 24 hours after the administration of APAP, ethanol or CCl4. Interestingly, the nature and the intensity of isoforms were different depending on the hepatotoxic substance. In a cohort of cirrhotic patients, the inventors were able to identify up to 14 albumin isoforms, all of which were also present in control patients. However, the inventors observed that the increase in the HSA-DA isoform was specific to patients with cirrhosis due to alcohol abuse, HSA+SGGS and HSA+2Glyc were increased specifically in NASH patients, and HSA-DA+Cys with HSA+SO2H were increased only in patients with the mixed form. In addition, we did not observe a specific isoform able to clearly discriminate the different stages of liver disease, but principal component analysis of the MS dataset perfectly separated cirrhosis patients with different Child-Pugh scores and control patients. The present invention thus relates to the use of albumin isoforms profiles for the characterization of the etiology and severity of liver injuries.
[post_date] => 2024-10-22 10:15:02
[post_modified] => 2024-10-22 10:15:02
[ID] => 8108
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => 1e15b7aa-905c-11ef-b885-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 2022-10-07
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO22116-D1
[keywords] => Liver Injuries, Liver Transplant, NASH, MASH, Mass spectrometry
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => EL BALKHI Souleiman,SAINT-MARCOUX Franck,SAUVAGE François-Ludovic,RAHALI Mohamed-Ali,MARQUET Pierre
[number_application] => European Procedure (Patents) (EPA) - 07 Oct. 2022 - 22 306 513.7
PCT/EP2023/077721 on 06/10/2023
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => mass_spectrometry
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
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[first_name] => Inserm
[last_name] => Transfert
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[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 22
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Gastrointestinal Diseases, Human POC, Liver Disease, Mass spectrometry, Method
[taxonomieurl] =>
Biomarker,
Biomarker,
Gastrointestinal Diseases,
Human POC,
Liver Disease,
Mass spectrometry,
Method
)
[23] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => USE OF AN AGENT CAPABLE OF INHIBITING THE ACTIVATION OF MAIT CELLS FOR THE TREATMENT OF RHEUMATOID ARTHRITIS
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-an-agent-capable-of-inhibiting-the-activation-of-mait-cells-for-the-treatment-of-rheumatoid-arthritis/
[post_content] => Rheumatoid arthritis (RA) is the most common form of inflammatory rheumatism involving small joints which are the seat for swelling and pain with structural damage, responsible for functional disabilities if no treatment is proposed. The inventors show that circulating MAIT cells were reduced and exhibited an activated and anti-apoptotic phenotype in RA patients compared to healthy controls. MAIT cell levels were also found to be increased in the synovial fluid as compared with the peripheral blood, suggesting that circulating MAIT cell deficiency is due to the migration of MAIT cells into the joint. Severity of arthritis induced by mBSA was reduced in mice depleted in MAIT cells. This data suggest that MAIT cells contribute to exacerbation of arthritis. Thus the present invention relates to the use of an agent capable of inhibiting the activation of MAIT cells for the treatment of rheumatoid arthritis.
[post_date] => 2024-10-09 07:45:01
[post_modified] => 2024-10-09 07:45:01
[ID] => 8102
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => f3b78c0a-860f-11ef-a34f-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] =>
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO22036-T1
[keywords] => MAIT cells, rheumatoid arthritis
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http://technology-offers.inserm-transfert.com/wp-content/uploads/BIO22036-T1_Avouac.pdf
[rare_disease] => 0
[second_indication] => 0
[inventors] => AVOUAC Jérôme,LESTURGIE Manon,LEHUEN-MONTEIRO Agnès,GONZALEZ Virginie
[number_application] => European Procedure (Patents) (EPA) - 02 Sept. 2022 - 22 306 303.3
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 23
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] =>
[taxonomieurl] =>
)
[24] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHODS FOR THE TREATMENT OF TH2-MEDIATED DISEASES
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-the-treatment-of-th2-mediated-diseases/
[post_content] => Voltage-dependent calcium channels (Cav1) contribute to T-cell activation. The inventors previously showed that Th2 cells co-express Cav1.2 and Cav1.3 calcium channels acting in a non-redundant and concerted way to initiate early TCR-driven calcium influx required for cytokine production and Th2-cell functions. While they have demonstrated that both channels have to be present on the same T-cell to induce allergic asthma, how these channels are regulated under TCR engagement is yet unknown. They investigated the relationship between PKCu03b1 and the Cav1.2/Cav1.3 duo channels in Th2 cells. They showed that PKC activation was sufficient to trigger Cav1-dependent calcium response and Th2 cytokine production. Cav1 channels, and especially Cav1.3, expression increased at the cell membrane of Th2 cells upon TCR stimulation and PKCu03b1 selectively associated with Cav1.3 upon activation. They showed that PKCu03b1 antisense oligonucleotides (PKCu03b1-AS) decreased Th2-cell functions and were beneficial in active and passive models of Th2-mediated airway inflammation induced by OVA. Altogether these results show that PKCu03b1 by interacting selectively with Cav1.3 after TCR engagement regulates Cav1.2/Cav1.3 duo-dependent calcium signaling and probably by this way impairs Th2-cell functions and their potential to mediate inflammation.
[post_date] => 2024-10-08 16:55:02
[post_modified] => 2024-10-08 16:55:02
[ID] => 8099
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => 22b78b02-774e-11ef-a1f1-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] =>
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO22179-T1
[keywords] => TH2-MEDIATED DISEASES, Voltage-dependent calcium channels, Cav, PKCu03b1
[pub_scient_inv_dispo] => Giang, Nicolas et al. /u201cPKCu03b1 interacts with Cav 1.3 calcium channels to promote the Cav 1.2/Cav 1.3 duo tuning Th2 functions./u201d Allergy vol. 78,3 (2023): 879-882. doi:10.1111/all.15611
[access_to_detailed_offer] => http://technology-offers.inserm-transfert.com/wp-content/uploads/BIO22179-T1_Savignac.pdf
[rare_disease] => 0
[second_indication] => 0
[inventors] => SAVIGNAC Magali,PELLETIER Lucette
[number_application] => European Procedure (Patents) (EPA) - 05 Août 2022 - 22 306 190.4
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 24
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Allergies, Basic research, Drug, Immunology
[taxonomieurl] =>
Allergies,
Basic research,
Drug,
Immunology
)
[25] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => USE OF HIF-1¿ STABILIZING AGENTS FOR THE TREATMENT OF TYPE I INTERFERONOPATHIES
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-hif-1-stabilizing-agents-for-the-treatment-of-type-i-interferonopathies/
[post_content] => Type I interferonopathies represent a subgroup of autoinflammatory diseases caused by mutations in genes associated with proteasome degradation or cytoplasmic RNA- and DNA- sensing pathways. Among them, Aicardi-Goutières syndrome (AGS) ischaracterised by both neurological and extra-neurological involvement with onset in childhood. Chronic inflammation in response to uncontrolled type I IFN production is, among other things, associated with IP-10 secretion. The inventors analysed, at the single-cell transcriptomic levels, peripheral blood samples from patients bearing mutations in three AGS-causing genes, i.e., SAMHD1, RNASEH2B or ADAR1 genes. Using machine-learning approaches and differential gene expression performed on these single-cell data, they identified a drastic loss of transcription factor hypoxia induced factor 1 u03b1 (HIF-1u03b1) expression associated with features of a metabolic switch and mitochondrial stress in monocytes/dendritic cells of patients. Chemical stabilization of HIF-1u03b1, with a synthetic drug (DMOG) in an in vitro model of AGS, allowed the inventors to reverse the energy metabolic switch, attenuate mitochondrial stress and markedly reduce IP-10 production. The inventors therefore propose that inappropriate energy metabolic switch contributes to exacerbated chronic inflammation in AGS, and that targeting this pathway might represent a promising therapeutic approach.
[post_date] => 2024-10-03 16:10:01
[post_modified] => 2024-10-03 16:10:01
[ID] => 8095
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => d486ca54-819f-11ef-8dcd-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] =>
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO23003-T1
[keywords] => Type I interferonopathy, Aicardi-Goutières syndrome,HIF-1u03b1
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http://technology-offers.inserm-transfert.com/wp-content/uploads/BIO23003-T1_Menager.pdf
[rare_disease] => 0
[second_indication] => 0
[inventors] => MENAGER Mickaël,BATIGNES Maxime
[number_application] => European Procedure (Patents) (EPA) - 06 Févr. 2023 - 23 305 153.1
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 25
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Immunology, Inflammation, Target
[taxonomieurl] =>
Immunology,
Inflammation,
Target
)
[26] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHODS FOR THE TREATMENT OF FOOD ALLERGY
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-the-treatment-of-food-allergy/
[post_content] => The incidence of food allergy has dramatically increased over the last three decades in industrialized countries, now affecting more than 200 million people worldwide. Treatment options for food allergy are still limited: lifelong avoidance of the allergen is the main approach, followed by allergen-specific oral immunotherapy, which carries inherent risks. Food allergy occurs when type 2 immune responses are dysregulated, leading to production of allergen- specific IgE, and IgE-mediated mast cell degranulation upon re-exposure to the same allergen. Here, the Inventors demonstrate that dietary fructo-oligosaccharides, which are a major class of FODMAPs, can aggravate food allergic reactions through a mechanism involving formation of AGEs and activation of the receptor RAGE, implying that inhibition of the AGE/AGE pathway represents a potential therapeutic strategy in food allergy.
[post_date] => 2024-10-03 15:25:02
[post_modified] => 2024-10-03 15:25:02
[ID] => 8093
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => 8f4285ec-8199-11ef-9473-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] =>
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO22178-T1
[keywords] => RAGE, AGE, food allergy, FODMAPs
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http://technology-offers.inserm-transfert.com/wp-content/uploads/BIO22178-T1_Reber.pdf
[rare_disease] => 0
[second_indication] => 0
[inventors] => REBER Laurent,KAMPHUIS Jasper
[number_application] => European Procedure (Patents) (EPA) - 08 Mars 2023 - 23 305 306.5
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 26
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Allergies, Drug, Immunology, Product, Target
[taxonomieurl] =>
Allergies,
Drug,
Immunology,
Product,
Target
)
[27] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHODS AND COMPOSITIONS FOR REPARING AIRWAY EPITHELIAL CELL IN FIBROSIS CYSTIC PATIENT
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-compositions-for-reparing-airway-epithelial-cell-in-fibrosis-cystic-patient/
[post_content] => The present invention relates to the treatment of fibrosis cystic. The inventors have demonstrated that specialised pro-resolution lipid mediators (SPMs) regulate tight junction formation and prevent its disruption during Aspergillus fumigatus infection of CF airway epithelial cells. Moreover, they have demonstrated that these SPMs repair the CF airway epithelial cells. Thus, the invention relates to methods and pharmaceutical compositions for the treatment of cystic fibrosis. The present invention also relates to methods and pharmaceutical compositions for treating or preventing Aspergillus fumigatus infection in patient suffering from cystic fibrosis.In cystic fibrosis (CF), impaired mucociliary clearance leads to chronic infection and inflammation. However, cilia beating features in a CF altered environment, consisting of dehydrated airway surface liquid layer and abnormal mucus, have not been fully characterized. Furthermore, acute inflammation is normally followed by an active resolution phase requiring specialized proresolving lipid mediators (SPMs) and allowing return to homeostasis. However, altered SPMs biosynthesis has been reported in CF. Here, we explored cilia beating dynamics in CF airways primary cultures and its response to the SPMs, resolvin E1 (RvE1) and lipoxin B4 (LXB4). Human nasal epithelial cells (hNECs) from CF and non-CF donors were grown at air-liquid interface. The ciliary beat frequency, synchronization, orientation, and density were analyzed from high-speed video microscopy using a multiscale Differential Dynamic Microscopy algorithm and an in-house developed method. Mucins and ASL layer height were studied by qRT-PCR and confocal microscopy. Principal component analysis showed that CF and non-CF hNEC had distinct cilia beating phenotypes, which was mostly explained by differences in cilia beat organization rather than frequency. Exposure to RvE1 (10 nM) and to LXB4 (10 nM) restored a non-CF-like cilia beating phenotype. Furthermore, RvE1 increased the airway surface liquid (ASL) layer height and reduced the mucin MUC5AC thickness. The calcium-activated chloride channel, TMEM16A, was involved in the RvE1 effect on cilia beating, hydration, and mucus. Altogether, our results provide evidence for defective cilia beating in CF airway epithelium and a role of RvE1 and LXB4 to restore the main epithelial functions involved in the mucociliary clearance.
[post_date] => 2024-10-01 16:25:01
[post_modified] => 2024-10-01 16:25:01
[ID] => 8090
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => c8b8f6de-800f-11ef-8d0c-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] =>
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO22248-T1
[keywords] => Cystic fibrosis, SPMs, RvE1, LXB4, Aspergillus fumigatus
[pub_scient_inv_dispo] => Briottet, Maëlle et al. /u201cSpecialized proresolving mediator resolvin E1 corrects the altered cystic fibrosis nasal epithelium cilia beating dynamics./u201d Proceedings of the National Academy of Sciences of the United States of America vol. 121,5 (2024): e2313089121.
[access_to_detailed_offer] => http://technology-offers.inserm-transfert.com/wp-content/uploads/BIO22248-T1_Urbach.pdf
[rare_disease] => 0
[second_indication] => 0
[inventors] => URBACH Valerie,SY Khadeeja Adam,BOTTEREL Françoise
[number_application] => European Procedure (Patents) (EPA) - 07 Juin 2022 - 22 305 824.9
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 27
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Cystic Fibrosis, Drug, Respiratory Disease, Target
[taxonomieurl] =>
Cystic Fibrosis,
Drug,
Respiratory Disease,
Target
)
[28] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHODS AND COMPOSITIONS FOR TREATMENT OF RAC2 MONOGENIC DISORDERS
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-compositions-for-treatment-of-rac2-monogenic-disorders/
[post_content] => A growing number of patients presenting severe combined immunodeficiencies attributed to monoallelic RAC2 variants have been identified. The expression of the RHO GTPase RAC2 is restricted to the hematopoietic lineage. RAC2 variants have been described to cause immunodeficiencies associated with high frequency of infection, leukopenia, and autoinflammatory features. Here, we show that specific RAC2 activating mutations induce the NLRP3 inflammasome activation leading to the secretion of IL-1u03b2 and IL-18 from macrophages. This activation depends on the activation state of the RAC2 variant and is mediated by the downstream kinase PAK1. Inhibiting the RAC2-PAK1-NLRP3 inflammasome pathway might be considered as a potential treatment for these patients.
[post_date] => 2024-10-01 15:15:02
[post_modified] => 2024-10-01 17:15:03
[ID] => 8088
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => b631af7e-8005-11ef-b70d-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] =>
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO22092-T1
[keywords] => Rac2, NLRP3, inflammation, inflammasome
[pub_scient_inv_dispo] => Doye, Anne et al. /u201cRAC2 gain-of-function variants causing inborn error of immunity drive NLRP3 inflammasome activation./u201d The Journal of experimental medicine vol. 221,10 (2024): e20231562. doi:10.1084/jem.20231562
[access_to_detailed_offer] => http://technology-offers.inserm-transfert.com/wp-content/uploads/BIO22092-T1_Boyer.pdf
[rare_disease] => 0
[second_indication] => 0
[inventors] => BOYER (NICE) Laurent
[number_application] =>
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 28
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Immunology, Target
[taxonomieurl] =>
Immunology,
Target
)
[29] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => USE OF LET-7B OR MIR-21 INHIBITORS FOR THE TREATMENT INFLAMMATORY BOWEL DISEASES
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-let-7b-or-mir-21-inhibitors-for-the-treatment-inflammatory-bowel-diseases/
[post_content] => Inflammatory bowel diseases (IBD) etiology is multifactorial. Luminal microRNAs (miRNAs) have been suspected to play a role in the promotion of chronic inflammation, but the extent to which fecal miRNAs are interacting with the intestinal ecosystem in a way that contribute to diseases, including IBD, remains unknown. Here, fecal let-7b and miR-21 were found elevated, associated with inflammation, and correlating with multiple bacteria in IBD patients and IL-10-/- mice, model of spontaneous colitis. Using an in vitro microbiota modeling system, we revealed that these two miRNAs can directly modify the composition and function of complex human microbiota, increasing their proinflammatory potential. In vivo investigations revealed that luminal increase of let-7b drastically alters the intestinal microbiota and enhances macrophagesu2019 associated proinflammatory cytokines (TNF, IL-6, and IL-1u03b2). Such proinflammatory effects are resilient and dependent on the bacterial presence. Moreover, we identified that besides impairing the intestinal barrier function, miR-21 increases myeloperoxidase and antimicrobial peptides secretion, causing intestinal dysbiosis. More importantly, in vivo inhibition of let-7b and miR-21 with anti-miRNAs significantly improved the intestinal mucosal barrier function and promoted a healthier host-microbiota interaction in the intestinal lining, which altogether conferred protection against colitis. In summary, we provide evidence of the functional significance of fecal miRNAs in host-microbiota communication, highlighting their therapeutic potential in intestinal inflammation and dysbiosis-related conditions, such as IBD.
[post_date] => 2024-09-25 16:00:02
[post_modified] => 2024-09-25 16:00:02
[ID] => 8085
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => bc758758-7b54-11ef-a6b2-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] =>
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO22444-T1
[keywords] => Inflammatory bowel disease, IBD, let-7b, miR-21, miRNA
[pub_scient_inv_dispo] => Casado-Bedmar M, Roy M, Berthet L, Hugot JP, Yang C, Manceau H, Peocu2019h K, Chassaing B, Merlin D, Viennois E. Fecal let-7b and miR-21 directly modulate the intestinal microbiota, driving chronic inflammation. Gut Microbes. 2024 Jan-Dec;16(1):2394249. doi: 10.1080/19490976.2024.2394249.
[access_to_detailed_offer] => http://technology-offers.inserm-transfert.com/wp-content/uploads/BIO22444-T1_Viennois.pdf
[rare_disease] => 0
[second_indication] => 0
[inventors] => CASADO BEDMAR Maria Teresa; VIENNOIS Emilie
[number_application] =>
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 29
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Drug, Gastrointestinal Diseases, Inflammatory Bowel Disease / Crohn's Disease, Target
[taxonomieurl] =>
Drug,
Gastrointestinal Diseases,
Inflammatory Bowel Disease / Crohn's Disease,
Target
)
[30] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHODS FOR THE DIAGNOSIS, TREATMENT AND ANALYSIS OFNLRP3-ASSOCIATED AUTOINFLAMMATORY DISEASES
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-the-diagnosis-treatment-and-analysis-ofnlrp3-associated-autoinflammatory-diseases/
[post_content] => NLRP3-associated autoinflammatory disease is a heterogenous group of monogenic conditions caused by NLRP3 gain-of-function mutations. The poor functional characterization of most NLRP3 variants hinders diagnosis despite efficient anti-IL-1 treatments. Additionally, while NLRP3 is controlled by priming and activation signals, gain-of-functions have only been investigated in response to priming. Here, we characterize 34 NLRP3 variants in vitro, evaluating their activity upon induction, priming, and/or activation signals, and their sensitivity to four inhibitors. We highlight the functional diversity of the gain-of-function mutants and describe four groups based on the signals governing their activation, correlating partly with the symptom severity. We identify a new group of NLRP3 mutants responding to the activation signal without priming, associated with frequent misdiagnoses. Our results identify key NLRP3 residues controlling inflammasome activity and sensitivity to inhibitors, and antagonistic mechanisms with broader efficacy for therapeutic strategies. They provide new insights into NLRP3 activation, an explanatory mechanism for NLRP3-AID heterogeneity, and original tools for NLRP3-AID diagnosis and drug development.
[post_date] => 2024-09-25 11:55:01
[post_modified] => 2024-09-25 13:55:03
[ID] => 8083
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => d3139418-7b32-11ef-80b1-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] =>
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO23231-T1
[keywords] => NLRP3, inflammasome, NLRP3-AID
[pub_scient_inv_dispo] => Cosson, Camille et al. /u201cFunctional diversity of NLRP3 gain-of-function mutants associated with CAPS autoinflammation./u201d The Journal of experimental medicine vol. 221,5 (2024): e20231200. doi:10.1084/jem.20231200
[access_to_detailed_offer] => http://technology-offers.inserm-transfert.com/wp-content/uploads/BIO23231-T1_PY.pdf
[rare_disease] => 0
[second_indication] => 0
[inventors] => PY Bénédicte
[number_application] =>
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 30
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Basic research, Biomarker, Drug, Immunology, Target
[taxonomieurl] =>
Basic research,
Biomarker,
Drug,
Immunology,
Target
)
[31] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => USE OF BRANCHED CHAIN FATTY ACIDS (BCFAS) FOR THETREATMENT OF INFLAMMATORY BOWEL DISEASES
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-branched-chain-fatty-acids-bcfas-for-thetreatment-of-inflammatory-bowel-diseases/
[post_content] => The gut microbiota produces a wide variety of metabolites, which interact with intestinal cells by modulating either gene transcription or post-translational modifications of gut proteins. The effect of gut commensal bacteria on SUMOylation, an essential ubiquitin-like modification in intestinal physiology, remains however unknown. Here, the inventors show that branched chain fatty acids (BCFAs) increase protein SUMOylation in different intestinal cell lines. They demonstrated that the hyperSUMOylation induced by BCFAs inhibits the activation of the NF-u03baB pathway by blocking the degradation of the inhibitory factor u0399u03baBu03b1 in response to TNFu03b1. This results in a decrease in pro-inflammatory cytokines expression as well as a decrease in intestinal epithelial permeability in response to TNFu03b1. Accordingly, the present invention relates to the use of Branched Chain Fatty Acids (BCFAs) for the treatment of diseases associated with intestinal inflammation such as Inflammatory Bowel Diseases and Irritable Bowel Syndrome.
[post_date] => 2024-09-20 12:50:01
[post_modified] => 2024-09-20 12:50:01
[ID] => 8066
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => e4143df6-774c-11ef-92f9-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] =>
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO19110-T1
[keywords] => IBD, BCFA, inflammatory bowel disease
[pub_scient_inv_dispo] => Ezzine, Chaima et al. /u201cFatty acids produced by the gut microbiota dampen host inflammatory responses by modulating intestinal SUMOylation./u201d Gut microbes vol. 14,1 (2022): 2108280. doi:10.1080/19490976.2022.2108280
[access_to_detailed_offer] => http://technology-offers.inserm-transfert.com/wp-content/uploads/BIO19110-T1_Ribet.pdf
[rare_disease] => 0
[second_indication] => 0
[inventors] => RIBET David,DECHELOTTE Pierre,EZZINE Chaima
[number_application] => European Procedure (Patents) (EPA) - 31 Août 2021 - 21306182.3
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 31
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Basic research, Concept and/or application formulated, Drug, Gastrointestinal Diseases, Inflammatory Bowel Disease / Crohn's Disease, Target
[taxonomieurl] =>
Basic research,
Concept and/or application formulated,
Drug,
Gastrointestinal Diseases,
Inflammatory Bowel Disease / Crohn's Disease,
Target
)
[32] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHODS AND PHARMACEUTICAL COMPOSITIONS FOR REPAIRING INTESTINAL MUCOSAL
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-pharmaceutical-compositions-for-repairing-intestinal-mucosal/
[post_content] => In the management of patients with inflammatory bowel diseases (IBD), there is a need to identify druggable biological pathways to improve mucosal repair and efficacy of TNF alpha biologics. Based on the VIVA transgenic model of Vnn1 overexpression on intestinal cells, the inventors show that the epithelial pantetheinase Vnn1 has a dual effect on colon: (1) its enzymatic products, cysteamine and pantothenic acid (vitamin B5) enhance coenzyme A regeneration and colon fitness through metabolic rewiring; (2) they favor microbiota-dependent accumulation of butyrate, previously shown to regulate mucosal energetics and to be reduced in IBD patients. Upon dextran sodium sulfate (DSS)-induced colitis, Vnn1 exerts a cytoprotective role on colonocytes and reinforces the mucosal barrier. Remarkably, this global pro-healing phenotype is recapitulated by treating control mice with the substrate (pantethine) or the products of pantetheinase activity prior to exposure to DSS. Therefore, enhancement of vitamin B5-driven metabolism should improve mucosal healing and maintain colon fitness and might enhance the efficacy of anti-inflammatory anti-TNF alpha therapy.
[post_date] => 2024-09-19 14:45:02
[post_modified] => 2024-09-19 14:45:02
[ID] => 8063
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => 0854fa52-7694-11ef-be47-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] =>
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO18084-T1
[keywords] => Inflammatory bowel disease, IBD, Vnn1, vitamin B5, anti-TNF alpha
[pub_scient_inv_dispo] => Millet, Virginie et al. /u201cHarnessing the Vnn1 pantetheinase pathway boosts short chain fatty acids production and mucosal protection in colitis./u201d Gut vol. 72,6 (2023): 1115-1128. doi:10.1136/gutjnl-2021-325792
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => NAQUET Philippe,MILLET Virginie,GALLAND Franck
[number_application] => European Procedure (Patents) (EPA) - 02 Nov. 2021 - 21 306 537.8
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 32
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Drug, Immunology, Inflammation, Target
[taxonomieurl] =>
Drug,
Immunology,
Inflammation,
Target
)
[33] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => Nlrp6 supports diurnal oscillation of host-microbiota interactions through casein kinase 2
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=7440
[post_content] => The present invention relates to the treatment of microbiome dysregulations. Said dysregulations may subsequently contribute to the development of several chronic diseases. Thus characterization of new post-biotic compounds inducing beneficial changes on host-microbiota interactions may be highly desirable. The inventors showed that Nlrp6 diurnally coordinates cyclical adaptation of the gut microbiota diversity to epithelial plasticity in response to a treatment with a Csnk2 inhibitor. The invention therefore relates to an inhibitor of Csnk2, for use in the treatment of microbiome dysregulations notably associated with circadian clock disruption. Said inhibitor may be selected among chemically synthetized or natural selective Csnk2 inhibitors such as flavones.
[post_date] => 2024-09-11 13:44:23
[post_modified] => 2024-09-18 18:25:02
[ID] => 7440
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => 4c9f0ec6-8d37-4f71-b61c-6a4ff803dca9
[etat_fiche_online] => en_ligne
[date_application] => 2016-05-20
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO16079-T1
[keywords] => Nlrp6; Csnk2 inhibitor, Microbiome
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] =>
[number_application] => European Procedure (Patents) (EPA) - 20 Mai 2016 - 16 305 585.8
[technology_engineering] =>
[multidisciplinary_field] => microbiota
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 33
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Basic research, Drug, Immunology, Microbiota, Product, Small Molecule
[taxonomieurl] =>
Basic research,
Drug,
Immunology,
Microbiota,
Product,
Small Molecule
)
[34] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHODS AND PHARMACEUTICAL COMPOSITIONS FOR THE TREATMENT OF SYSTEMIC MASTOCYTOSIS
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-pharmaceutical-compositions-for-the-treatment-of-systemic-mastocytosis/
[post_content] => The present invention relates to methods and pharmaceutical compositions for the treatment of systemic mastocytosis. The inventors showed the effect of KPT-251 treatment on SCF-dependent human Mast cell (MC) line without KIT mutation (WT ROSA) and on two factor-independent MC lines with KIT mutations : ROSA u0394 417-419 insY and ROSA D816V. KPT is a Selective Inhibitor of Nuclear Export (SINE) that specifically inhibits the activity of the exportin-1 (XPO1). KPT-251 treatment induces minimal toxicity in non-cancerous hematopoietic cells both in vitro and in vivo. In particular, the present invention relates a method of treating systemic mastocytosis in patient in need thereof comprising administering to the patient a therapeutically effective amount of a XPO1 inhibitor.
[post_date] => 2024-09-11 13:43:44
[post_modified] => 2024-09-26 15:35:02
[ID] => 7402
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => a27d83b5-c5aa-15d9-8428-5ab8f08c26a2
[etat_fiche_online] => en_ligne
[date_application] => 2016-09-16
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO16342-T1
[keywords] => Systemic mastocytosis, XPO1 inhibitor, exportin-1
[pub_scient_inv_dispo] => Guillem, Flavia et al. /u201cXPO1 regulates erythroid differentiation and is a new target for the treatment of u03b2-thalassemia./u201d Haematologica vol. 105,9 2240-2249. 1 Sep. 2020, doi:10.3324/haematol.2018.210054
[access_to_detailed_offer] => http://technology-offers.inserm-transfert.com/wp-content/uploads/BIO16342-T1_HERMINE.pdf
[rare_disease] => 1
[second_indication] => 0
[inventors] => HERMINE Olivier,DAMAJ Gandhi,LADRAA Sophia,GUILLEM Flavia
[number_application] => European Procedure (Patents) (EPA) - 16 Sept. 2016 - 16 306 181.5
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 34
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Drug, Identification, Immunology, Method, Target
[taxonomieurl] =>
Drug,
Identification,
Immunology,
Method,
Target
)
[35] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => Lymphotoxin alpha regulates the immunosuppressive functions of Regulatory T cells
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=7345
[post_content] => The present invention relates to regulatory T cell and uses thereof. By their immunosuppressive and anti-inflammatory activities, regulatory T cells play a central role in peripheral tolerance and thus critically prevent the development of autoimmune and inflammatory disorders. The inventors showed that Foxp3+CD4+ Tregs express high levels of LT?, which negatively regulates their immunosuppressive signature. They demonstrated that the adoptive transfer of LT?-/- Tregs or the adoptive transfer of Tregs previously incubated with soluble lymphotoxin-? receptor in mice protects from dextran sodium sulfate (DSS)-induced colitis and attenuates inflammatory bowel disease (IBD), multi-organ autoimmunity and the development of CAC. The inventors also showed that by mixed bone marrow chimeras that LT? expression specifically in hematopoietic cells negatively controls the immunosuppressive signature of Tregs. In particular, the present invention relates to a method of treating or preventing autoimmune disorders and inflammatory-associated cancers in a subject in need thereof comprising the step of administrating to the subject a therapeutically effective amount of regulatory T cells which have been previously incubated with effective amount of soluble lymphotoxin-? receptor.
[post_date] => 2024-09-11 13:43:10
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[ID] => 7345
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[post_title] => GSK3B AND USES THEREOF IN THE DIAGNOSTIC AND TREATMENT OF HYPOPIGMENTATION DISORDERS
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=7313
[post_content] => The present invention relates to the identification of the glycogen synthase kinase-3 beta (GSK3B or GSK-3P) as a therapeutic target of pigmentation disorder and as biomarker of pigmentation status. The invention in particular relates to products and methods for treating a hypopigmentation disorder. The invention also relates to products and methods for detecting, diagnosing, staging or monitoring the course of hypopigmentation disorder and is particularly suited for human subjects.
[post_date] => 2024-09-24 11:55:02
[post_modified] => 2024-09-24 11:55:04
[ID] => 7313
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[number_application] => European Procedure (Patents) (EPA) - 18 Déc. 2014 - 14307090.2
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[post_title] => DIAGNOSIS, PROGNOSIS AND TREATMENT OF A DISEASE RELATED TO A DECREASE OF F. PRAUSNITZII
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=7242
[post_content] => The invention relates to a method comprising a step of determining the number, concentration and/or proportion of T lymphocytes with a CD4+ CD8u03b1u03b1low phenotype and further expressing CCR6 and/or CXCR6, for (i) diagnosing, (ii) prognosing outcome of, or (iii) predicting the risk of developing a disease related to a decrease of F. prau. The invention also concerns the treatment of said disease by administering a population of these specific T lymphocytes. The Inventors have indeed identified two markers, CCR6 and CXCR6, enabling to select a population of F. prau-specific cells among CD4+ CD8u03b1u03b1low T lymphocytes, from a blood sample and without needing to assess their F. prauspecificity. T lymphocytes with a CD4+ CD8u03b1u03b1low CCR6+ CXCR6+ phenotype are for example significantly decreased in IBD patients. The disease related to a decrease of F. prauis particularly an inflammatory bowel disease (IBD), such as Crohnu2019s disease.
[post_date] => 2024-09-24 11:35:05
[post_modified] => 2024-09-24 11:35:05
[ID] => 7242
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[keywords] => IBD, inflammatory bowel disease, F. prausnitzii, CCR6
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[inventors] => JOTEREAU Francine,GODEFROY Emmanuelle,SARRABAYROUSE Guillaume,SOKOL Harry,ALTARE Frédéric
[number_application] => European Procedure (Patents) (EPA) - 01 Juin 2018 - 18305677.9
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[post_title] => REGULATORY T CELLS GENETICALLY MODIFIED FOR THE LYMPHOTOXIN ALPHA GENE AND USES THEREOF
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=7232
[post_content] => The present invention relates to regulatory T cell and uses thereof. By their immunosuppressive and anti-inflammatory activities, regulatory T cells play a central role in peripheral tolerance and thus critically prevent the development of autoimmune and inflammatory disorders. The inventors showed that Foxp3+CD4+ Tregs express high levels of LTu03b1, which negatively regulates their immunosuppressive signature. They demonstrated that the adoptive transfer of LTu03b1/u2212//u2212 Tregs in mice protects from dextran sodium sulfate (DSS)-induced colitis and attenuates inflammatory bowel disease (IBD), multi-organ autoimmunity and the development of CAC. The inventors also showed that by mixed bone marrow chimeras that LTu03b1 expression specifically in hematopoietic cells negatively controls the immunosuppressive signature of Tregs. In particular, the present invention relates to regulatory T cell characterized in that it does not express or expresses reduced levels of lymphotoxin alpha.
[post_date] => 2024-09-24 11:20:01
[post_modified] => 2024-09-24 11:20:04
[ID] => 7232
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[pub_scient_inv_dispo] => Borelli, Alexia et al. /u201cLymphotoxin limits Foxp3+ regulatory T cell development from Foxp3lo precursors via IL-4 signaling./u201d Nature communications vol. 15,1 6976. 14 Aug. 2024, doi:10.1038/s41467-024-51164-5
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[rare_disease] => 0
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[inventors] => IRLA Magali
[number_application] => European Procedure (Patents) (EPA) - 14 Nov. 2017 - 17 306 579.8
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[post_categoryname] => Therapeutic
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[taxonomie] => Immunology
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[39] => stdClass Object
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[post_title] => METHODS FOR THE DIAGNOSIS AND TREATMENT OF T CELL-LYMPHOMAS CCR8
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-the-diagnosis-and-treatment-of-t-cell-lymphomas-ccr8-2/
[post_content] => T-cell lymphomas are a heterogeneous group of malignancies involving T lymphocytes and generally characterized by a poor prognosis. Among them, cutaneous T-cell lymphomas involve primarily the skin. Mycosis fungoides and Sézary syndrome are the most frequent cutaneous T-cell lymphomas. The inventors studied the regulatory T phenotype of Sézary cells and showed the expression of CCR8 (CD198) by Sézary cells and other T-cell lymphoma cell lines. CCR8 therefore appears as a useful diagnostic, prognostic and follow-up marker, and as a potential therapeutic target in T-cell lymphomas. Therapeutic depletion of CCR8-expressing cancer cells would eliminate tumor cells and also activate the anti-tumor immunity in T-cell lymphomas.
[post_date] => 2024-08-28 10:25:27
[post_modified] => 2024-09-11 15:45:45
[ID] => 6508
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[date] =>
[bd_referent] => Aymeric EMPEREUR
[bd_referent_id] =>
[contact_email] => aymeric.empereur@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO21120-T1
[keywords] => CTCL; CCR8, Sézary Syndrome
[pub_scient_inv_dispo] => Giustiniani J, Dobos G, Moins-Teisserenc H, Eustaquio T, Battistella M, Ortonne N, Ram-Wolff C, Bouaziz JD, Marie-Cardine A, Mourah S, Bagot M, Kupper TS, Clark RA, Bensussan A, de Masson A. CCR8 is a new therapeutic target in cutaneous T-cell lymphomas. Blood Adv. 2022 Jun 14;6(11):3507-3512. doi: 10.1182/bloodadvances.2021006512. PMID: 35201316; PMCID: PMC9198911.
[access_to_detailed_offer] => http:/
[rare_disease] => false
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[inventors] => BENSUSSAN Armand,DE MASSON Adele,BATTISTELLA Maxime,GIUSTINIANI Jérôme,BAGOT Martine,ORTONNE Nicolas,MARIE-CARDINE Anne
[number_application] => European Procedure (Patents) (EPA) - 23 Mars 2021 - 21 305 356.4
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[post_categoryname] => Therapeutic
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[taxonomie] => Antibody, Biologic, Biomarker, Drug, Lymphoma, Method, Oncology, Protein, Sezary syndrome
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Drug,
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[post_title] => USE OF SPLICE SWITCHING OLIGONUCLEOTIDES FOR EXON SKIPPING-MEDIATED KNOCKDOWN OF PIM2
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-splice-switching-oligonucleotides-for-exon-skipping-mediated-knockdown-of-pim2/
[post_content] => PIM2 kinase deregulation has been reported in several cancers. In particular, PIM2 isconsidered in multiple myeloma as part of the oncogenic process and several PIM kinaseinhibitors have been developed showing encouraging results in preclinical studies and clinical trials. Now the inventors have developed an antisense RNA strategy based on a splice-switching oligonucleotide (SSO) so as to induce efficient knockdown of PIM2 expression. This SSOmediated knockdown is a powerful approach to for cancer treatments. Accordingly, the present invention relates to the use of splice switching oligonucleotides for exon skipping-mediated knockdown of PIM2.
[post_date] => 2024-08-28 10:25:10
[post_modified] => 2024-09-11 15:45:30
[ID] => 6506
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[date] =>
[bd_referent] => Aymeric EMPEREUR
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[reference_online] => BIO21121-T1
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[pub_scient_inv_dispo] => Haas M, Caron G, Chatonnet F, Manenti S, Alaterre E, Devin J, Delaloy C, Bertolin G, Viel R, Pignarre A, Llamas-Gutierrez F, Marchalot A, Decaux O, Tarte K, Delpy L, Moreaux J, Fest T. PIM2 kinase has a pivotal role in plasmablast generation and plasma cell survival, opening up novel treatment options in myeloma. Blood. 2022 Apr 14;139(15):2316-2337. doi: 10.1182/blood.2021014011. PMID: 35108359.
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[inventors] => FEST Thierry,MOREAUX Jérôme,MARCHALOT Anne,LACOMBE Gersende,HAAS Marion,DELPY Laurent
[number_application] => European Procedure (Patents) (EPA) - 19 Avr. 2021 - 21 305 513.0
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[technological_platform] =>
[post_categoryname] => Therapeutic
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[taxonomie] => Drug, Multiple myeloma, Oligonucleotide, Oncology, Target
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[post_title] => ANTI-ROBO4 HUMAN MONOCLONAL ANTIBODIES AND USESTHEREOF FOR THE TREATMENT OF CANCER
[guid] => https://technology-offers.inserm-transfert.com/offer/anti-robo4-human-monoclonal-antibodies-and-usesthereof-for-the-treatment-of-cancer/
[post_content] => There is an interest to develop anti-ROBO4 antibodies that can be suitable for the treatment of cancer. The inventors produced new human antibodies directed against ROBO4 were by aphage display strategy and the antibody selection was performed by using HEK and HEK stably expressing ROBO4 (HEK-ROBO4) cell lines. As a first step, a batch of 6 differentantibodies named D3, H3, H9, E11, H11 and G12 was tested for their binding properties. Theantibodies were then tested for their ability to inhibit the attachment of tumor cells toosteoblastic cells in monolayers. Finally the inventors showed that the anti-ROBO4 antibodies E11 and G12 inhibits significantly the formation of the tumor spheroid. The present invention thus relates to anti-ROBO4 human monoclonal antibodies and uses thereof for the treatment of cancer.
[post_date] => 2024-08-28 10:25:07
[post_modified] => 2024-09-11 15:45:29
[ID] => 6504
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[inventors] => CLEZARDIN Philippe,ECKEL Bénédicte,DIAZ-LATOUD Chantal,CLEMENT-DEMANGE Lise,BERNARD Margaux,CHENTOUF Myriam,ROBERT Bruno,MARTINEAU Pierre
[number_application] => European Procedure (Patents) (EPA) - 16 Févr. 2022 - 22305173.1
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[post_title] => METHOD FOR TREATING CANCER
[guid] => https://technology-offers.inserm-transfert.com/offer/method-for-treating-cancer/
[post_content] => The present invention relates to a method of treating HER2EU overexpressing cancers. The inventors discovered that the heme-mediated formation of dimers and in general oligomers of Trastuzumab is associated with an improved complement-mediated cytotoxicity on breast cancer cells. The present data highlight that the sensitivity to heme of Trastuzumab, may have major repercussion on its therapeutic activity. Thus the invention relates to the combination of an HER2eu antibody with a heme and/or of its oligomers and its therapeutic composition in the HER2EU characteristic cancer treatment.
[post_date] => 2024-08-28 10:25:05
[post_modified] => 2024-09-11 15:45:13
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[date_application] => 10-09-2018
[date] =>
[bd_referent] => Aymeric EMPEREUR
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[contact_email] => aymeric.empereur@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO17187-T1
[keywords] =>
[pub_scient_inv_dispo] =>
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[rare_disease] => false
[second_indication] => false
[inventors] => DIMITROV Jordan,MAREY JAROSSAY Annaelle,LACROIX-DESMAZES Sébastien
[number_application] => European Procedure (Patents) (EPA) - 10 Sept. 2018 - 18 306 187.8
[technology_engineering] =>
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[post_categoryname] => Therapeutic
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[post_title] => TREATMENT OF LIVER CANCERS BY DISRUPTING THE BETA-CATENIN/TCF-4 BINDING SITE LOCATED UPSTREAM OF MEG3 IN THE DLK1/DIO3 LOCUS
[guid] => https://technology-offers.inserm-transfert.com/offer/treatment-of-liver-cancers-by-disrupting-the-beta-catenin-tcf-4-binding-site-located-upstream-of-meg3-in-the-dlk1-dio3-locus/
[post_content] => Activating mutations in CTNNB1 gene encoding u03b2-catenin is encountered in approximately 30% of hepatocellular carcinoma (HCC) and in more than 80% of hepatoblastoma. In Apcu0394hep model, the inventors unravel the biggest cluster of non-coding RNAs identified called the DLK1/DIO3 locus as the most significantly induced region in response to u03b2-catenin activation regarding transcription of coding and non-coding elements. Using in vivo Crispr/cas9 strategy, the inventors were able to demonstrate that u03b2-catenin and its cofactor TCF-4 directly bind on a WRE-containing site located upstream of Meg3 to create an active enhancer regulatory region engaged in chromatin remodeling in the direct vicinity of this binding site but also at distance by long range DNA-DNA contacts to promote transcription of the entire locus. TheseCrispr/cas9 constructs have also proved to be a valuable strategy to impair the locus expression in the murine models mimicking HCC and hepatoblastoma (Apcu0394hep and u03b2-catenin Exon3 tumors) but also in two cell lines with activating mutations in u03b2-catenin encoding gene, the murine Hepa1-6 and human HuH6 cells. In transformed cells, it significantly impaired cell proliferation in vitro and HuH6 stemness capacities but also tumor progression in Hepa1-6 allografts. In mouse models, the locus editing during early steps of tumorigenesis decreased the proliferation of Apcu0394hep preneoplastic hepatocytes but also those of Apcu0394hep and u03b2-catenin Exon3 tumor cell resulting in impairment of tumor size. In conclusion, the results demonstrate that disrupting the-catenin/TCF-4 binding site located upstream of Meg3 in the DLK1/DIO3 locus represents a very interesting approach for the treatment of liver cancers.
[post_date] => 2024-08-28 10:24:59
[post_modified] => 2024-09-11 15:45:32
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[pub_scient_inv_dispo] => Sanceau J, Poupel L, Joubel C, Lagoutte I, Caruso S, Pinto S, Desbois-Mouthon C, Godard C, Hamimi A, Montmory E, Dulary C, Chantalat S, Roehrig A, Muret K, Saint-Pierre B, Deleuze JF, Mouillet-Richard S, Forné T, Grosset CF, Zucman-Rossi J, Colnot S, Gougelet A. DLK1/DIO3 locus upregulation by a u03b2-catenin-dependent enhancer drives cell proliferation and liver tumorigenesis. Mol Ther. 2024 Apr 3;32(4):1125-1143. doi: 10.1016/j.ymthe.2024.01.036. Epub 2024 Feb 3. PMID: 38311851; PMCID: PMC11163201.
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[inventors] => GOUGELET Angélique,POUPEL Lucie,SANCEAU Julie,COLNOT Sabine
[number_application] => European Procedure (Patents) (EPA) - 14 Févr. 2022 - 22 305 162.4
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[post_title] => COMBINATION TREATMENT OF PANCREATIC CANCER
[guid] => https://technology-offers.inserm-transfert.com/offer/combination-treatment-of-pancreatic-cancer/
[post_content] => PI3K signalling is the most increased pathway in human cancers. The four isoforms of PI3K are thought to be activated by different redundant mechanisms leading to a common downstream signalling. The inventors questioned this concept, by mapping differential isoformspecific downstream signalling in response to their constant selective inhibition in pancreatic cancer, a disease currently without therapy. They identified common and specific signals activated by each PI3K isoform. These data make the rational for the development of highly selective PI3K isoform drugs used in combination, instead of compounds inhibiting all PI3Ks. In particular, the inventors showed that combined p110? and p110? inhibition is the most efficient strategy for pancreatic cancer patients.
[post_date] => 2024-08-28 10:24:56
[post_modified] => 2024-09-11 15:45:11
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[inventors] => GUILLERMET-GUIBERT Julie,CINTAS Célia,REICHERT Maximilian
[number_application] => European Procedure (Patents) (EPA) - 13 Oct. 2017 - 17 306 391.8
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[post_title] => A XPO1 inhibitor for the treatment of Myelodysplastic syndromes
[guid] => https://technology-offers.inserm-transfert.com/offer/a-xpo1-inhibitor-for-the-treatment-of-myelodysplastic-syndromes/
[post_content] => The present invention provides methods and pharmaceutical compositions designed to intervene in this defective process and to promote or restore erythrocyte maturation in individuals suffering from a myelodysplastic syndrome. The methods involve maintaining the activity of GATA-1 by preventing sequestration of Hsp70 in the cytoplasm. Accordingly, it is an object of this invention to provide methods of restoring or increasing erythrocyte maturation in a subject suffering from a myelodysplastic syndrome by preventing proteolytic inactivation of GATA-1. In some embodiments, preventing is achieved by administering to the subject a compound that inhibits the XPO1 nuclear transporter.
[post_date] => 2024-08-28 10:24:55
[post_modified] => 2024-09-11 15:45:11
[ID] => 6492
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[inventors] => FONTENAY Michaela,ARLET Jean-benoît,GUILLEM Flavia,COURTOIS Genevieve
[number_application] => European Procedure (Patents) (EPA) - 10 Juin 2014 - 14 305 873.3
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[post_title] => USE OF A L-ASPARAGINASE IN COMBINATION WITH A FERROPTOSIS INDUCER FOR THE TREATMENT OF EXTRANODAL NATURAL KILLER/TCELL LYMPHOMA
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-a-l-asparaginase-in-combination-with-a-ferroptosis-inducer-for-the-treatment-of-extranodal-natural-killer-tcell-lymphoma/
[post_content] => Extranodal natural killer/T-cell lymphoma (ENKTCL) is an aggressive haematological malignancy. The treatment of ENKTCL is dependent on the extent of the tumor. However the use of L-asparaginase-containing regimens obtained impressive outcomes as induction or salvage treatment for ENKTCL. Although more than 70% of early-stage patients can achievelong-term survival, patients with advanced-stage disease had extremely poor prognosis even after asparaginase-based chemotherapy regimens. There is thus a medical need for improving the treatment of ENKTCL with L-asparaginase. Now the inventors demonstrate the interest of the use of L-asparaginase in combination with a ferroptosis inducer for the treatment of ENKTCL. In particular, combination of APR-246 and Erwinase® has synergistic effects in KHYG-1 cells. The present invention thus relates to the use of a L-asparaginase in combination with a ferroptosis inducer for the treatment of ENKTCL.
[post_date] => 2024-08-28 10:24:54
[post_modified] => 2024-09-11 15:45:34
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[keywords] => Combination treatment; ENKTCL; Ferroptosis
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[inventors] => HERMINE Olivier,COURONNE Lucile,SIMONIN Mathieu,ANDRIEU Guillaume,MAROUF Amira,ASNAFI Vahid
[number_application] => European Procedure (Patents) (EPA) - 04 Juil. 2022 - 22 305 993.2
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[taxonomie] => Drug, Lymphoma, Method, Oncology
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[post_title] => EXTRACELLULAR VESICLES FUNCTIONALIZED WITH AN ERV SYNCITIN AND USES THEREOF FOR CARGO DELIVERY
[guid] => https://technology-offers.inserm-transfert.com/offer/extracellular-vesicles-functionalized-with-an-erv-syncitin-and-uses-thereof-for-cargo-delivery/
[post_content] => EVs are being recognized as vectors for drug delivery. In particular, EV loading with targeting and therapeutic agents brings along an interesting opportunity to translate EVs into a biomimetic selective delivery system. Indeed, EVs constitute a physiological carrier being potentially less immunogenic than artificial delivery vehicles. The inventors now developed a novel method to control the loading of a cargo into EVs on demand. These EVs are equipped, if necessary, with non-viral fusogen, therefore enhancing EV-cargo delivery into acceptor cells. To acutely measure this process, they follow the fate of a luciferase-tagged cargo. Cargo loading was enabled through a drug-reversible inducible dimerization system. Briefly, donor cells were transfected with plasmids encoding for FKBP-tagged CD63, a classical membrane EV marker, and FRB-Nanoluciferase (NLuc) that is normally cytosolic. Upon addition of the dimerizing drug, FRB-Nluc interacts with FKBP-CD63 and is recruited into secreted EVs. This is accompanied by an enhanced delivery into acceptor cells. This phenomenon can be further enhanced when EVs are equipped with syncitin1, a mammalian fusogenic protein that trigger fusion between EV membrane and the plasma membrane of acceptor cells. Using this novel process, the inventors further demonstrated that the catalytic domain of the Diphteria toxin (DTA), that is responsible for protein synthesis inhibition and ultimately cell death, can be delivered to acceptor cells via functionalized EVs. This led to protein synthesis inhibition and death of acceptor cells. This novel method and the derived applications promise to open new doors in precision care medicine, especially when EVs will be equipped with antibodies raised against cell specific antigens.
[post_date] => 2024-08-28 10:24:52
[post_modified] => 2024-09-11 15:45:35
[ID] => 6488
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[bd_referent] => Aymeric EMPEREUR
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[reference_online] => BIO22268-T1
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[pub_scient_inv_dispo] => Bui S, Dancourt J, Lavieu G. Virus-Free Method to Control and Enhance Extracellular Vesicle Cargo Loading and Delivery. ACS Appl Bio Mater. 2023 Mar 20;6(3):1081-1091. doi: 10.1021/acsabm.2c00955. Epub 2023 Feb 13. PMID: 36781171; PMCID: PMC10031566.
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[rare_disease] => false
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[inventors] => LAVIEU Grégory,BUI Shéryl,DANCOURT Julia
[number_application] => European Procedure (Patents) (EPA) - 21 Juil. 2022 - 22 306 089.8
[technology_engineering] =>
[multidisciplinary_field] =>
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[post_categoryname] => Therapeutic
[parent_category] => 195
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[contact_email] => contact@inserm-transfert.fr
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[taxonomie] => Biologic, Drug, Method, Oncology
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Oncology
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[post_title] => METHODS FOR CONTROLLING THE TUMOR CELL KILLING BY LIGHT
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-controlling-the-tumor-cell-killing-by-light/
[post_content] => The inventors have developed a new system of optogenetics-based recombinant system allowing to target tumor cells to control in space and time tumor cell lysis by cytotoxic T lymphocytes (CTLs) with light. To do so, they have coupled tumor-specific antigen antibody to a photoreceptor protein that can bind an optogenetic domain linked to a Fab fragment derived from an agonistic antibody targeting the TCR. They demonstrated that these new system allow the spatio-temporal control of the tumor cell killing by CTLs in vitro, in response to light. The present invention relates to methods of activating on demand an immune cell or a plurality of immune cells, and methods for treating cancer.
[post_date] => 2024-08-28 10:24:50
[post_modified] => 2024-09-11 15:45:36
[ID] => 6485
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[pub_scient_inv_dispo] => Jaeger M, Anastasio A, Chamy L, Brustlein S, Vincentelli R, Durbesson F, Gigan J, Thépaut M, Char R, Boussand M, Lechelon M, Argüello RJ, Marguet D, He HT, Lasserre R. Light-inducible T cell engagers trigger, tune, and shape the activation of primary T cells. Proc Natl Acad Sci U S A. 2023 Sep 26;120(39):e2302500120. doi: 10.1073/pnas.2302500120. Epub 2023 Sep 18. PMID: 37722050; PMCID: PMC10523538.
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[inventors] => LASSERRE Remi,JAEGER Morgane
[number_application] => European Procedure (Patents) (EPA) - 14 Avr. 2022 - 22 305 545.0
[technology_engineering] =>
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[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
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Drug,
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Oncology
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[post_title] => Methods and pharmaceutical composition for cancer immunotherapy
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-pharmaceutical-composition-for-cancer-immunotherapy/
[post_content] => The present invention relates to a method for enhancing the potency of an immune checkpoint inhibitor administered to a subject as part of a treatment regimen for cancer, the method comprising: administering a pharmaceutically effective amountof a TNFalpha blocking agent to a subject in combination with the immune checkpoint inhibitor.
[post_date] => 2024-08-28 10:24:49
[post_modified] => 2024-09-11 15:45:08
[ID] => 6483
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[idSugar] => 26ae119e-22e0-41a9-9126-0db92541e8a7
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[date_application] => 28-03-2016
[date] =>
[bd_referent] => Aymeric EMPEREUR
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[contact_email] => aymeric.empereur@inserm-transfert.fr
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[reference_online] => BIO15452-T1
[keywords] => TNF alpha blocking agent, immune checkpoint inhibitor, combination
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => SEGUI Bruno,BERTRAND Florie,ANDRIEU-ABADIE Nathalie,MEYER Nicolas,COLACIOS Céline
[number_application] => European Procedure (Patents) (EPA) - 28 Janv. 2016 - 16 305 085.9
[technology_engineering] =>
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[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[post_title] => METHODS AND PHARMACEUTICAL COMPOSITIONS FOR TREATING CANCER
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-pharmaceutical-compositions-for-treating-cancer/
[post_content] => Tumour-specific molecular targets and alternative therapeutic strategies for triplenegative breast cancer (TNBC) are urgently needed. The protease cathepsin D (cath-D) is aberrantly secreted and a marker of poor prognosis in breast cancer. Using degradomic analyses by TAILS, we discovered that the matricellular protein SPARC is a substrate of extracellular cath-D. In vitro, cath-D induced limited proteolysis of SPARC C-terminal extracellular Ca2+ binding domain at acidic pH, leading to the production of SPARC fragments (34-, 27-, 16-, 9-, and 6-kDa). SPARC cleavage also occurred in vivo in TNBC and mouse mammary tumours.Moreover, the C-terminal 9-kDa SPARC fragment inhibited MDA-MB-231 TNBC celladhesion and spreading on fibronectin, and stimulated their migration, endothelial transmigration and invasion more potently than full-length SPARC. These results highlight a novel crosstalk between proteases and matricellular proteins in the TNBC microenvironment through limited proteolysis of SPARC, and reveal that the 9-kDa C-terminal SPARC fragment is an attractive therapeutic target for TNBC.Thus, the invention relates to an inhibitor of SPARC fragment for use for treating cancer, and in particularly triple cancer negative breast cancer.
[post_date] => 2024-08-28 10:24:47
[post_modified] => 2024-09-11 15:45:42
[ID] => 6480
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[pub_scient_inv_dispo] => Alcaraz LB, Mallavialle A, Mollevi C, Boissière-Michot F, Mansouri H, Simony-Lafontaine J, Laurent-Matha V, Chardès T, Jacot W, Turtoi A, Roger P, Guiu S, Liaudet-Coopman E. SPARC in cancer-associated fibroblasts is an independent poor prognostic factor in non-metastatic triple-negative breast cancer and exhibits pro-tumor activity. Int J Cancer. 2023 Mar 15;152(6):1243-1258. doi: 10.1002/ijc.34345. Epub 2022 Nov 30. PMID: 36346290; PMCID: PMC10099777.
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[inventors] => LIAUDET-COOPMAN Emmanuelle,MALLAVIALLE Aude,ALCARAZ CACCHIA Lindsay
[number_application] => European Procedure (Patents) (EPA) - 21 Oct. 2020 - 20 306 254.2
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[post_title] => COMBINATION FOR TREATING CANCER
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[post_content] => The present invention relates to the treatment of cancer and particularly of lung cancer. In the present study, the inventors analyzed the role of the Notch pathway in EGFR-driven lung adenocarcinoma (LUAD) using complex genetic mouse models and patient derived xenografts. They found that, similarly to KRAS-driven LUAD, EGFR-driven LUAD shows both Notch pathway hyperactivation and addiction to its activity. Importantly, combination of EGFR tyrosine Kinase Inhibitors (TKIs) with Notch inhibition re-sensitizes LUAD cells harboring gatekeeper mutations EGFRT790M or EGFRC797S to gefitinib and osimertinib, respectively. Moreover, they show that pSTAT3, which is known to increase upon EGFR TKI treatment, directly binds to the HES1 promoter and represses HES1 expression. Finally, high HES1 expression levels correlate with shorter progression free survival and its expression increases upon progression in EGFR mutated patients under TKI treatment. Thus, the present invention relates to a combination of a tyrosine-kinase inhibitor (TKI) against epidermal growth factor receptor (EGFR) and an inhibitor of the Notch signalling pathway for use in the treatment of a cancer in a subject in need thereof.
[post_date] => 2024-08-28 10:24:41
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[inventors] => MARAVER Antonio,BOUSQUET Emilie
[number_application] => European Procedure (Patents) (EPA) - 19 Juil. 2018 - 18 305 991.4
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[post_title] => METHODS OF TREATMENT OF CANCER DISEASE BY TARGETING AN EPIGENETIC FACTOR
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[post_content] => The present invention relates to a method for preventing or treating a cancer disease by targeting the epigenetic factor Chromodomain on Y-like 2 (CDYL2). The inventors found that CDYL2 is commonly over-expressed in cancer and high CDYL2 levels correlate with poor prognosis in a number of cancer types even in drug resistant cancer. CDYL2 upregulation in a breast cancer cell line induced migration, invasion, stem-like phenotypes, as well as an epithelial-to-mesenchymal transition (EMT). Due to the importance of EMT and stemness in therapeutic resistance and relapse in cancer, the inventors propose that CDYL2 inhibition will also be beneficial to the treatment of such cancers. Furthermore RNAi inhibition of CDYL2 diminished these same EMT-associated processes in the mesenchymal-like breast cancer cell line. Finally ablating the expression of CDYL2 with RNAi 1) stimulates the expression of genes associated with an anti-tumor immune response (such as gene involved in interferon response) and 2) inhibits lung tumorigenesis in a preclinical model (mouse injected with the triple negative MDA-MB-231 cell line). These results show that CDYL2 as a strong candidate proto-oncogene and therapeutic target in cancer and also contributes to the anti-tumoral immune response escape.
[post_date] => 2024-08-28 10:24:39
[post_modified] => 2024-09-11 15:45:25
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[pub_scient_inv_dispo] => Siouda M, Dujardin AD, Barbollat-Boutrand L, Mendoza-Parra MA, Gibert B, Ouzounova M, Bouaoud J, Tonon L, Robert M, Foy JP, Lavergne V, Manie SN, Viari A, Puisieux A, Ichim G, Gronemeyer H, Saintigny P, Mulligan P. CDYL2 Epigenetically Regulates MIR124 to Control NF-u03baB/STAT3-Dependent Breast Cancer Cell Plasticity. iScience. 2020 Jun 26;23(6):101141. doi: 10.1016/j.isci.2020.101141. Epub 2020 May 6. PMID: 32450513; PMCID: PMC7251929.
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[inventors] => MULLIGAN Peter,SAINTIGNY Pierre,SIOUDA Maha
[number_application] => European Procedure (Patents) (EPA) - 05 Févr. 2020 - 20 305 101.6
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Drug,
Oncology,
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Target,
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[post_title] => ANTI-MÜLLERIAN INHIBITING SUBSTANCE ANTIBODIES AND USES THEREOF
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[post_content] => In ovarian carcinoma, Müllerian Inhibiting Substance (MIS) type II receptor (MISRII) and the MIS/MISRII signaling pathway are potential therapeutic targets. Conversely, the role of the three MIS type I receptors (MISRI; ALK2, ALK3 and ALK6) in this cancer needs to be clarified. Using four ovarian cancer cell lines and ovarian cancer cells isolated from patientsu2019 tumor ascites, the inventors found that ALK2 and ALK3 are the two main MISRIs involved in MIS signaling at low and high MIS concentrations, respectively. Moreover, high MIS concentrations were associated with apoptosis and decreased clonogenic survival, whereas low MIS concentrations improved cancer cell viability. Finally, the inventors showed that anti-MIS antibody B10 inhibited MIS pro-survival effect. These last results open the way to an innovative therapeutic approach to suppress MIS proliferative effect, instead of administering high doses of MIS to induce cancer cell apoptosis.
[post_date] => 2024-08-28 10:24:37
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[pub_scient_inv_dispo] => Chauvin M, Garambois V, Choblet S, Colombo PE, Chentouf M, Gros L, De Brauwere DP, Duonor-Cerutti M, Dumas K, Robert B, Jarlier M, Martineau P, Navarro-Teulon I, Pépin D, Chardès T, Pèlegrin A. Anti-Müllerian hormone concentration regulates activin receptor-like kinase-2/3 expression levels with opposing effects on ovarian cancer cell survival. Int J Oncol. 2021 Jul;59(1):43. doi: 10.3892/ijo.2021.5223. Epub 2021 May 20. PMID: 34013359; PMCID: PMC8131086.
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[inventors] => PELEGRIN André,CHAUVIN Maëva,DI CLEMENTE RENAULD-BESSE Nathalie,MARTINEAU Pierre,CHENTOUF Myriam,ROBERT Bruno
[number_application] => European Procedure (Patents) (EPA) - 27 Sept. 2019 - 19 306 213.0
[technology_engineering] =>
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[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[post_title] => METHOD TO GENERATE IMPROVING CAR-T CELLS
[guid] => https://technology-offers.inserm-transfert.com/offer/method-to-generate-improving-car-t-cells/
[post_content] => The present invention relates to the adoptive therapy using notably CAR-T cells. Herethe inventors used a lentiviral vector approach to silence RINF expression in a shRNA dependent manner and evaluate the consequences of RINF silencing on human CAR-T cells proliferation ex vivo and their functionality and capacity to eradicate tumor cells in vivo. More, the proposed methodology to improve CAR-T cells persistence and efficacy by disrupting RINF/CXXC5 is not restricted to patients suffering from hematological or solid cancers (anti-CD19, anti-EGFR, anti-BCMAu2026) but could be also used to improve the efficacy of ACT in non-cancer diseases by such as lupus (1), cardiac fibrosis (2) or aging related-disorders (3).Thus, the present invention relates to an immune cell characterized in that it is defective for RINF.
[post_date] => 2024-08-28 10:24:37
[post_modified] => 2024-09-11 15:45:24
[ID] => 6465
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[bd_referent] => Aymeric EMPEREUR
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[reference_online] => BIO21116-T1
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[pub_scient_inv_dispo] => Astori A, Matherat G, Munoz I, Gautier EF, Surdez D, Zermati Y, Verdier F, Zaidi S, Feuillet V, Kadi A, Lauret E, Delattre O, Lefèvre C, Fontenay M, Ségal-Bendirdjian E, Dusanter-Fourt I, Bouscary D, Hermine O, Mayeux P, Pendino F. The epigenetic regulator RINF (CXXC5) maintains SMAD7 expression in human immature erythroid cells and sustains red blood cells expansion. Haematologica. 2022 Jan 1;107(1):268-283. doi: 10.3324/haematol.2020.263558. PMID: 33241676; PMCID: PMC8719099.
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[second_indication] => false
[inventors] => PENDINO Frédéric,DONNADIEU Emmanuel,AN Dongjie,FUMAGALLI Mattia
[number_application] => European Procedure (Patents) (EPA) - 07 Oct. 2022 - 22 306 511.1
[technology_engineering] =>
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[post_categoryname] => Therapeutic
[parent_category] => 195
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[post_title] => Bispecific antibody targeting transferrin receptor 1 and soluble antigen
[guid] => https://technology-offers.inserm-transfert.com/offer/bispecific-antibody-targeting-transferrin-receptor-1-and-soluble-antigen/
[post_content] => The invention relates to a bispecific antibody targeting TfR1 and a soluble antigen. The inventors demonstrate that the unique mode of interaction of the bispecific antibody with TfR1 increases its persistence in vivo through an FcRn-like mechanism. It has been demonstrated on MCF7 cell line that the bispecific antibody induces soluble antigen (IL6) uptake through TfR1 mediated endocytosis. Effects of the bispecific antibody on XG6 cell lines viability have been demonstrated, notably on iron and IL-6 deprivation. Hence, the inventors design an improved sweeping antibody which can specifically target tumors and inflammatory cells expressing TfR1. By its unique mode of interaction with TfR1, its ability to induce soluble uptake antigen through TfR1 mediated endocytosis and its capacity to deprive cells of iron, known for being required in tumors growth and progression and development of inflammatory pathologies, the bispecific antibody can be used in the treatment of cancer and inflammatory pathologies.
[post_date] => 2024-08-28 10:24:33
[post_modified] => 2024-09-11 15:45:21
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[pub_scient_inv_dispo] => Neiveyans M, Melhem R, Arnoult C, Bourquard T, Jarlier M, Busson M, Laroche A, Cerutti M, Pugnière M, Ternant D, Gaborit N, Chardès T, Poupon A, Gouilleux-Gruart V, Pèlegrin A, Poul MA. A recycling anti-transferrin receptor-1 monoclonal antibody as an efficient therapy for erythroleukemia through target up-regulation and antibody-dependent cytotoxic effector functions. MAbs. 2019 Apr;11(3):593-605. doi: 10.1080/19420862.2018.1564510. Epub 2019 Feb 18. PMID: 30604643; PMCID: PMC6512944.
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[rare_disease] => false
[second_indication] => false
[inventors] => POUL Marie-Alix,LAROCHE Adrien
[number_application] => European Procedure (Patents) (EPA) - 20 Nov. 2018 - 18 306 524.2
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[post_title] => BAY-1895344 (Elimusertib) from Bayer in adult and pediatric liver cancers
[guid] => https://technology-offers.inserm-transfert.com/offer/bay-1895344-elimusertib-from-bayer-in-adult-and-pediatric-liver-cancers/
[post_content] => Pediatric liver cancers (PLC) are rare tumors. In particular, hepatoblastomas are usually treated with cisplatin-based neoadjuvant chemotherapy followed by surgical removal of the tumor and adjuvant chemotherapy. However, some hepatoblastomas develop resistance to chemotherapy during the initial neoadjuvant chemotherapy or after tumor recurrence, and the molecular determinants of cisplatin resistance are yet to be discovered. In contrast to hepatoblastomas, pediatric HCCs respond poorly to chemotherapy, and as in adults, they have a poor prognosis if not completely removed by surgery. There is thus an urgent need for new therapeutic strategies to overcome this resistance. Now the inventors demonstrate that Elimusertib and Cisplatin combination shows synergistic efficacy on tumor cell viability inhibition in pediatric liver cancer cell lines. The present invention thus relates to the combination of cisplatin and Elimusertib for the treatment of pediatric liver cancers.
[post_date] => 2024-08-28 10:24:30
[post_modified] => 2024-09-11 15:45:18
[ID] => 6456
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[rare_disease] => false
[second_indication] => false
[inventors] => REBOUISSOU Sandra,NAULT Jean-charles,PILET Jill,HIRSCH Théo,ZUCMAN-ROSSI Jessica,MOREL-RIBEIRO Pierre
[number_application] => European Procedure (Patents) (EPA) - 21 Déc. 2021 - 21 306 870.3
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[post_title] => New method for treating melanoma using a TNFalpha blocking agent
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[post_content] => TNF alpha blocking agent for use in the treatment and prevention of melanoma in a subject in whom melanoma cells express MHCI and in whom stroma cells exhibit TNF alpha expression.
[post_date] => 2024-08-28 10:24:26
[post_modified] => 2024-09-11 15:44:59
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[reference_online] => BIO14057-T1
[keywords] => melanoma, TNFalpha inhibitors; MHC1
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[access_to_detailed_offer] => http:/
[rare_disease] => false
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[inventors] => COLACIOS Céline,LEVADE Thierry,ANDRIEU-ABADIE Nathalie,ROCHAIX Philippe,ROCHOTTE Julia,BENOIST Hervé,BERTRAND Florie
[number_application] => European Procedure (Patents) (EPA) - 12 Mai 2014 - 14 305 687.7
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[post_title] => SK2 INHIBITOR FOR THE TREATMENT OF PANCREATIC CANCER
[guid] => https://technology-offers.inserm-transfert.com/offer/sk2-inhibitor-for-the-treatment-of-pancreatic-cancer/
[post_content] => Pancreatic Ductal Adenocarcinoma (PDAC) still represents a therapeutic dead-end. Theinventors report that the K+ channel SK2 is stimulated by secreted cues from cancer-associated fibroblasts (CAF) leading to the activation of an Integrin-EGFR-AKT signaling axis whichparticipates to the acquisition of pro-metastatic features. The inventors show that SK2 acts as a pivotal signaling regulator as being both a direct target of AKT and an amplifier of AKT downstream transduction. The present invention relates to a method of treatment of pancreaticcancer in a patient in need thereof comprising a therapeutically effective amount of SK2inhibitor.
[post_date] => 2024-08-28 10:24:24
[post_modified] => 2024-09-11 15:44:58
[ID] => 6448
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[pub_scient_inv_dispo] => Rapetti-Mauss R, Nigri J, Berenguier C, Finetti P, Tubiana SS, Labrum B, Allegrini B, Pellissier B, Efthymiou G, Hussain Z, Bousquet C, Dusetti N, Bertucci F, Guizouarn H, Melnyk P, Borgese F, Tomasini R, Soriani O. SK2 channels set a signalling hub bolstering CAF-triggered tumourigenic processes in pancreatic cancer. Gut. 2023 Apr;72(4):722-735. doi: 10.1136/gutjnl-2021-326610. Epub 2022 Sep 1. PMID: 36882214.
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[inventors] => SORIANI Olivier,RAPETTI-MAUSS Raphaël,BORGESE Mauro Franck,TOMASINI Richard
[number_application] => European Procedure (Patents) (EPA) - 10 Août 2022 - 22 306 211.8
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[post_title] => SIGMAR1 LIGAND FOR THE TREATMENT OF PANCREATIC CANCER
[guid] => https://technology-offers.inserm-transfert.com/offer/sigmar1-ligand-for-the-treatment-of-pancreatic-cancer/
[post_content] => Here the inventors applied PDAC-derived CAF secretome on pancreatic cancer cellsand evaluated Sig-1R implication in stromal cues integration by PCC from signalingtransmission to biological outcomes, at the cellular and physiological level. They demonstrated that the loss of Sig-1R in epithelial cells inhibits stromal-induced tumor growth and metastatic process. Thus, the inventors demonstrate that Sig-1R is a key actor of the dialog between stromal and cancer cell compartmentsThe present invention relates to method for the treatment of pancreatic cancer in apatient in need thereof comprising a therapeutically effective amount of a Sig-1R ligand
[post_date] => 2024-08-28 10:24:24
[post_modified] => 2024-09-11 15:44:58
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[pub_scient_inv_dispo] => Potier-Cartereau M, Raoul W, Weber G, Mahéo K, Rapetti-Mauss R, Gueguinou M, Buscaglia P, Goupille C, Le Goux N, Abdoul-Azize S, Lecomte T, Fromont G, Chantome A, Mignen O, Soriani O, Vandier C. Potassium and Calcium Channel Complexes as Novel Targets for Cancer Research. Rev Physiol Biochem Pharmacol. 2022;183:157-176. doi: 10.1007/112_2020_24. PMID: 32767122.
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[inventors] => SORIANI Olivier,BORGESE Mauro Franck,RAPETTI-MAUSS Raphaël,TOMASINI Richard,MELNYK Patricia
[number_application] => European Procedure (Patents) (EPA) - 10 Août 2022 - 22 306 212.6
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Oncology,
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Target
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[post_title] => METHODS AND COMPOSITIONS FOR TREATING MELANOMA
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-compositions-for-treating-melanoma-4/
[post_content] => Inventors have shown that targeting DDR1 and DDR2 collagen receptors by Imatinib resensitizes melanoma tumors to BRAFV600E to targeted therapy and normalizes the fibrotic stromal reaction. These findings provide the rationale to combine Imatinib (or other DDR inhibitors) and MAPK-targeting agents to disrupt the influence of the matrix microenvironment in order to delay or prevent the emergence of therapy-resistant cells. They have shown that inhibition of DDR1 and DDR2 kinase activities by Imatinib suppressed the protection of melanoma cells against Vemurafenib (BRAFi) and Trametinib (MEKi) co-drugging and led to cell cycle arrest and cell death. Similar biochemical cell cycle and apoptotic events were promoted in presence of Nilotinib. They validated this anti-tumor activity of Imatinib combined with Vemurafenib in a pre-clinical xenograft model of melanoma. Accordingly, the present invention relates to a method for treating melanoma in a subject in need thereof comprising a step of administering said subject with a therapeutically effective amount of : i) an inhibitor of BRAF, ii) an inhibitor of MEK, and iii) an inhibitor of DDR1/2.
[post_date] => 2024-08-28 10:24:23
[post_modified] => 2024-09-11 15:44:57
[ID] => 6446
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[idSugar] => 4a2b2be8-a311-c19b-de78-5b8015a9e476
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[date_application] => 20-06-2018
[date] =>
[bd_referent] => Aymeric EMPEREUR
[bd_referent_id] =>
[contact_email] => aymeric.empereur@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO18220-T1
[keywords] =>
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => TARTARE-DECKERT Sophie,BERESTJUK Ilona,DECKERT Marcel
[number_application] => European Procedure (Patents) (EPA) - 20 Juin 2018 - 18 305 776.9
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[nickname] => aymeric.empereur@inserm-transfert.fr
[first_name] => Aymeric
[last_name] => Empereur
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[contact_description] =>
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[comteur] => 60
[terms] => Array
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[taxonomie] => Drug, Melanoma, Method, Oncology, Target, Validation in vivo
[taxonomieurl] =>
Drug,
Melanoma,
Method,
Oncology,
Target,
Validation in vivo
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[post_title] => METHODS AND COMPOSITIONS FOR TREATING LUNG CANCER
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-compositions-for-treating-lung-cancer/
[post_content] => Cholesterol efflux pathways have anti-inflammatory and anti-proliferative properties that could be exploited in tumor biology to unravel cancer vulnerabilities. Using a mouse model of lung tumor bearing KRASG12D mutation, the inventors identified that disruption of cholesterol efflux pathways by specific inactivation of Abca1 and Abcg1 in epithelial cancer progenitor cells and to some extent in macrophages promoted a pro-tolerogenic tumor microenvironment (TME). In particular, the inventors show that cholesterol removal therapy with cyclodextrin inhalation also reduced tumor burden in progressing tumor by suppressing the proliferation and expansion of epithelial progenitor cells of tumor-origin. The inventorsu2019 results position cholesterol removal therapy as a putative metabolic target in lung cancer progenitor cells. The presentinvention relates to a method for the treatment of a lung cancer in a patient in need thereof comprising administering to the patient a therapeutically effective amount of cyclodextrin.
[post_date] => 2024-08-28 10:24:21
[post_modified] => 2024-09-11 15:44:56
[ID] => 6442
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[date_application] =>
[date] =>
[bd_referent] => Aymeric EMPEREUR
[bd_referent_id] =>
[contact_email] =>
[contact_phone] =>
[reference_online] => BIO21062-T1
[keywords] =>
[pub_scient_inv_dispo] => Guilbaud E, Barouillet T, Ilie M, Borowczyk C, Ivanov S, Sarrazy V, Vaillant N, Ayrault M, Castiglione A, Rignol G, Brest P, Bazioti V, Zaitsev K, Lebrigand K, Dussaud S, Magnone V, Bertolotto C, Marchetti S, Irondelle M, Goldberg I, Huby T, Westerterp M, Gautier EL, Mari B, Barbry P, Hofman P, Yvan-Charvet L. Cholesterol efflux pathways hinder KRAS-driven lung tumor progenitor cell expansion. Cell Stem Cell. 2023 Jun 1;30(6):800-817.e9. doi: 10.1016/j.stem.2023.05.005. PMID: 37267915.
[access_to_detailed_offer] =>
[rare_disease] => false
[second_indication] => false
[inventors] => YVAN-CHARVET Laurent,ILIE Marius,HOFMAN Paul
[number_application] => European Procedure (Patents) (EPA) - 31 Mai 2023 - 23 305 858.5
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[thera_area] => Therapy Area
[type_of_patent] => Type of patent
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[first_name] => Inserm
[last_name] => Transfert
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 61
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Drug, Lung cancer, Method, Oncology
[taxonomieurl] =>
Drug,
Lung cancer,
Method,
Oncology
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[62] => stdClass Object
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[post_title] => METHODS FOR THE TREATMENT OF ANAPLASTIC LARGE CELL LYMPHOMA
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-the-treatment-of-anaplastic-large-cell-lymphoma/
[post_content] => Anaplastic large cell lymphoma (ALCL) is a rare and aggressive peripheral T-cell lymphomaaffects lymph nodes and extra-nodal sites with characteristic skin lesions. Approximatively half of the tumors express the NPM1-ALK fusion from the translocation t(2;5)(p23;q32). In the present study, the inventors identify ROR2 as progressively up regulated thoughttumorigenesis. Patient samples show a significantly high ROR2 expression (transcriptomicdata) as well as a strong ROR2 protein expression (IHC) with some tumors displaying a clearmembrane signal. ROR2 mRNA expression level is also positively correlated to NPM-ALKexpression level in tumor cells and is not expressed in normal T cells. In addition, ROR2 protein level is significantly increased in resistant cells to the ALK inhibitor, crizotinib, used in clinical trials for children with refractory tumors. This result opens the road to ROR2 specific therapies: ROR2 inhibitors, monoclonal antibodies therapies or even ROR2 specific CAR cells, including for ALCL ALK(+) resistant tumors.
[post_date] => 2024-08-28 10:24:18
[post_modified] => 2024-09-11 15:44:55
[ID] => 6440
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[date_application] =>
[date] =>
[bd_referent] => Aymeric EMPEREUR
[bd_referent_id] =>
[contact_email] => aymeric.empereur@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO21072-T1
[keywords] =>
[pub_scient_inv_dispo] => Babin L, Darchen A, Robert E, Aid Z, Borry R, Soudais C, Piganeau M, De Cian A, Giovannangeli C, Bawa O, Rigaud C, Scoazec JY, Couronné L, Veleanu L, Cieslak A, Asnafi V, Sibon D, Lamant L, Meggetto F, Mercher T, Brunet E. De novo generation of the NPM-ALK fusion recapitulates the pleiotropic phenotypes of ALK+ ALCL pathogenesis and reveals the ROR2 receptor as target for tumor cells. Mol Cancer. 2022 Mar 4;21(1):65. doi: 10.1186/s12943-022-01520-0. PMID: 35246138; PMCID: PMC8895835.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => BRUNET Erika,LAMANT Laurence,MERCHER Thomas,MEGGETTO-PRADELLE Fabienne,BABIN Loélia,DARCHEN Alice,ROBERT Elie
[number_application] => European Procedure (Patents) (EPA) - 09 Avr. 2021 - 21 305 467.9
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[contact_description] =>
[contact_email] =>
[contact_phone] =>
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[comteur] => 62
[terms] => Array
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[taxonomie] => Drug, Lymphoma, Method, Oncology
[taxonomieurl] =>
Drug,
Lymphoma,
Method,
Oncology
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[63] => stdClass Object
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[post_title] => CHIMERIC PROTEINS AND METHODS OF IMMUNOTHERAPY
[guid] => https://technology-offers.inserm-transfert.com/offer/chimeric-proteins-and-methods-of-immunotherapy/
[post_content] => Chimeric proteins for cancer immunotherapy can combine different activities bydisplaying both agonistic and antagonistic properties on a single molecule. However, those usually exhibit toxicities related to their potency being exerted in the entire organism and notonly in tissues relevant for cancer treatment. This may be solved by using appropriatevectorization of the chimeric proteins to the tumour microenvironment, where immune cells interact with tumour cells expressing immunomodulatory molecules.The present invention relates to a nucleic acid encoding a chimeric protein or a chimericprotein having a general structure of: N terminus - (a) - (b) - (c) - C terminus, wherein: (a) is a signaling and/or targeting domain, (b) is a linker (b) is a functional linker and (c) is a signaling and/or targeting domain or N terminus - (c) - (b) - (a) - C terminus, wherein: (c) is a signaling and/or targeting domain, (b) is a linker (b) is a functional linker and (a) is a signaling and/or targeting domain.
[post_date] => 2024-08-27 11:33:07
[post_modified] => 2024-09-11 15:44:54
[ID] => 6433
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[date] =>
[bd_referent] => Aymeric EMPEREUR
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[contact_phone] =>
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[keywords] =>
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => false
[second_indication] => false
[inventors] => BOISGERAULT Nicolas,PETITHOMME Tacien
[number_application] => European Procedure (Patents) (EPA) - 30 Juil. 2021 - 21306069.2
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 63
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Biologic, Drug, Hit - validation in vitro, Oncology, Product, Protein, Recombinant protein
[taxonomieurl] =>
Biologic,
Drug,
Hit - validation in vitro,
Oncology,
Product,
Protein,
Recombinant protein
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[post_title] => METHODS AND COMPOSITIONS FOR TREATING MELANOMA
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=6429
[post_content] => Metastatic uveal melanomas are highly resistant to all existing treatments. Here, a kinome-wide CRISPR-Cas9 knockout screen, revealed that the LKB1-SIK2 module plays a critical role in constraining uveal melanoma cell tumorigenesis. The inventorsu2019 results demonstrate that a combination of SLC8A1 inhibitor and mitochondria-targeted antioxidant has an enhanced cell death efficacy in LKB1 and SIK2-negative uveal melanoma cells. They also designed a LKB1 loss gene signature that is predictive of patient survival and treatment response. Their data thus identify new prognosis markers, and metabolic vulnerability, thereby providing a therapeuticstrategy for these subtypes of metastatic uveal melanomas.The present invention relates to a method for treating melanoma in a subject in need thereof comprising a step of administering said subject with a therapeutically effective amount of a combination of SLC8A1 inhibitor and mitochondria-targeted antioxidant.
[post_date] => 2024-08-27 11:33:04
[post_modified] => 2024-09-11 15:44:52
[ID] => 6429
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[date_application] =>
[date] =>
[bd_referent] => Aymeric EMPEREUR
[bd_referent_id] =>
[contact_email] =>
[contact_phone] =>
[reference_online] => BIO23060-T1
[keywords] =>
[pub_scient_inv_dispo] => Proteau S, Krossa I, Husser C, Guéguinou M, Sella F, Bille K, Irondelle M, Dalmasso M, Barouillet T, Cheli Y, Pisibon C, Arrighi N, Nahon-Estève S, Martel A, Gastaud L, Lassalle S, Mignen O, Brest P, Mazure NM, Bost F, Baillif S, Landreville S, Turcotte S, Hasson D, Carcamo S, Vandier C, Bernstein E, Yvan-Charvet L, Levesque MP, Ballotti R, Bertolotto C, Strub T. LKB1-SIK2 loss drives uveal melanoma proliferation and hypersensitivity to SLC8A1 and ROS inhibition. EMBO Mol Med. 2023 Dec 7;15(12):e17719. doi: 10.15252/emmm.202317719. Epub 2023 Nov 15. PMID: 37966164; PMCID: PMC10701601.
[access_to_detailed_offer] =>
[rare_disease] => false
[second_indication] => false
[inventors] => BERTOLOTTO Corine
[number_application] => European Procedure (Patents) (EPA) - 26 Mai 2023 - 23 305 842.9
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[tags_order_view] => stdClass Object
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[first_name] => Inserm
[last_name] => Transfert
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[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 64
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Drug, Melanoma, Method, Oncology
[taxonomieurl] =>
Drug,
Melanoma,
Method,
Oncology
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[65] => stdClass Object
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[post_title] => METHODS FOR TREATING NOTCH1-DRIVEN CANCERS
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-treating-notch1-driven-cancers/
[post_content] => T-cell acute lymphoblastic leukemias (T-ALL) are aggressive hematological malignancies associated with poor clinical outcome. TP53 alterations (TP53Alt) were rarely identified in TALL at diagnosis and their prognostic impact remains unclear. In a cohort of 476 adults and pediatric T-ALL, TP53Alt were observed in 4% of cases and were associated with chemoresistance and poor prognosis. APR-246, a small compound which restores wild-type configuration to mutated p53, showed efficacy in T-ALL harboring TP53 mutations. More importantly, in TP53 germline T-ALL, Notch1 pathway gain of function mutations were associated with substantial sensitivity to APR-246. Mechanistically, Notch1 activation via p53 downregulation and subsequent ferroptosis induction led to preferential APR-246 sensitivity.Given that Notch1 pathway oncogenic activation is present in more than 70% of T-ALLs, these observations pave the way for promising perspectives in T-ALL treatment which could benefit from the Achilles heel associated with Notch1 activation sensitizing leukemia cells to APR-246-induced ferroptosis, thus extending the use of APR-246 in T-ALL beyond TP53 alterations.
[post_date] => 2024-08-27 11:33:00
[post_modified] => 2024-09-11 15:44:50
[ID] => 6423
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[inventors] => ASNAFI Vahid,SIMONIN Mathieu,HERMINE Olivier
[number_application] => International Procedure (PCT) - 26 Nov. 2021 - PCT/IB2021/000837
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Drug,
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Oncology,
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[post_title] => METHODS FOR THE TREATMENT OF ADULT T-CELL LEUKEMIA/LYMPHOMA
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-the-treatment-of-adult-t-cell-leukemia-lymphoma/
[post_content] => Adult T-cell leukemia/lymphoma (ATL) is an aggressive proliferation of mature activated CD4+ T cells associated with the human T-cell lymphotropic virus type I (HTLV-I). The inventors performed an integrated genomic analysis of a retrospective cohort of 62 ATL patients mainly originating from Africa and the Caribbean area. In particular, they identified a subset of mutations in the TCRF-?B pathway (PLCG1, CARD11, PRKCB, CBLB, IRF4, CSNK1A1, FYN, RHOA, VAV1). Furthermore, the inventors investigated the effects of an anti-CD3 antibody (OKT3) exposure on 4 ATL samples including 2 cases harboring CARD11 and PRKCB gain of function alterations and 2 cases without any TCR pathway mutation. The data suggest that ATL harboring TCR pathway mutations clearly responded to anti-CD3 (Fig. 1B, red + OKT3) and died by apoptosis possibly by a mechanism resembling AICD. Importantly, these TCR-pathwayFKB mutated patients also showed poorer outcome as compared to unmutated cases. Accordingly, the present invention relates to a method of treating adult T-cell leukemia/lymphoma (ATL) in a patient in need thereof comprising administering to the patient a therapeutically effective amount of an anti-CD3 antibody.
[post_date] => 2024-08-27 11:32:58
[post_modified] => 2024-09-11 15:44:50
[ID] => 6422
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[date] =>
[bd_referent] => Aymeric EMPEREUR
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[inventors] => ASNAFI Vahid,GHYSDAEL Jacques,HERMINE Olivier,MARÇAIS Ambroise
[number_application] => European Procedure (Patents) (EPA) - 02 Oct. 2019 - 19 306 263.5
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[terms] => Array
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[taxonomie] => Drug, Leukemias, Method, Oncology, Target
[taxonomieurl] =>
Drug,
Leukemias,
Method,
Oncology,
Target
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[67] => stdClass Object
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[post_title] => Nanoblade technology: High efficiency delivery of CRISPRs components in primary cells by Virus Like Particles.
[guid] => https://technology-offers.inserm-transfert.com/offer
anoblade-technology-high-efficiency-delivery-of-crisprs-components-in-primary-cells-by-virus-like-particles/
[post_content] => The present invention relates to a virus-derived particle comprising one or more Cas protein(s), as well as to kits and methods using the same for altering a target nucleic acid.
[post_date] => 2024-08-27 11:15:14
[post_modified] => 2024-09-11 15:44:44
[ID] => 6412
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[date] =>
[bd_referent] => Elodie ACLOQUE
[bd_referent_id] =>
[contact_email] => Elodie.ACLOQUE@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO15247-T1
[keywords] => CRISPR; Cas9; Virology; Gene editing; Gene therapy
[pub_scient_inv_dispo] => Efficient genome editing in primary cells and in vivo using viral-derived u2019Nanobladesu2019 loaded with Cas9/sgRNA ribonucleoproteins https:/www.biorxiv.org/content/early/2017/10/12/202010
[access_to_detailed_offer] => http:/
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[second_indication] => false
[inventors] =>
[number_application] =>
[technology_engineering] => gene_editing
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[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
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[type_of_patent] => Type of patent
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[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
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[comteur] => 67
[terms] => Array
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[0] => Therapeutic
)
[taxonomie] => Drug, Gene editing, Hit - validation in vitro, Oncology, Others, Product, Product
[taxonomieurl] =>
Drug,
Gene editing,
Hit - validation in vitro,
Oncology,
Others,
Product,
Product
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[68] => stdClass Object
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[post] => stdClass Object
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[post_title] => Exon skipping therapy of Erythropoietic Protoporphyria
[guid] => https://technology-offers.inserm-transfert.com/offer/exon-skipping-therapy-of-erythropoietic-protoporphyria/
[post_content] => The present invention relates to methods and pharmaceutical compositions for the treatment of Erythropoietic Protoporphyria. In particular, the present invention relates to a method for increasing the amount of functional FECH in a erythroid cell carrying the hypomorphic allele IVS3 48C/T (rs2272783) in trans to a deleterious mutation in the FECH gene comprising the step of consisting of bringing the erythroid cell into contact with at least one antisense oligonucletotide (ASO) comprising the sequence 5u2019 gcagcctgagaaatgtttt 3u2019 to prevent splicing of the cryptic exon inserted into the mutant IVS3 48C/T (rs2272783) FECH mRNA.
[post_date] => 2024-08-27 11:14:04
[post_modified] => 2024-09-11 15:40:34
[ID] => 6411
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[idSugar] => 8c75fd78-97b2-40f1-b673-6aeda1fd4c41
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[date_application] => 13-06-2013
[date] =>
[bd_referent] => Elodie ACLOQUE
[bd_referent_id] =>
[contact_email] => Elodie.ACLOQUE@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO12380-T1
[keywords] => Exon Skipping; Erythropoietic Protoporphyria; Orphan Drug Disease, Ferrochelatase
[pub_scient_inv_dispo] => Am J Hum Genet. 2014 Apr 3;94(4):611-7. doi: 10.1016/j.ajhg.2014.02.010. Epub 2014 Mar 27.
[access_to_detailed_offer] => /wp-content/uploads/BIO12380-T1_GOUYA.pdf
[rare_disease] => true
[second_indication] => false
[inventors] => DEYBACH Jean-charles,OUSTRIC Vincent,PUY Hervé
[number_application] => European Procedure (Patents) (EPA) - 13 Juin 2013 - 13 305 796.8
[technology_engineering] => gene_therapy
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
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[type_of_patent] => Type of patent
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[user] => stdClass Object
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 68
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Antisense Oligonucleotide, Drug, Gene therapy, Genetic Disorders, Hit - validation in vitro, Oligonucleotide, Product, Product
[taxonomieurl] =>
Antisense Oligonucleotide,
Drug,
Gene therapy,
Genetic Disorders,
Hit - validation in vitro,
Oligonucleotide,
Product,
Product
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[69] => stdClass Object
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[post] => stdClass Object
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[post_title] => NOVEL MELANOMA ANTIGEN PEPTIDE AND USES THEREOF
[guid] => https://technology-offers.inserm-transfert.com/offer
ovel-melanoma-antigen-peptide-and-uses-thereof/
[post_content] => The invention relates to peptides derived from the MELOE antigen for therapeutic vaccination against cancer. A phase I clinical trial for ex-vivo therapy of melonama is ongoing.
[post_date] => 2024-08-27 11:14:04
[post_modified] => 2024-09-11 15:40:31
[ID] => 6410
)
[post_meta] => stdClass Object
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[application] =>
[idSugar] => 10e34f65-25b2-44b6-9ada-6b8aa6a00e56
[etat_fiche_online] => en_ligne
[date_application] => 22-05-2012
[date] =>
[bd_referent] => Elodie ACLOQUE
[bd_referent_id] =>
[contact_email] => Elodie.ACLOQUE@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO12113-T1
[keywords] => MELOE, antigen, cancer, melanoma, TIL, vaccination
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => ROGEL Anne,LANG François,BOBINET Mathilde
[number_application] => International Procedure (PCT) - 22 Mai 2012 - PCT/IB2012/001310
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
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[type_of_patent] => Type of patent
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[user] => stdClass Object
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[author] => 1
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[wp_user_level] => 2
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 69
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Biologic, Cell therapy, Clinical Trial, Drug, Melanoma, Oncology, Phase 1, Product
[taxonomieurl] =>
Biologic,
Cell therapy,
Clinical Trial,
Drug,
Melanoma,
Oncology,
Phase 1,
Product
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[70] => stdClass Object
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[post] => stdClass Object
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[post_title] => Hydrophobically modified Antisense Oligonucleotides comprising a cetal group or a triple alkyl chain to improve intracellular delivery and efficacy of antisense oligonucleiotide
[guid] => https://technology-offers.inserm-transfert.com/offer/hydrophobically-modified-antisense-oligonucleotides-comprising-a-cetal-group-or-a-triple-alkyl-chain-to-improve-intracellular-delivery-and-efficacy-of-antisense-oligonucleiotide/
[post_content] => The present invention concerns an oligonucleotide modified by substitution at the 3u2019 or the 5u2019 end by at least triple alkyl chain or at least one ketal functional group, wherein the ketal carbon bears two hydrocarbon chains. The invention also concerns the use of the hydrophobically modified oligonucleotides as a medicament, in particular for use for treating cancer. The autors show lipid conjugate Antisense Oligonucleotide (L-ASO) are capable of inhibiting prostate cancer in vivo and have no toxicity in mice (Karaki S et al. 2017 J Control Release, 258:1-9). The addition of a lipid chain on the 5u2019 part of the antisense oligonucleotide enables inhibiting specifically u201cUD proteinu201d, even in the absence of the transfection agent. The lipid modification strongly enhances the ability of ASO to reduce u201cUD proteinu201d expression leading to a strong reduction of tumor progression in a murin xenograft model of Castration Resistant prostate cancer. The L-ASO have been validated in others therapeutic indications. These modifications allow advantages over standard ASO: 1/ Delivery enhancement, Stability, biodisponibility; 2/ Internalisation without any transfection agents; 3/ Encapsulation of different molecules like chemotherapies (L-ASOs self-assembly give sphericals nanoparticles, which are prone to host drug molecules within their hydrophobic cores: for instance Paclitaxel).
[post_date] => 2024-08-27 11:14:03
[post_modified] => 2024-09-11 15:40:29
[ID] => 6409
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => 9feb2cd5-4695-4988-8688-b1305f763336
[etat_fiche_online] => en_ligne
[date_application] => 05-06-2013
[date] =>
[bd_referent] => Elodie ACLOQUE
[bd_referent_id] =>
[contact_email] => Elodie.ACLOQUE@inserm-transfert.fr
[contact_phone] =>
[reference_online] => CHIM13035-T1
[keywords] => Nucleic acids, Antisense, Oligonuceotides; Encapsulation; Nanoparticles.
[pub_scient_inv_dispo] => J Control Release. 2017 Jul 28;258:1-9. doi: 10.1016/j.jconrel.2017.04.042. Epub 2017 May 1.Bioconjug Chem. 2013 Aug 21;24(8):1345-55.Chem Soc Rev. 2011 Dec;40(12):5844-54. doi: 10.1039/c1cs15038c. Epub 2011 May 24.
[access_to_detailed_offer] => /wp-content/uploads/CHIM13035-T1_BARTHELEMY.pdf
[rare_disease] => false
[second_indication] => false
[inventors] => ACUNZO Julie,OUMZIL Khalid,GISSOT Arnaud,ROCCHI Palma
[number_application] => International Procedure (PCT) - 05 Juin 2013 - PCT/IB2013/001516
[technology_engineering] => drug_delivery
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
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[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
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[user] => stdClass Object
(
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[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
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[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 70
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Antisense Oligonucleotide, Drug, Drug delivery, Hit - validation in vivo, Oligonucleotide, Oncology, Product, Product, Prostate Cancer
[taxonomieurl] =>
Antisense Oligonucleotide,
Drug,
Drug delivery,
Hit - validation in vivo,
Oligonucleotide,
Oncology,
Product,
Product,
Prostate Cancer
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[71] => stdClass Object
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[post] => stdClass Object
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[post_title] => Novel target and mAb candidates for the treatment of HCMV infection
[guid] => https://technology-offers.inserm-transfert.com/offer
ovel-target-and-mab-candidates-for-the-treatment-of-hcmv-infection/
[post_content] => The present invention relates to a method for treating an infection, particularly HCMV infection. To date, there are very few reports on the role of DC-SIGN+ dendritic cells in very early phases of viral infections. By using four anti-human DC-SIGN monoclonal antibodies, the inventors have demonstrated that DC-SIGN might be considered as the most important receptor for both pre- and post-fusion HCMV gB on monocyte-derived dendritic cells (MDDCs). In particular, the invention relates to a method for treating an infection in a subject in need thereof comprising a step of administering to said subject an agent that blocks the interaction between DC-SIGN and an infectious ligand.
[post_date] => 2024-08-27 11:14:02
[post_modified] => 2024-09-11 15:40:20
[ID] => 6408
)
[post_meta] => stdClass Object
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[application] =>
[idSugar] => a4c4fde4-5d4b-4ed4-a90e-76b7676c4c5d
[etat_fiche_online] => en_ligne
[date_application] => 23-01-2017
[date] =>
[bd_referent] => Elodie ACLOQUE
[bd_referent_id] =>
[contact_email] => Elodie.ACLOQUE@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO16304-T1
[keywords] => Infectious Diseases, Antivirals, HCMV, DC-SIGN
[pub_scient_inv_dispo] => Org Biomol Chem. 2017 Sep 20;15(36):7660-7671. doi: 10.1039/c7ob01569k.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => HALARY Franck,PIN Jean-Jacques,RAZANAJAONA-DOLL Diane
[number_application] => European Procedure (Patents) (EPA) - 23 Janv. 2017 - 17305064.2
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
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[user] => stdClass Object
(
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[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
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[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 71
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Antibody, Biologic, Drug, Infectious Diseases, Lead - validation in vivo, Product, Product, Protein
[taxonomieurl] =>
Antibody,
Biologic,
Drug,
Infectious Diseases,
Lead - validation in vivo,
Product,
Product,
Protein
)
[72] => stdClass Object
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[post] => stdClass Object
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[post_title] => Improved vector for driving the targeted integration of a transgene into an eukaryotic genome.
[guid] => https://technology-offers.inserm-transfert.com/offer/improved-vector-for-driving-the-targeted-integration-of-a-transgene-into-an-eukaryotic-genome/
[post_content] => The present invention relates to polypeptide for engineering integrase chimeric proteins and their use in gene therapy. A key challenge for gene transfer based on the use of retroviral vectors is to achieve stable transgene expression while minimizing insertional mutagenesis and induction of the DNA damage response due to the presence of double stranded DNA. One approach to avoid insertional mutagenesis is to target the transgene integration to a specific location on the genome.Here autors describe an interaction between Ty1 integrase and the AC40 subunit of Pol III and demonstrate that AC40 is the predominant determinant targeting Ty1 integration upstream of Pol IIIu2013transcribed genes. Lack of an integrase-AC40 interaction dramatically alters target site choice, leading to a redistribution of Ty1 insertions in the genome, mainly to chromosome ends. The mechanism of target specificity allows Ty1 to proliferate and yet minimizes genetic damage to its host. Accordingly, the domain of Ty1 responsible for the interaction with the RNA polymerase III is suitable to engineering integrase of retrovirus so as to drive the targeted integration of a transgene into a eukaryotic genome.
[post_date] => 2024-08-27 11:14:01
[post_modified] => 2024-09-11 15:42:48
[ID] => 6407
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => cc69e496-7878-4ba2-8f9f-a0c91cc90782
[etat_fiche_online] => en_ligne
[date_application] => 13-02-2015
[date] =>
[bd_referent] => Elodie ACLOQUE
[bd_referent_id] =>
[contact_email] => Elodie.ACLOQUE@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO15039-T1
[keywords] => polypeptide, retroviral vector, integrase, Ty1, AC40, retrotransposon, insertional mutagenesis
[pub_scient_inv_dispo] => Science. 2015 May 1;348(6234):585-8. doi: 10.1126/science.1259114.
[access_to_detailed_offer] => /wp-content/uploads/BIO15039-T1_LESAGE.pdf
[rare_disease] => false
[second_indication] => false
[inventors] => BRIDIER-NAHMIAS Antoine,WERNER Michel
[number_application] => European Procedure (Patents) (EPA) - 13 Févr. 2015 - 15305217.0
[technology_engineering] => gene_therapy
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
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[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 72
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Biologic, Drug, Gene Therapy, Gene therapy, Hit - validation in vitro, Others, Product, Product
[taxonomieurl] =>
Biologic,
Drug,
Gene Therapy,
Gene therapy,
Hit - validation in vitro,
Others,
Product,
Product
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[post_title] => Nanoparticle based glue, Biocompatible sealant for surgery
[guid] => https://technology-offers.inserm-transfert.com/offer
anoparticle-based-glue-biocompatible-sealant-for-surgery/
[post_content] => The present invention relates to methods for adhering tissue surfaces and materials and biomedical uses thereof. In particular the present invention relates to a method for adhering a first tissue surface to a second tissue surface in a subject in need thereof, comprising the steps of adsorbing a layer of nanoparticles on at least one of the tissue surfaces, and approximating the surfaces for a time sufficient for allowing the surfaces to adhere to each other. The present invention also relates to a method for adhering a material to a biological tissue in a subject in need thereof, comprising the steps of adsorbing a layer of nanoparticles on the surface of the material and/or the biological tissue and approximating the material and the biological tissue for a time sufficient for allowing the material and the biological tissue to adhere to each other.Inventors demonstrated that rapid and strong adhesion by aqueous solutions of nanoparticles can be advantageously used in very different clinical situations. For skin wounds a remarkable aesthetic healing was obtained and repair procedure does not require any specific preparation or training. Bleeding control and tissue repair by nanobridging shown here in the case of liver could be used on spleen, kidney, heart, and lungs surgeries. When tight sealing is needed nanobridging could complement anastomosis and classical suturing protocols. The possibility of securing medical devices could open new applications in repair and regenerative medicine. From chemistry standpoint, the principle illustrated here has used silica and iron oxide nanoparticles but not limited to these nanoparticle and they are many possible choices of sizes, forms and surface chemistries. In particular, nanoparticles with intrinsic biological effects such as silver nanoparticles for skin infection or drug delivery systems could provide useful options. Translation to clinical practice will require careful safety and toxicity investigations. A better understanding of biological mechanisms of the adhesion by nanobridging will guide the design of future-generation tissue adhesives.
[post_date] => 2024-08-27 11:14:01
[post_modified] => 2024-09-11 15:42:46
[ID] => 6406
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[date] =>
[bd_referent] => Elodie ACLOQUE
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[contact_email] => Elodie.ACLOQUE@inserm-transfert.fr
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[reference_online] => BIO13377-T1
[keywords] => Nanoparticles; Biomaterials; Regenerative medecine; skin wounds; tissue repair; Bleeding control; tight sealing; liver surgeries; spleen surgeries, kidney surgeries, heart surgeries, lungs surgeries
[pub_scient_inv_dispo] => Angew Chem Int Ed Engl. 2014 Jun 16;53(25):6369-73. doi: 10.1002/anie.201401043. Epub 2014 Apr 16.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => MARCELLAN Alba,LEIBLER Ludwik,PELLE Anne
[number_application] => European Procedure (Patents) (EPA) - 10 Déc. 2013 - 13 306 692.8
[technology_engineering] => biomaterials
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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)
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[terms] => Array
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[taxonomie] => Biomaterials, Drug, Hit - validation in vivo, Others, Polymer, Product, Product
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Biomaterials,
Drug,
Hit - validation in vivo,
Others,
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Product,
Product
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[post_title] => Ex vivo gene therapy based vaccine with nucleic acid molecule encoding for CD70 for the treatment of B-cell malignancies
[guid] => https://technology-offers.inserm-transfert.com/offer/ex-vivo-gene-therapy-based-vaccine-with-nucleic-acid-molecule-encoding-for-cd70-for-the-treatment-of-b-cell-malignancies/
[post_content] => The present invention relates to a method of treating a B-cell malignancy in a subject using a vaccine composition comprising a population of malignant B cells from said subject transformed with a nucleic acid molecule encoding for a CD70 polypeptide.Epstein-Barr virus (EBV) infection in humans is a major trigger of malignant and non-malignant B cell proliferations. The inventors showed that EBV-specific T lymphocytes cannot expand properly when stimulated with CD70-deficient EBV-infected cells, while expression of CD70 restores expansion. In particular, the present invention relates to a method of treating a B-cell malignancy in a subject in need thereof comprising i) providing a sample of malignant B cells obtained from the subject ii) isolating and culturing a population of malignant B cells from the sample of step i), iii) introducing in the population malignant B cells of step ii) a nucleic acid molecule encoding for a CD70 polypeptide and iv) administering to the subject a therapeutically effective amount of the population of malignant B cells of step iii).
[post_date] => 2024-08-27 11:14:00
[post_modified] => 2024-09-11 15:42:42
[ID] => 6405
)
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[date_application] => 22-04-2016
[date] =>
[bd_referent] => Elodie ACLOQUE
[bd_referent_id] =>
[contact_email] => Elodie.ACLOQUE@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO16135-T1
[keywords] => B-malignancies, CD70, CD27, cell therapy ,B leukemia, lymphoma, Epstein-Barr virus, Vaccine, ex vivo gene therapy
[pub_scient_inv_dispo] => J Exp Med. 2017 Jan;214(1):73-89. doi: 10.1084/jem.20160784. Epub 2016 Dec 23.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => FISCHER Alain,IZAWA Kazushi,MARTIN (INSERM) Emmanuel
[number_application] => European Procedure (Patents) (EPA) - 22 Avr. 2016 - 16 305 471.1
[technology_engineering] => gene_therapy
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 74
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Burkitt Lymphoma, Drug, Gene therapy, Lymphoma, Method, Oligonucleotide, Oncology, Target, Validation in vitro
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Burkitt Lymphoma,
Drug,
Gene therapy,
Lymphoma,
Method,
Oligonucleotide,
Oncology,
Target,
Validation in vitro
)
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[post] => stdClass Object
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[post_title] => CtIP fusion to Cas9 enhances transgene integration by homology-dependent repair
[guid] => https://technology-offers.inserm-transfert.com/offer/ctip-fusion-to-cas9-enhances-transgene-integration-by-homology-dependent-repair-2/
[post_content] => The present invention relates to nuclease protein fusions for enhancing genome editing by homology-directed transgene integration (HDI).The inventors found that the rate of HDI mediated by the CRISPR/Cas9 system may be substantially improved by providing the Cas9 nuclease in the form of a fusion protein with at least the N-terminal domain of the CtIP protein. CtIP proteins are involved in the early steps of homologous recombination. In addition, the inventors identified the subdomains of the N-terminal domain of the CtIP protein that are important for improving the HDI rate.Thus, the invention relates to fusion proteins comprising a Cas9 protein, a tetramerization domain of a CtIP protein and a dimerization domain of a CtIP protein. Particularly, the inventors have tested these fusion proteins HEK293 cells, RG37DR cells and Sprague-Dawley rats.
[post_date] => 2024-08-27 11:13:59
[post_modified] => 2024-09-11 15:42:38
[ID] => 6404
)
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[application] =>
[idSugar] => 74038319-c062-4172-871e-71068b58c043
[etat_fiche_online] => en_ligne
[date_application] => 09-03-2018
[date] =>
[bd_referent] => Elodie ACLOQUE
[bd_referent_id] =>
[contact_email] => Elodie.ACLOQUE@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO16366-T1
[keywords] => Genome editing, homologuous recombinant integration
[pub_scient_inv_dispo] => Nat Commun. 2018 Mar 19;9(1):1133. doi: 10.1038/s41467-018-03475-7.
[access_to_detailed_offer] => /wp-content/uploads/BIO16366-T1_CONCORDET.pdf
[rare_disease] => false
[second_indication] => false
[inventors] => CONCORDET Jean-Paul,ANEGON Ignacio,LOPEZ Bernard,GIOVANNANGELI Carine,CHARPENTIER Marine
[number_application] => European Procedure (Patents) (EPA) - 10 Mars 2017 - 17 305 260.6
[technology_engineering] => gene_editing
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
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[first_name] => Inserm
[last_name] => Transfert
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(
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)
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 75
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Drug, Gene editing, Lead - validation in vitro, Oligonucleotide, Others, Product, Product
[taxonomieurl] =>
Drug,
Gene editing,
Lead - validation in vitro,
Oligonucleotide,
Others,
Product,
Product
)
[76] => stdClass Object
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[post] => stdClass Object
(
[post_title] => MitoCeption: novel method for the intracellular transfer of isolated mitochondria in recipient cells
[guid] => https://technology-offers.inserm-transfert.com/offer/mitoception-novel-method-for-the-intracellular-transfer-of-isolated-mitochondria-in-recipient-cells/
[post_content] => The present invention relates to a method for the intercellular transfer of an amount of mitochondria isolated from a population of donor cells into a population of recipient cells.Mitochondria activity is central to cell and tissue homeostasis. Mitochondrial dysfunction and the energy metabolism reprogramming it induces are the hallmarks of many genetic diseases. They also play a key role in tumor progression and resistance to therapy. These essential roles of mitochondria, added to their recently documented cell-cell transfer capacity, explain the current burst of interest they trigger. Here a methodology (MitoCeption) that allows the quantitative transfer of mitochondria, isolated from cell type A, to cell type B is described. Autors validated and quantified the effective mitochondria transfer on different cell types, by confocal imaging and flow cytometry.
[post_date] => 2024-08-27 11:13:52
[post_modified] => 2024-09-11 15:41:53
[ID] => 6403
)
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[idSugar] => 2daa9dcb-41b6-4c97-83c9-faa8417b4241
[etat_fiche_online] => en_ligne
[date_application] => 16-07-2014
[date] =>
[bd_referent] => Elodie ACLOQUE
[bd_referent_id] =>
[contact_email] => Elodie.ACLOQUE@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO12385-T1
[keywords] => Mesenchymal Steml Cell, Mesenchymal Stroma Cell, mitochondria transfers, tumor, intercellular, MitoCeption
[pub_scient_inv_dispo] => Sci Rep. 2015 Mar 13;5:9073. doi: 10.1038/srep09073.J Vis Exp. 2017 Feb 22;(120). doi: 10.3791/55245.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] =>
[number_application] =>
[technology_engineering] => cell_therapy
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
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[first_name] => Inserm
[last_name] => Transfert
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(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 76
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Biologic, Cell therapy, Cell therapy, Drug, Method, Oncology
[taxonomieurl] =>
Biologic,
Cell therapy,
Cell therapy,
Drug,
Method,
Oncology
)
[77] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => CDC25A phosphatase inhibitor for use in thetreatment of a drug resistant cancer and/or in the prevention of tumor relapse
[guid] => https://technology-offers.inserm-transfert.com/offer/cdc25a-phosphatase-inhibitor-for-use-in-thetreatment-of-a-drug-resistant-cancer-and-or-in-the-prevention-of-tumor-relapse/
[post_content] => The invention relates to a CDC25A phosphatase inhibitor for use in the treatment of drug resistant cancer or for use in the prevention of tumor relapse in a patient suffering or having suffered from cancer.In a preferred embodiment, the drug resistant cancer according to the invention is associated with a mutated FLT3-ITD such as Acute Myeloid Leukemia (AML).Autors demonstrate that inhibiting CDC25A reduces proliferation and induces monocytic differentiation of FLT3-ITD-positive AML cells in vitro and in vivo, and they argue for a central function of this phosphatase in the hematopoieticdifferentiation arrest of these cells.
[post_date] => 2024-08-27 11:13:46
[post_modified] => 2024-09-11 15:41:39
[ID] => 6402
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => 65442075-db31-4991-a3e0-f273f1332f95
[etat_fiche_online] => en_ligne
[date_application] => 24-09-2014
[date] =>
[bd_referent] => Elodie ACLOQUE
[bd_referent_id] =>
[contact_email] => Elodie.ACLOQUE@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO14117-T1
[keywords] => CDC25A phosphatase inhibitor, AML, FLT3-ITD, antisense oligonucleotide
[pub_scient_inv_dispo] => Oncotarget. 2015 Nov 10;6(35):38061-78. doi: 10.18632/oncotarget.5706.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => BERTOLI Sarah
[number_application] => European Procedure (Patents) (EPA) - 26 Sept. 2014 - 14 306 492.1
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
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)
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[role] => member
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[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 77
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Acute Myelocytic Leukemia (AML), Drug, Leukemias, Oncology, Target, Target, Validation in vivo
[taxonomieurl] =>
Acute Myelocytic Leukemia (AML),
Drug,
Leukemias,
Oncology,
Target,
Target,
Validation in vivo
)
[78] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => Pharmacologically Active Microcarriers for efficient integration of transplanted cells in the host tissue
[guid] => https://technology-offers.inserm-transfert.com/offer/pharmacologically-active-microcarriers-for-efficient-integration-of-transplanted-cells-in-the-host-tissue/
[post_content] => This invention results from Pharmacologically Active Microcarriers (PAM) which are based on a biocompatible and biodegradable material. These particles made with poly(D,L-lactic-coglycolic acid) (PLGA) and coated with adhesion molecules may serve as a support for cell culture and may be used as cell carriers presenting a controlled delivery of active protein. They can thus support the survival and differentiation of the transported cells as well as their microenvironment and allow efficient integration of transplanted cells in the host tissue.The autors have demonstrated the therapeutic potential of PAM in various clinical applications (parkinson disease, cartilage repair, ischaemic stroke, regeneration of post-ischemic tissues,...).Exclusive license available outside cell therapy for animal osteoarticular and pulmonary diseases.
[post_date] => 2024-08-27 11:13:45
[post_modified] => 2024-09-11 15:41:37
[ID] => 6401
)
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[application] =>
[idSugar] => 742e47ee-1016-47e8-8279-2c327533fe25
[etat_fiche_online] => en_ligne
[date_application] => 03-05-2002
[date] =>
[bd_referent] => Elodie ACLOQUE
[bd_referent_id] =>
[contact_email] => Elodie.ACLOQUE@inserm-transfert.fr
[contact_phone] =>
[reference_online] => GBM01306-T1
[keywords] => cartilage repair, ischaemic stroke, regeneration of post-ischemic tissues, microparticle, Biomaterial, cell therapy, Regenerative medecine, cell delivery, Polymer
[pub_scient_inv_dispo] => - Technology: Biomaterials. 2005 Jun;26(17):3727-37.Eur J Pharm Biopharm. 2008 Sep;70(1):127-36. doi: 10.1016/j.ejpb.2008.03.006. Epub 2008 Mar 16.Eur J Pharm Sci. 2012 Jan 23;45(1-2):128-37. doi: 10.1016/j.ejps.2011.10.030. Epub 2011 Nov 9.- Cartilage repair:Biomaterials. 2010 Sep;31(25):6485-93. doi: 10.1016/j.biomaterials.2010.05.013. Epub 2010 Jun 8.J Control Release. 2013 Aug 28;170(1):99-110. doi: 10.1016/j.jconrel.2013.04.017. Epub 2013 May 3.- Parkinson disease: Cell Transplant. 2004;13(5):573-83.Biomaterials. 2007 Apr;28(11):1978-88. Epub 2007 Jan 4.Bone. 2007 Feb;40(2):360-73. Epub 2006 Nov 3.Biomaterials. 2011 Feb;32(6):1560-73. doi: 10.1016/j.biomaterials.2010.10.041. Epub 2010 Nov 12.Stem Cells Transl Med. 2015 Jun;4(6):670-84. doi: 10.5966/sctm.2014-0139. Epub 2015 Apr 29.- Ischaemic stroke: J Neurochem. 2011 Dec;119(5):972-88. doi: 10.1111/j.1471-4159.2011.07272.x. Epub 2011 May 13.Acta Biomater. 2015 Mar;15:77-88. doi: 10.1016/j.actbio.2014.12.017. Epub 2014 Dec 31.- Regeneration of post-ischemic tissues:Eur J Pharm Biopharm. 2012 Aug;81(3):609-16. doi: 10.1016/j.ejpb.2012.04.014. Epub 2012 Apr 26.J Cell Mol Med. 2013 Jan;17(1):192-204. doi: 10.1111/j.1582-4934.2012.01662.x. Epub 2013 Jan 11.
[access_to_detailed_offer] => /wp-content/uploads/GBM01306-T1_MONTERO-MENEI.pdf
[rare_disease] => false
[second_indication] => false
[inventors] => VENIER Marie-Claire,BENOIT Jean-Pierre,MENEI Philippe,TATARD Valérie
[number_application] => France (NP) - 03 Mai 2002 - 02 05574
[technology_engineering] => biomaterials
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 78
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Biologic, Biomaterials, Cell therapy, Central Nervous System, Drug, Hit - validation in vivo, Parkinson's Disease, Product, Product, Stem cell therapy
[taxonomieurl] =>
Biologic,
Biomaterials,
Cell therapy,
Central Nervous System,
Drug,
Hit - validation in vivo,
Parkinson's Disease,
Product,
Product,
Stem cell therapy
)
[79] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHODS OF DIAGNOSING ACUTE CIRCULATORY FAILURE
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-of-diagnosing-acute-circulatory-failure/
[post_content] => Circulatory failure generates hypoxia and leads to accumulation of reductive species in tissue and circulatory failure monitoring tools are needed but rare. Cardiopulmonary bypass (CPB) is known to promote brief circulatory failure during its initiation. In the present study, the Inventors demonstrate a correlation between whole blood redox potential and circulatory failure during (CPB). They made a prospective study with 17 patients eligible for cardiac surgery with cardiopulmonary bypass. They demonstrated a frank reduction of the whole blood redox potential during circulatory failure during the initiation of CPB. They also demonstrated that they were able to classify patients in 3 groups, one of them presenting an unfavorable post-operative outcome. Accordingly, the present invention relates to a method of diagnosing acute circulatory failure in a patient comprising determining the level of redox potential in a sample obtained from said patient, wherein the level of redox potential indicates whether the patient suffers or not from an acute circulatory failure.
[post_date] => 2024-07-08 13:19:50
[post_modified] => 2024-09-11 15:54:20
[ID] => 6377
)
[post_meta] => stdClass Object
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[application] =>
[idSugar] => 8b126ed0-3ab1-11ef-a77a-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 06-10-2022
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO22443-D1
[keywords] => acute circulatory failure, Blood Redox potential, Diagnosis, Prognosis, Cardiopulmoanry bypass (CBP)
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => false
[second_indication] => false
[inventors] => GALINIER Anne,LABASTE François,PEY Vincent,MINVILLE Vincent,STEPHAN Marion,DRAY Cédric
[number_application] => European Procedure (Patents) (EPA) - 06 Oct. 2022 - 22 306 499.9 - PCT/EP2023/077580 on 05/10/2023
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => other
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
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(
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[first_name] => Inserm
[last_name] => Transfert
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[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 79
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Acute heart failure, Biomarker, Biomarker, Cardiovascular Diseases, Devices, Human POC, In vitro diagnostic medical device, Other, Product
[taxonomieurl] =>
Acute heart failure,
Biomarker,
Biomarker,
Cardiovascular Diseases,
Devices,
Human POC,
In vitro diagnostic medical device,
Other,
Product
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[80] => stdClass Object
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[post_title] => Use of Hedgehog inhibitors for the treatment of mastocytosis
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-hedgehog-inhibitors-for-the-treatment-of-mastocytosis/
[post_content] => The inventors demonstrate for the first time the activation of the Hedgehog (HH) signaling pathway in normal and abnormal human mast cells (MCs). These results prompt the inventors to explore the consequence of the inhibition of the HH pathway, especially the canonical pathway, on MC proliferation. They demonstrate that Hedgehog inhibitors inhibit proliferation and induces apoptosis of mast cells. Accordingly the present invention relates to a method of treating a mast cell disease in a patient in need there of comprising administering to the patient a therapeutically effective amount of a Hedgehog inhibitor.
[post_date] => 2024-06-07 09:32:46
[post_modified] => 2024-09-11 15:45:04
[ID] => 6292
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[date_application] => 18-05-2017
[date] =>
[bd_referent] => Aymeric EMPEREUR
[bd_referent_id] =>
[contact_email] => anne.cochi@inserm-transfert.fr
[contact_phone] => +33 1 80 05 86 41
[reference_online] => BIO17083-T1
[keywords] => mastocytosis, combination
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[second_indication] => false
[inventors] => MAOUCHE-CHRETIEN Leila,BODEMER Christine,HERMINE Olivier,POLIVKA Laura
[number_application] => European Procedure (Patents) (EPA) - 18 Mai 2017 - 17 305 573.2
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[bd_referent] => Anne COCHI
[contact_description] => Business Development Manager
[contact_email] => anne.cochi@inserm-transfert.fr
[contact_phone] => +33 1 80 05 86 41
)
[comteur] => 80
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Drug, Method, Oncology, Target, Validation in vivo
[taxonomieurl] =>
Drug,
Method,
Oncology,
Target,
Validation in vivo
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[81] => stdClass Object
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[post_title] => METHODS FOR THE DIAGNOSIS AND THETREATMENT OF GRAFT-VERSUS-HOST DISEASE
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-the-diagnosis-and-thetreatment-of-graft-versus-host-disease/
[post_content] => The invention relates to methods for the prediction and the treatment of risk of acute graft versus host disease. The inventors demonstrated that an alteration of CD73-mediated regulatory function of DP8u03b1 Tregs could contribute to the acute GvHD pathophysiology. In particular, the present invention relates to method of determining whether a subject has or is at 0 a risk of developing graft-versus-host disease (GvHD) comprising the steps of: i) determining the level of CD73 expression by DP8u03b1 TREGS in a sample obtained from the subject, ii) comparing the level determined at step i) with a predetermined reference value wherein detecting differential between the level of CD73 expression by DP8u03b1 TREGS determined at step i) and the predetermined reference value is indicative of whether a subject has or is at a risk of developing graft-versus-host disease (GvHD).
[post_date] => 2024-06-07 09:32:27
[post_modified] => 2024-09-19 15:00:02
[ID] => 6291
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[date_application] =>
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO20418-T1
[keywords] =>
[pub_scient_inv_dispo] => Blood. 2022; Godefroy et al. CD73-Expressing Microbiota-Reactive DP8u03b1 Regulatory T Cells Are Lacking in Acute GvHD Patients and Prevent Disease Development in a Pre-Clinical In Vivo Humanized Mouse Model of GvHD
[access_to_detailed_offer] => http://technology-offers.inserm-transfert.com/wp-content/uploads/BIO20418-Godefroy_T1.pdf
[rare_disease] => 0
[second_indication] => 0
[inventors] => GODEFROY Emmanuelle,CHEVALLIER Patrice,ALTARE Frédéric,JOTEREAU Francine
[number_application] => European Procedure (Patents) (EPA) - 04 Nov. 2020 - 20 306 320.1
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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)
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[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 81
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Drug, Graft Versus Host Disease (GVHD), Immunology, Method, Target, Transplantation
[taxonomieurl] =>
Drug,
Graft Versus Host Disease (GVHD),
Immunology,
Method,
Target,
Transplantation
)
[82] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => FC-engineered anti-human IgE antibodies and methods of use
[guid] => https://technology-offers.inserm-transfert.com/offer/fc-engineered-anti-human-ige-antibodies-and-methods-of-use/
[post_content] => The present invention relates to the treatment of IgE-mediated disease. The inventors hypothesized that formation of immune complexes between Omalizumab and IgE might be responsible for some of the adverse reactions observed in highly atopic patients (i.e. patients with a history of anaphylaxis and/or high IgE titers). Immune complexes can induce inflammation through activation of Fc gamma receptors (Fcu03b3Rs) and/or the complement cascade. They identified that Omalizumab:hIgE immune complexes activate human Fcu03b3Rs in vitro. Moreover, similarly to some of the reported side effects observed in human, Omalizumab:hIgE immune complexes can induce anaphylaxis when injected in mice expressing human Fcu03b3Rs. Using publicly available omalizumab VH and VL sequences, they cloned and produced two mutant versions of omalizumab in which residues in the Fc portion of the Ab were mutated. These variants did not induce anaphylaxis when injected into mice expressing human Fcu03b3Rs and could be thus used for the treatment of IgE-mediated disease. Thus invention relates to a recombinant immunoglobulin heavy chain protein which comprises at least one mutation in the Fc portion and recombinant antibody comprising said heavy chain protein.
[post_date] => 2024-06-07 09:31:27
[post_modified] => 2024-09-20 14:25:02
[ID] => 6290
)
[post_meta] => stdClass Object
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[object] =>
[application] =>
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[etat_fiche_online] => en_ligne
[date_application] =>
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] =>
[contact_phone] =>
[reference_online] => BIO60360-T1
[keywords] => Inflammation - Anaphylaxis - Antibody - Side effect
[pub_scient_inv_dispo] => The anti-IgE mAb omalizumab induces adverse reactions by engaging Fcu03b3 receptors Balbino B. et al. J Clin Invest. 2020 Mar 2;130(3):1330-1335
[access_to_detailed_offer] => http://technology-offers.inserm-transfert.com/wp-content/uploads/BIO60360-T1_Reber.pdf
[rare_disease] => 0
[second_indication] => 0
[inventors] => REBER Laurent,BRUHNS Pierre,BALBINO Bianca
[number_application] => United States Of America (PSP) - 13 Avr. 2018 - 62/657,401
[technology_engineering] => antibodies_nanobodies
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
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(
[author] => 1
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)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 82
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Antibodies nanobodies, Biologic, Drug, Immunology, Inflammation, Method, Product
[taxonomieurl] =>
Antibodies nanobodies,
Biologic,
Drug,
Immunology,
Inflammation,
Method,
Product
)
[83] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => USE OF ETV3 or ETV6 INHIBITORS FOR BLOCKING THE DIFFERENTIATION OF MONOCYTES INTO DENDRITIC CELLS
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-etv3-or-etv6-inhibitors-for-blocking-the-differentiation-of-monocytes-into-dendritic-cells/
[post_content] => In inflamed tissues, monocytes differentiate into macrophages (mo-Mac) or dendritic cells (mo-DC). In chronic non-resolving inflammation, mo-DC are major drivers of pathogenic events. Manipulating monocyte differentiation would therefore represent an attractive therapeutic strategy. Here the inventors show that the transcriptional repressors ETV3 and ETV6 control monocyte differentiation into mo-DC. To validate the physiological relevance of these findings, the inventors generated mice deficient for ETV6 in monocytes. Deficient mice show spontaneous expression of interferon-stimulated genes, confirming that ETV6 regulates interferon responses in vivo. Furthermore, deficient mice display impaired mo-DC differentiation during peritonitis and less severe symptoms in experimental autoimmune encephalomyelitis. The findings identify ETV3 and ETV6 as a therapeutic target to redirect monocyte differentiation in inflammatory disorders.
[post_date] => 2024-06-07 09:31:27
[post_modified] => 2024-09-20 15:05:02
[ID] => 6289
)
[post_meta] => stdClass Object
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[object] =>
[application] =>
[idSugar] => 56490a45-58c8-75c3-ab30-616836acead6
[etat_fiche_online] => en_ligne
[date_application] => 2021-09-01
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO21335-T1
[keywords] =>
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => SEGURA Elodie,VILLAR Javiera
[number_application] => European Procedure (Patents) (EPA) - 01 Sept. 2021 - 21 306 195.5
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
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[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 83
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Drug, Immunology, Inflammation, Oligonucleotide, Target, Target
[taxonomieurl] =>
Drug,
Immunology,
Inflammation,
Oligonucleotide,
Target,
Target
)
[84] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHODS FOR MODULATING INNATE LYMPHOID CELL ACTIVITY, ANTIBODY DRUG CONJUGATES AND USES IN THERAPY
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-modulating-innate-lymphoid-cell-activity-antibody-drug-conjugates-and-uses-in-therapy/
[post_content] => The present invention relates to methods for modulating innate lymphoid cell activity, antibody drug conjugates and uses in therapy. The inventors showed in a model of murine cytomegalovirus infection, that glucocorticoid receptor expression in innate lymphoid cells plays an essential early role in regulating host protection against inflammation-induced tissue damage. Mechanistically, they demonstrated for the first time that endogenous glucocorticoids produced shortly after infection promote the expression of the immune checkpoint PD1 on the surface of natural killer cells. This glucocorticoid-PD1 pathway acts to limit the production of interferon-u03b3 by NK cells. The modulation of the glucocorticoid-PD1 pathway in order to increase or decrease the activity of ILCs would permit to treat either cancers and infectious diseases or autoimmune and inflammatory diseases. In particular, the present invention relates to a method of modulating innate lymphoid cell activity which comprises modulating the activity of glucocorticoid receptor.
[post_date] => 2024-06-07 09:31:26
[post_modified] => 2024-09-11 15:44:41
[ID] => 6288
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => 9fba0eb1-e710-a7a7-03cd-5afc3f31d179
[etat_fiche_online] => en_ligne
[date_application] => 22-03-2018
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => Soraya.SIN-MONNOT@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO17668-T1
[keywords] => Innate lymphoid cell - Innate immunity - glucocorticoid receptor - inflammation-induced tissue damage - immune checkpoint PD1
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => UGOLINI Sophie,QUATRINI Linda
[number_application] => European Procedure (Patents) (EPA) - 22 Mars 2018 - 18 305 319.8
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 84
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Drug, Immunology, Inflammation
[taxonomieurl] =>
Drug,
Immunology,
Inflammation
)
[85] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => USE OF TCR-DEFICIENT CAR-TREGS IN COMBINATION WITH ANTI-TCR COMPLEX MONOCLONAL ANTIBODIES FOR INDUCING DURABLE TOLERANCE
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-tcr-deficient-car-tregs-in-combination-with-anti-tcr-complex-monoclonal-antibodies-for-inducing-durable-tolerance/
[post_content] => The present invention is defined by the claims. In particular, the present invention relates to the use of TCR-deficient CAR-Tregs in combination with anti-TCR complex monoclonal antibodies for inducing durable tolerance.
[post_date] => 2024-06-07 09:31:25
[post_modified] => 2024-09-20 15:55:02
[ID] => 6287
)
[post_meta] => stdClass Object
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[object] =>
[application] =>
[idSugar] => bb50d920-b37e-11ee-91a7-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] =>
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] =>
[contact_phone] =>
[reference_online] => BIO22067-T1
[keywords] => TCR-deficient CAR-Treg - Anti-TCR complex - Stability of CAR-Treg
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http://technology-offers.inserm-transfert.com/wp-content/uploads/BIO22067-T1_Zuber.pdf
[rare_disease] => 0
[second_indication] => 0
[inventors] => ZUBER Julien,CHARBONNIER Soeli,BLEIN Tifanie
[number_application] => European Procedure (Patents) (EPA) - 18 Févr. 2022 - 22 305 182.2
[technology_engineering] => cell_therapy
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 85
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Biologic, Cell therapy, Cell therapy, Cellular immunotherapy, Drug, Identification, Immunology, Inflammation, Target, Target
[taxonomieurl] =>
Biologic,
Cell therapy,
Cell therapy,
Cellular immunotherapy,
Drug,
Identification,
Immunology,
Inflammation,
Target,
Target
)
[86] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => USE OF TG2 INHIBITORS FOR IMPROVING MUCOCILIARY CLEARANCE IN RESPIRATORY DISEASES
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-tg2-inhibitors-for-improving-mucociliary-clearance-in-respiratory-diseases/
[post_content] => In asthma, modification of gel-forming respiratory mucins leading to their tethering to the apical pole of epithelial cells, are believed to participate in airway obstruction by mucus plugs. These changes have been linked to local production of Th2 cytokines, resulting in mucus cell hyperplasia and increased MUC5AC production. The inventors showed that severe eosinophil asthma was associated with overexpression of transglutaminase 2 (TG2), an enzyme recently involved in intestinal mucin reticulation. Moreover, the bronchial epithelium from asthmatic patients or control subjects was reconstituted in vitro by culturing cells at the air-liquid interface and the hypersecretory differentiation was modeled by exposing control bronchial epithelial to IL-13. The inventors showed TG2 expression was upregulated upon IL-13-mediated hypersecretory differentiation and correlated with MUC5AC expression. IL-13 promoted MU5AC tethering to in vitro reconstituted hypersecretory epithelium, and this was blocked by a TG2 inhibitor. In conclusion, the inventors showed that TG2 participates in respiratory mucin modifications in asthma, and contribute to mucus tethering to the airway wall, supporting the use of TG2 inhibitors for improving mucociliary clearance in asthma, but more generally in respiratory diseases
[post_date] => 2024-06-07 09:31:25
[post_modified] => 2024-09-20 17:00:02
[ID] => 6286
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => 6cd93c8f-f3b8-b3c6-bff8-60e71bd2126e
[etat_fiche_online] => en_ligne
[date_application] =>
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO20412-T1
[keywords] =>
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => LETUVE Severine,GUILLOT Loïc,TAILLE Camille,ROBBE MASSELOT Catherine,SALLON Céline
[number_application] => European Procedure (Patents) (EPA) - 15 Oct. 2020 - 20 306 214.6
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 86
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] =>
[taxonomieurl] =>
)
[87] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => USE OF IL-36 INHIBITORS FOR THE TREATMENT OF NETHERTON SYNDROME
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-il-36-inhibitors-for-the-treatment-of-netherton-syndrome/
[post_content] => Netherton syndrome (NS) is a rare recessive skin disorder caused by loss-of-function mutations in SPINK5 encoding the protease inhibitor LEKTI. NS patients present with typical ichthyosis linearis circumflexa (NS-ILC) or scaly erythroderma (NS-SE). Here the inventors employed a combination of several molecular profiling methods to comprehensively characterize the skin, immune cells and allergic phenotypes of NS-ILC and NS-SE patients. In particular, they studied a cohort of 13 NS patients comprising 9 NS-ILC and 4 NS-SE. Integrated multi-omics revealed abnormal epidermal proliferation and differentiation and IL-17/IL-36 signatures in lesion skin and in blood in both NS endotypes. This study thus identifies IL-17/IL-36 as predominant signaling axes in both NS endotypes and unveils molecular features distinguishing NS-ILC and NS-SE. In particular, blocking of IL36 signaling would therefore represent a novel therapeutic strategy for NS, in particular in NS-SE patients.
[post_date] => 2024-06-07 09:31:25
[post_modified] => 2024-09-23 19:15:02
[ID] => 6285
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => f086e2c7-6249-18d2-0488-62ed193923f2
[etat_fiche_online] => en_ligne
[date_application] =>
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO20216-T1
[keywords] =>
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http://technology-offers.inserm-transfert.com/wp-content/uploads/BIO20216-T1_Hovnanian.pdf
[rare_disease] => 1
[second_indication] => 0
[inventors] => HOVNANIAN Alain,BARBIEUX Claire,PETROVA Evgeniya,GOUIN Olivier
[number_application] => European Procedure (Patents) (EPA) - 12 Juil. 2021 - 21 305 968.6
[technology_engineering] =>
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[comteur] => 87
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[taxonomie] => Dermatology, Method
[taxonomieurl] =>
Dermatology,
Method
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[88] => stdClass Object
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[post_title] => METHODS FOR PREDICTING AND PREVENTING POSTOPERATIVE COMPLICATIONS AFTER CARDIAC SURGERY WITH CARDIOPULMONARY BY-PASS
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-predicting-and-preventing-postoperative-complications-after-cardiac-surgery-with-cardiopulmonary-by-pass/
[post_content] => Cardiopulmonary by-pass (CBP) during cardiac surgery leads to deleterious systemic inflammatory response. In a prospective cohort of 46 patients older than 18 years and eligible for non-urgent cardiac surgery with CPB, measurement of sTREM-1 in the plasma was performed immediately after the onset of anesthesia (H0) and 2 and 24 hours after CBP. After CBP, sTREM-1 significantly increased at H2 and at H24 (p
[post_date] => 2024-06-07 09:26:03
[post_modified] => 2024-09-11 15:54:07
[ID] => 6284
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[date_application] => 11-10-2021
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO21316-D1
[keywords] => Cardiopulmonary by-pass (CBP), sTrem-1, severe organ failure, prognosis
[pub_scient_inv_dispo] => Front Cardiovasc Med, 2023 Jul 13, Vandestienne et al., Soluble TREM-1 plasma levels are associated with acute kidney injury, acute atrial fibrillation and prolonged ICU stay after cardiac surgery- a proof-concept stud, doi: 10.3389/fcvm.2023.1098914.
[access_to_detailed_offer] =>
[rare_disease] => false
[second_indication] => false
[inventors] => AIT-OUFELLA Hafid,CLAVIER Thomas
[number_application] => European Procedure (Patents) (EPA) - 11 Oct. 2021 - 21 306 422.3
[technology_engineering] =>
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[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 88
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Cardiovascular Diseases, Immunoassay, Pre-Analytic Validation
[taxonomieurl] =>
Biomarker,
Cardiovascular Diseases,
Immunoassay,
Pre-Analytic Validation
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[89] => stdClass Object
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[post] => stdClass Object
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[post_title] => METHOD FOR DIAGNOSING COLLAGEN DEGRADATATION ASSOCIATED DISEASE
[guid] => https://technology-offers.inserm-transfert.com/offer/method-for-diagnosing-collagen-degradatation-associated-disease/
[post_content] => The Inventors have developed an ELISA of a new molecular marker detecting a neoepitope generated from the cleavage of the u03b11 chain of type III collagen within its helical domain. Serum levels of this marker were significantly increased in patients with RA and is significantly associated to CRP and ESR levels. Indeed, they demonstrated that the median serum HELIX-III levels were significantly higher in patients with moderate (p=0027) and active RA (p=00004) compared with those in age-matched controls. The present invention relates to an antibody recognizing an epitope having SEQ ID NO :1 of collagen protein and its uses for diagnostic, prognostic and monitoring purposes.
[post_date] => 2024-06-07 09:26:02
[post_modified] => 2024-09-11 15:54:07
[ID] => 6283
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[date_application] => 01-02-2022
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO21443-D1
[keywords] => Rheumatoid Arthritis, collagene degradation, prognosis
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => false
[second_indication] => false
[inventors] => CHAPURLAT Roland,GARNERO Patrick,GINEYTS Evelyne
[number_application] => European Procedure (Patents) (EPA) - 01 Févr. 2022 - 22 305 111.1
[technology_engineering] =>
[multidisciplinary_field] =>
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[post_categoryname] => Diagnostic
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[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 89
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Analytic validation, Biomarker, Immunoassay, Immunology, Protype kit, Rheumatoid Arthritis
[taxonomieurl] =>
Analytic validation,
Biomarker,
Immunoassay,
Immunology,
Protype kit,
Rheumatoid Arthritis
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[90] => stdClass Object
(
[post] => stdClass Object
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[post_title] => METHODS FOR THE DIAGNOSIS AND TREATMENT OF T CELL-LYMPHOMAS
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-the-diagnosis-and-treatment-of-t-cell-lymphomas/
[post_content] => T-cell lymphomas are a heterogeneous group of malignancies involving T lymphocytes and generally characterized by a poor prognosis. Among them, cutaneous T-cell lymphomas involve primarily the skin. Mycosis fungoides and Sézary syndrome are the most frequent cutaneous T-cell lymphomas. The Inventors showed that malignant T cells express CD33 in patients with Sézary syndrome, mycosis fungoides and Hepatosplenic T-cell lymphoma (HSTL). CD33 therefore appears as a useful diagnostic, prognostic and follow-up marker, and as a potential therapeutic target in T-cell lymphomas.
[post_date] => 2024-06-07 09:26:02
[post_modified] => 2024-09-11 15:54:12
[ID] => 6282
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[date_application] => 15-04-2022
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] =>
[contact_phone] =>
[reference_online] => BIO22146-D1
[keywords] => CD33, Diagnostic, Treatment Prediction, T-cell Lymphoma, Sézary Syndrome, Flow-Cytometry
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => false
[second_indication] => false
[inventors] => BENSUSSAN Armand,BAGOT Martine,DE MASSON Adele,GIUSTINIANI Jérôme
[number_application] => European Procedure (Patents) (EPA) - 15 Avr. 2022 - 22 305 558.3 and PCT/EP2023/059761 on 14/04/2023
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
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[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 90
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Human POC, Immunoassay, Lymphoma, Oncology, Sezary syndrome
[taxonomieurl] =>
Biomarker,
Human POC,
Immunoassay,
Lymphoma,
Oncology,
Sezary syndrome
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[91] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHODS FOR THE DIAGNOSIS AND TREATMENT OF ACUTE LYMPHOBLASTIC LEUKEMIA
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-the-diagnosis-and-treatment-of-acute-lymphoblastic-leukemia/
[post_content] => The present invention relates to a method of treating acute lymphoblastic leukemia in a patient in need thereof comprising administering to the patient a therapeutically effective amount of an agent capable of inducing cell death of CCR8 expressing cancer cells. The present invention also relates to a method of diagnosing acute lymphoblastic leukemia in a patient comprising detecting the expression level of CCR8 in a sample obtained from the patient.
[post_date] => 2024-06-07 09:26:01
[post_modified] => 2024-09-11 15:54:14
[ID] => 6280
)
[post_meta] => stdClass Object
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[application] =>
[idSugar] => 9d45c4d6-bc4d-11ee-87ca-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 30-06-2022
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] =>
[contact_phone] =>
[reference_online] => BIO22280-D1
[keywords] => acute lymphoblastic leukemia, diagnostic, Predictive, Compagnon diagnostic, CCR8
[pub_scient_inv_dispo] => not published
[access_to_detailed_offer] =>
[rare_disease] => false
[second_indication] => false
[inventors] => BENSUSSAN Armand,ORTONNE Nicolas,DE MASSON Adele,BAGOT Martine,GIUSTINIANI Jérôme,LEMONNIER François,SOULIER Jean,GACHET Stéphanie,CLAPPIER Emmanuelle
[number_application] => European Procedure (Patents) (EPA) - 30 Juin 2022 - 22 305 958.5 and PCT/EP2023/067924 on 09/01/2024
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
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[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 91
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Acute Lymphocytic Leukemia (ALL), Biomarker, Biomarker, Immunoassay, In vitro poc, Leukemias, Method, Oncology, Target
[taxonomieurl] =>
Acute Lymphocytic Leukemia (ALL),
Biomarker,
Biomarker,
Immunoassay,
In vitro poc,
Leukemias,
Method,
Oncology,
Target
)
[92] => stdClass Object
(
[post] => stdClass Object
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[post_title] => GARP AS A BIOMARKER AND BIOTARGET IN T-CELL MALIGNANCIES
[guid] => https://technology-offers.inserm-transfert.com/offer/garp-as-a-biomarker-and-biotarget-in-t-cell-malignancies/
[post_content] => The present study of the regulatory T phenotype of Sézary cells led to the discovery of the expression of GARP (LRRC32) by Sézary cells. GARP has also been shown to be overexpressed in samples from patients with acute lymphoblastic leukemia. GARP therefore appears as a diagnostic marker, for monitoring T-cell malignancies, and as a therapeutic target. Accordingly, the present invention relates to methods for the diagnosis and treatment of T-cell malignancies.
[post_date] => 2024-06-07 09:26:01
[post_modified] => 2024-09-11 15:54:15
[ID] => 6279
)
[post_meta] => stdClass Object
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[application] =>
[idSugar] => 45aa7cfa-bc69-11ee-8024-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 22-07-2022
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] =>
[contact_phone] =>
[reference_online] => BIO22282-D1
[keywords] => Sezary Syndrome, GARP, Diagnostic, Compagnon Diagnostic, Flow Cytometry
[pub_scient_inv_dispo] => Not Published
[access_to_detailed_offer] =>
[rare_disease] => false
[second_indication] => false
[inventors] => BENSUSSAN Armand,DE MASSON Adele,BAGOT Martine,LEMONNIER François,ORTONNE Nicolas,GIUSTINIANI Jérôme
[number_application] => European Procedure (Patents) (EPA) - 22 Juil. 2022 - 22 306 100.3 and PCT/EP2023/070250 on 04/08/2023
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
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[type_of_patent] => Type of patent
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[user] => stdClass Object
(
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[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
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[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 92
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Human POC, Immunoassay, Lymphoma, Method, Oncology, Sezary syndrome, Target
[taxonomieurl] =>
Biomarker,
Biomarker,
Human POC,
Immunoassay,
Lymphoma,
Method,
Oncology,
Sezary syndrome,
Target
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[93] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHODS AND COMPOSITION TO IDENTIFY AND TREAT SUBJECTS RESISTING TO CHEMOTHERAPY TREATMENT
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-composition-to-identify-and-treat-subjects-resisting-to-chemotherapy-treatment-2/
[post_content] => The present invention relates to a method for treating a subject suffering from a cancer comprising a step of administering said subject with a therapeutically effective amount of an inhibitor of NETs. By in vitro experiments, inventors have demonstrated that inhibiting the formation of NETs with a PAD4 inhibitor or digesting the NET-DNA scaffold with DNase I during PMA-induced NET formation overcame the chemoresistance induced by the NET CM in vitro.They have also generated data in vivo and shown that targeting of NETs with either a PAD4 inhibitor or DNase I enhanced chemotherapy efficacy. PAD4 inhibition and DNase I treatment not only eliminated NETs in the metastatic lungs and in the plasma, but also reduced neutrophil recruitment to the lungs.
[post_date] => 2024-06-07 09:26:01
[post_modified] => 2024-09-11 15:54:15
[ID] => 6278
)
[post_meta] => stdClass Object
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[object] =>
[application] =>
[idSugar] => 41cb4076-c1da-11ee-8f59-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 05-07-2022
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO21413-D1
[keywords] => Breast Cancer, NETs, chemotherapy, treatment response prediction, prognosis
[pub_scient_inv_dispo] => Cancer Cell. 2023 Apr 10;41(4):757-775.e10. doi:10.1016/j.ccell.2023.03.008.
[access_to_detailed_offer] =>
[rare_disease] => false
[second_indication] => false
[inventors] => GAGGIOLI Cédric,MOUSSET Alexandra,ALBRENGUES Jean
[number_application] => European Procedure (Patents) (EPA) - 05 Juil. 2022 - 22 306 004.7 and PCT/EP2023/068444 on 04/07/2023
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
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[thera_area] => Therapy Area
[type_of_patent] => Type of patent
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[user] => stdClass Object
(
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[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 93
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Animal POC, Biomarker, Breast Cancer, Immunoassay, Oncology
[taxonomieurl] =>
Animal POC,
Biomarker,
Breast Cancer,
Immunoassay,
Oncology
)
[94] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => LRRC33 AS A BIOMARKER AND BIOTARGET IN CUTANEOUS T-CELL LYMPHOMAS
[guid] => https://technology-offers.inserm-transfert.com/offer/lrrc33-as-a-biomarker-and-biotarget-in-cutaneous-t-cell-lymphomas/
[post_content] => The present study of the regulatory T phenotype of Sézary cells led to the discovery of the expression of LRRC33 by Sézary cells. LRRC33 therefore appears as a diagnostic marker, for monitoring Sézary syndrome, and as a therapeutic target. Accordingly, the present invention relates to methods for the diagnosis and treatment of cutaneous T cell-lymphomas.
[post_date] => 2024-06-07 09:26:00
[post_modified] => 2024-09-11 15:54:16
[ID] => 6277
)
[post_meta] => stdClass Object
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[object] =>
[application] =>
[idSugar] => cd0699da-c1dd-11ee-a538-506b8df7f2c7
[etat_fiche_online] => en_ligne
[date_application] => 29-07-2022
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO22283-D1
[keywords] => Sezary Synrdome, Diagnostic, cutaneous T cell-lymphomas, Flow-Cytometry
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => false
[second_indication] => false
[inventors] => BENSUSSAN Armand,GIUSTINIANI Jérôme,DE MASSON Adele,ORTONNE Nicolas
[number_application] => European Procedure (Patents) (EPA) - 29 Juil. 2022 - 22 306 146.6 and PCT/EP2023/070960 on 28/07/2023
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
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[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
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[user] => stdClass Object
(
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[first_name] => Inserm
[last_name] => Transfert
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[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 94
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Human POC, Immunoassay, Lymphoma, Method, Oncology, Sezary syndrome, Target
[taxonomieurl] =>
Biomarker,
Biomarker,
Human POC,
Immunoassay,
Lymphoma,
Method,
Oncology,
Sezary syndrome,
Target
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[95] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => Novel B-Raf inhibitors devoid of rapid metabolism and of binding to Pregnane X Receptor
[guid] => https://technology-offers.inserm-transfert.com/offer
ovel-b-raf-inhibitors-devoid-of-rapid-metabolism-and-of-binding-to-pregnane-x-receptor/
[post_content] => The present invention relates to N-(3-(5-(pyrimidin-4-yl)thiazol-4-yl)phenylsulfonamide compounds which are useful as inhibitors of protein kinases, more specifically BRAF or mutant forms thereof, to pharmaceutical composition comprising such compounds, and to uses of such compounds in the treatment or prevention of diseases associated with deregulated protein kinase activity, such as cancer.
[post_date] => 2023-05-24 10:15:02
[post_modified] => 2024-09-11 15:45:10
[ID] => 4931
)
[post_meta] => stdClass Object
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[application] =>
[idSugar] => db16775c-4f9b-f329-849f-5f8955f49e80
[etat_fiche_online] => en_ligne
[date_application] => 05-12-2019
[date] =>
[bd_referent] => Aymeric EMPEREUR
[bd_referent_id] =>
[contact_email] => aymeric.empereur@inserm-transfert.fr
[contact_phone] =>
[reference_online] => CHIM18530-T1
[keywords] => BRAF inhibitors
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => /wp-content/uploads/BIO18530-T1_LABESSE.pdf
[rare_disease] => false
[second_indication] => false
[inventors] => LABESSE Gilles,COHEN-GONSAUD Martin,BOURGUET William,GELIN Muriel,GUICHOU Jean-François,BALAGUER Patrick,SCHNEIDER Mélanie
[number_application] => European Procedure (Patents) (EPA) - 05 Déc. 2019 - 19 306 579.4
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
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[thera_area] => Therapy Area
[type_of_patent] => Type of patent
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[user] => stdClass Object
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Hit - validation in vitro,
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[post_title] => METHODS AND COMPOSITION TO IDENTIFY AND TREAT SUBJECTS RESISTING TO CHEMOTHERAPY TREATMENT
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[post_content] => The present invention relates to a method for treating a subject suffering from a cancer comprising a step of administering said subject with a therapeutically effective amount of an inhibitor of NETs.By in vitro experiments, inventors have demonstrated that inhibiting the formation of NETs with a PAD4 inhibitor or digesting the NET-DNA scaffold with DNase I during PMAinduced NET formation overcame the chemoresistance induced by the NET CM in vitro.They have also generated data in vivo and shown that targeting of NETs with either a PAD4 inhibitor or DNase I enhanced chemotherapy efficacy. PAD4 inhibition and DNase I treatment not only eliminated NETs in the metastatic lungs and in the plasma, but also reduced neutrophil recruitment to the lungs.
[post_date] => 2023-05-23 13:15:01
[post_modified] => 2024-09-11 15:45:13
[ID] => 4929
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[date] =>
[bd_referent] => Aymeric EMPEREUR
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[reference_online] => BIO21413-T1
[keywords] => Metastasis, Breast Cancer, Chemotherapy resistance
[pub_scient_inv_dispo] => Cancer Cell. 2023 Apr 10;41(4):757-775.e10. doi:10.1016/j.ccell.2023.03.008.
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[rare_disease] => false
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[inventors] => GAGGIOLI Cédric,MOUSSET Alexandra,ALBRENGUES Jean
[number_application] => European Procedure (Patents) (EPA) - 05 Juil. 2022 - 22 306 004.7
[technology_engineering] =>
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Biomarker,
Breast Cancer,
Drug,
Enzyme,
Method,
Oncology,
Protein,
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Target,
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[post_title] => NEW STRATEGY TARGETING STROMA/TUMOR CELL CROSSTALK TO TREAT A CANCER
[guid] => https://technology-offers.inserm-transfert.com/offer
ew-strategy-targeting-stroma-tumor-cell-crosstalk-to-treat-a-cancer/
[post_content] => In this study, the Inventors report that CD9 is a key component of PC-associated CAFsderived ANXA6+-EVs. They determined that CD9 is expressed by PC-associated CAFs in vitro as well as in vivo. Targeting CD9 impaired CAFs-derived ANXA6+-EVs uptake by pancreatic cancer cells, which consequently decreases their migratory abilities. Signaling pathway arrays highlighted p38/MAPK as activated in pancreatic cancer cells following CAFs-derived ANXA6+/CD9+-EVs uptake. The use of CD9 blocking antibody, p38 siRNA or chemical inhibitors impaired pancreatic cancer cells abilities following incubation with CAFs-derived ANXA6+/CD9+-EVs. Finally, they revealed CD9 expression as an independent poor-prognosis marker in human PC samples. Collectively their data highlight the key role of CD9 in CAFs erived ANXA6+-EVs internalization by pancreatic cancer cells and the consequent, and mandatory, activation of p38/MAPK pathway to foster their migratory abilities. Measuring the oncogenic CAFs-derived ANXA6+/CD9+-EVs then limiting their action on pancreatic cancer cells abilities might be a promising option for PC stratification and treatment.
[post_date] => 2023-05-15 13:55:02
[post_modified] => 2024-09-11 15:43:28
[ID] => 4928
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[date] =>
[bd_referent] => Aymeric EMPEREUR
[bd_referent_id] =>
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[reference_online] => BIO21093-T1
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[pub_scient_inv_dispo] => Sci Signal. 2022 Aug 2;15(745):eabg8191. doi: 10.1126/scisignal.abg8191. Epub 2022 Aug 2.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => TOMASINI Richard,TUBIANA Sarah,NIGRI Jérémy
[number_application] => European Procedure (Patents) (EPA) - 22 Nov. 2021 - 21 306 624.4
[technology_engineering] =>
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[taxonomie] => Oncology, Pancreatic Cancer, Target
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Oncology,
Pancreatic Cancer,
Target
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[98] => stdClass Object
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[post_title] => MESENCHYMAL STEM CELL DERIVED EXTRACELLULAR VESICLES LOADED WITH AT LEAST ONE PHOTOSENSITIZER AND USES THEREOF FOR THE TREATMENT OF PERITONEAL CARCINOMATOSIS
[guid] => https://technology-offers.inserm-transfert.com/offer/mesenchymal-stem-cell-derived-extracellular-vesicles-loaded-with-at-least-one-photosensitizer-and-uses-thereof-for-the-treatment-of-peritoneal-carcinomatosis/
[post_content] => Several gastrointestinal and gynecological malignancies have the potential to disseminate and grow in the peritoneal cavity. The occurrence of peritoneal carcinomatosis (PC) has been shown to significantly decrease overall survival in patients. Treatment of residual microscopic disease remains a challenge with new anticancer modalities development. Now, the inventors propose an innovative therapeutic management of peritoneal carcinomatosis (PC) that is bio-inspired and tumor-targeted by engineering MSC-derived EVs to encapsulate a photosensitizer (mTHPC) for improved photodynamic therapy efficiency and safety. In this work, the inventors first evaluated the biodistribution of EVs-mTHPC in a murine PC model and highlighted superior accumulation of mTHPC in the tumor compared to other mTHPC formulations (free drug and liposomal one (Foslip®). The effectiveness of PDT mediated by mTHPC vectorized in EVs has then been evaluated in PC. In accordance with pharmacokinetics, the results revealed both an enhanced light-induced therapeutic efficiency in terms of tumoral cytotoxicity, safety for surrounding tissue after laser irradiation, immunomodulation and improved survival time. Thus, the present invention relates to mesenchymal stem cell derived extracellular vesicles loaded with at least one photosensitizer and uses thereof for the treatment of peritoneal carcinomatosis.
[post_date] => 2023-05-15 13:25:01
[post_modified] => 2024-09-11 15:45:01
[ID] => 4927
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[date] =>
[bd_referent] => Aymeric EMPEREUR
[bd_referent_id] =>
[contact_email] => aymeric.empereur@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO19434-T1
[keywords] => Oncology, photodynamic therapy, MSC, peritoneal
carcinomatosis, pleural metastasis
[pub_scient_inv_dispo] => Amandine Pinto et al. ACS Nano 2021, 15, 2, 3251u20133263
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => POCARD Marc,PIFFOUX Max,MARANGON Iris,WILHEM Claire,GAZEAU Florence,PINTO Amandine,SILVA (BRUN-GRAEPPI) Amanda K. Andriola
[number_application] => European Procedure (Patents) (EPA) - 21 Nov. 2019 - 19 306 495.3
[technology_engineering] => cell_therapy
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[comteur] => 98
[terms] => Array
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[taxonomie] => Biologic, Cell therapy, Cell therapy, Colorectal Cancer, Drug, Method, Oncology, Product, Stem cell therapy
[taxonomieurl] =>
Biologic,
Cell therapy,
Cell therapy,
Colorectal Cancer,
Drug,
Method,
Oncology,
Product,
Stem cell therapy
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[99] => stdClass Object
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[post_title] => Anti-PTF1a antibodies
[guid] => https://technology-offers.inserm-transfert.com/?p=4900
[post_content] => Two rabbits (A and B) were immunized with a mix of two synthetic peptides of murine PTF1a sequence (one N-term peptide, KSFDNIENEPPFEFVS (aa 309-324) and one C-term peptide, EDFFTDQSSRDPLED (aa 24-38)) conjugated to keyhole limpet haemocyanin. C-term and N-term peptides have 100 % identity with rat sequence and 93% with human sequence.We call our antibodies 7A (from rabbit A) and 7B (from rabbit B).We designed Biacore experiments with immobilized peptides to test their specificity against immunogenic peptides (see Figure 1). 7A recognizes C-term sequence better than N-term sequence. 7B recognizes C-term sequence but not N-term sequence (see Figure 1).Antibody 7B was purified against the « wrong peptide, N-term » but the flow through fraction has been kept. It has been tested and shows preserved immunoreactivity against C-terminal sequence (see Figure 1) and detects PTF1a in Western-Blot (see Figure 3).We successfully used antibodies 7A and 7B in immunohistochemistry on human and mouse pancreas (see publication 1 and 3 and also see immunofluorescence in Figure 2), in immunocytochemistry of rat pancreatic acinar cells (see publication 1), Western-blot analysis of nuclear and cytoplasmic extracts of rat pancreatic acinar cells (see publication 1), of murine pancreatic acinar protein extracts (see publication 2), of transfected HEK cells (see publication 2), and in immunoprecipitation experiments (see publication 2). Antibodies 7A and 7B are specific of pancreatic acinar cells and do not recognize any other proteins in Western-blot analysis of pancreatic ductal cells or COS cells (see Figure 3). Figure 3 also shows the absence of non specific bands. We can provide around 30 ml of 7A antibody, 2 ml of unpurified 7B and 6 ml of 7B flow-through.We also have lesser quantities of intermediate bleeds. Their specificity towards peptide antigens was also tested by Biacore, we can provide these results on demand in case of interest. We did not tested them in WB and IF/IHC.
[post_date] => 2023-03-31 16:40:02
[post_modified] => 2024-09-11 16:06:33
[ID] => 4900
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[keywords] => pancreatic acinar cells; acinar-to ductal metaplasia; development; reprogramming; embryonic nervous system; plasticity
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => false
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[number_application] =>
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[post_categoryname] => Antibodies
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[contact_description] =>
[contact_email] =>
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[comteur] => 99
[terms] => Array
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[0] => Antibodies
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[taxonomie] => Academic Research, Diabetes, ELISA (or compatible technique), Gastrointestinal Diseases, Immunocytochemistry, Immunofluorescence, Immunohistochemistry - Paraffin, Immunohistochemistry u2013 Frozen, Immunoprecipitation, Metabolic Disorders, Mouse, Oncology, Pancreatic Cancer, Pancreatic exocrine tumor, Pancreatitis, Rabbit, Type 1 Diabetes (Juvenile Diabetes), Western Blot
[taxonomieurl] =>
Academic Research,
Diabetes,
ELISA (or compatible technique),
Gastrointestinal Diseases,
Immunocytochemistry,
Immunofluorescence,
Immunohistochemistry - Paraffin,
Immunohistochemistry u2013 Frozen,
Immunoprecipitation,
Metabolic Disorders,
Mouse,
Oncology,
Pancreatic Cancer,
Pancreatic exocrine tumor,
Pancreatitis,
Rabbit,
Type 1 Diabetes (Juvenile Diabetes),
Western Blot
)
[100] => stdClass Object
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[post_title] => CD38 AS A BIOMARKER AND BIOTARGET IN CELL-LYMPHOMAS
[guid] => https://technology-offers.inserm-transfert.com/offer/cd38-as-a-biomarker-and-biotarget-in-cell-lymphomas/
[post_content] => T-cell lymphomas are a heterogeneous group of malignancies involving T lymphocytes and generally characterized by a poor prognosis. Among them, cutaneous T-cell lymphomas involve primarily the skin. Mycosis fungoides and Sézary syndrome are the most frequent cutaneous T-cell lymphomas. Now the inventors showed the expression of CD38 by Sézary cells and in CD4+ blood cells of patients with Sezary syndrome. CD38 therefore appears as a useful diagnostic, prognostic and follow-up marker, and as a potential therapeutic target in T-cell lymphomas. Therapeutic depletion of CD38-expressing cancer cells would eliminate tumor cells.
[post_date] => 2023-03-08 15:25:03
[post_modified] => 2024-09-11 15:53:59
[ID] => 4898
)
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[date_application] =>
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO22037-D1
[keywords] => cutaneous T-cell lymphoma, Sézary syndrome, Diagnostic, Treatment Response Prediction, Prognosis CD38
[pub_scient_inv_dispo] => J Invest Dermatol, 2023 Jan 28, Ta et al., CD38 Targeting in Aggressive, Treatment-Refractory Cutaneous T-Cell Lymphomas, doi: 10.1016/j.jid.2023.01.009. Online ahead of print.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => BENSUSSAN Armand,BAGOT Martine,BATTISTELLA Maxime,DE MASSON Adele,MOINS Hélène
[number_application] => European Procedure (Patents) (EPA) - 31 Janv. 2022 - 22 305 106.1
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => imaging,immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
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[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
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[user] => stdClass Object
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[first_name] => Inserm
[last_name] => Transfert
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 100
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Human POC, Imaging, Immunoassay, Lymphoma, Oncology, Sezary syndrome, Target
[taxonomieurl] =>
Biomarker,
Biomarker,
Human POC,
Imaging,
Immunoassay,
Lymphoma,
Oncology,
Sezary syndrome,
Target
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[101] => stdClass Object
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[post_title] => METHODS AND COMPOSITIONS FOR TREATING TRIPLE NEGATIVE BREAST CANCER (TNBC)
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-compositions-for-treating-triple-negative-breast-cancer-tnbc/
[post_content] => Inventors analyzed the prognostic value of tumor and stromal-derived SPARC in a large series that included 148 non-metastatic TNBC patients with a long follow-up by immunohistochemistry. They show that SPARC expression was detected in cancer cells (42.4%), cancer-associated fibroblasts (CAFs) (88.1%), TAMs (77.1%), endothelial cells (75.2%) and TILs (9.8%). Recurrence-free survival (RFS) was significantly lower for patients with a positive expression of SPARC in CAFs (SPARC+ CAFs) with a median follow-up of 5.4 years. SPARC expression in CAFs was found to be an independent prognostic factor in multivariate analysis. Accordingly, the present invention relates to a method for predicting the survival time of a subject suffering from triple-negative breast cancer (TNBC) comprising determining the expression level of Secreted Protein Acidic and Rich in Cysteine (SPARC) in cancer-associated fibroblasts (CAFs) in a biological sample obtained from the subject wherein said positive expression of SPARC in CAFs (SPARC+CAFs) correlates with a short survival time of the subject.
[post_date] => 2023-03-08 14:15:02
[post_modified] => 2024-09-11 15:53:59
[ID] => 4897
)
[post_meta] => stdClass Object
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[idSugar] => 354f3f52-e37a-ef4c-c595-64088c3184a7
[etat_fiche_online] => en_ligne
[date_application] =>
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO21444-D1
[keywords] => triple negative breast cancer (TNBC), Prognosis, Treatment Response Prediction, SPARC
[pub_scient_inv_dispo] => Int J Cancer, 2023 Mar 15, Alcaraz et al, SPARC in cancer-associated fibroblasts is an independent poor prognostic factor in non-metastatic triple-negative breast cancer and exhibits pro-tumor activity, doi: 10.1002/ijc.34345. Epub 2022 Nov 30.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => LIAUDET-COOPMAN Emmanuelle,ROGER Pascal,GUIU Séverine,ALCARAZ CACCHIA Lindsay
[number_application] => European Procedure (Patents) (EPA) - 03 Nov. 2021 - 21 306 545.1
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => imaging,transcriptomics
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
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[user] => stdClass Object
(
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[first_name] => Inserm
[last_name] => Transfert
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[wp_user_level] => 2
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 101
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Breast Cancer, Imaging, Method, Oncology, Pre-Analytic Validation, Target, Transcriptomics
[taxonomieurl] =>
Biomarker,
Biomarker,
Breast Cancer,
Imaging,
Method,
Oncology,
Pre-Analytic Validation,
Target,
Transcriptomics
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[102] => stdClass Object
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[post] => stdClass Object
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[post_title] => METHOD FOR DIAGNOSING COLORECTAL CANCER
[guid] => https://technology-offers.inserm-transfert.com/offer/method-for-diagnosing-colorectal-cancer/
[post_content] => The present invention relates to the diagnosing of colorectal cancer. The inventors have thus designed an efficient, rapid and cost-effective method to purify and analyse mRNA from small volumes of blood plasma. They found that the RPS28, B2M, TIMP-1 and CLU levels were significantly higher in metastatic colorectal cancer patients. Thus, the present invention relates to a method for diagnosing a colorectal cancer in a subject in need thereof comprising i) determining in a sample obtained from the subject the expression levels of at least one biomarker selected from the group consisting of RPS28, B2M, TIMP-1 and CLU mRNAs.
[post_date] => 2023-03-08 13:50:01
[post_modified] => 2024-09-11 15:53:58
[ID] => 4896
)
[post_meta] => stdClass Object
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[object] =>
[application] =>
[idSugar] => cdd61d66-d036-3cb7-28ca-640885f41931
[etat_fiche_online] => en_ligne
[date_application] => 08-02-2022
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO21297-D1
[keywords] => Colorectal Cancer, Metastatis Colorectal Cancer, Diagnosis, RNA signature
[pub_scient_inv_dispo] => Sci Rep, 2023 Feb 15, Grosgeorges et al., A straightforward method to quantify circulating mRNAs as biomarkers of colorectal cancer, doi: 10.1038/s41598-023-29948-4.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => BLACHE Philippe
[number_application] => European Procedure (Patents) (EPA) - 08 Févr. 2022 - 22305131.9
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => transcriptomics
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
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[thera_area] => Therapy Area
[type_of_patent] => Type of patent
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[last_name] => Transfert
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[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 102
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Colorectal Cancer, Oncology, Pre-Analytic Validation, Transcriptomics
[taxonomieurl] =>
Biomarker,
Biomarker,
Colorectal Cancer,
Oncology,
Pre-Analytic Validation,
Transcriptomics
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[103] => stdClass Object
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[post_title] => METHODS FOR IMPROVING THE EFFICACY OF HDAC INHIBITOR THERAPY AND PREDICTING THE RESPONSE TO TREATMENT WITH HDAC INHIBITOR
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-improving-the-efficacy-of-hdac-inhibitor-therapy-and-predicting-the-response-to-treatment-with-hdac-inhibitor/
[post_content] => Investigating the impact of Tau protein expression in cancer cell lines, Inventors have demonstrated that the Tau expression is associated with an increased resistance to HDAC inhibittors. Briefly in the present invention, inventors report that Tau expression in breast cancer cell lines causes resistance to the anti-cancer effects of histone deacetylase inhibitors, by preventing histone deacetylase inhibitor-inducible gene expression and remodeling of chromatin structure. Inventors identify Tau as a protein recognizing and binding to core histone when H3 and H4 are devoid of any post-translational modifications or acetylated H4 that increases the Tauu2019s affinity. In addition, they demonstrate that the interaction between Tau and histones prevents further histone H3 post-translational modifications induced by histone deacetylase-inhibitor treatment by maintaining a more compact chromatin structureThe present invention relates to means to improve the bioavailability of histone deacetylase (HDAC) inhibitor and thereby also improve the efficacy of histone deacetylase (HDAC) inhibitor treatments.
[post_date] => 2023-03-07 16:10:01
[post_modified] => 2024-09-11 15:53:57
[ID] => 4895
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[date_application] => 20-09-2021
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO20332-D1
[keywords] => Tau inhibitor, HDAC inhibitor, Treatment response prediction, Breast Cancer, Companion Diagnostics
[pub_scient_inv_dispo] => Front Cell Dev Biol, 2021 Oct 14, Rico et al, Tau Stabilzes Chromatin Compaction, doi: 10.3389/fcell.2021.740550.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => RICO Thomas,LEFEBVRE Bruno,BUEE Luc
[number_application] => European Procedure (Patents) (EPA) - 20 Sept. 2021 - 21 306 299.5
[technology_engineering] =>
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[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
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[taxonomie] => Biomarker, Biomarker, Breast Cancer, Immunoassay, In vitro poc, Method, Oncology
[taxonomieurl] =>
Biomarker,
Biomarker,
Breast Cancer,
Immunoassay,
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[post_title] => NEW BIOMARKERS OF ALCOHOL USE DISORDERS
[guid] => https://technology-offers.inserm-transfert.com/offer
ew-biomarkers-of-alcohol-use-disorders/
[post_content] => The present invention relates to a method for predicting alcohol use disorder. The objective of this study was to validate the possibility of performing a plasma assay and to quantify the value of four plasmatic biomarkers of brain damage in patient with AUD, either at the onset of alcohol withdrawal in patients admitted for alcohol cessation or in abstinent patients with history of AUD. The inventors also 1) analysed the correlation between the levels of these biomarkers; 2) compared patients in alcohol cessation and abstinent patients; 3) analysed the association of these biomarkers, in alcohol cessation group, with the severity of alcohol withdrawal expressed by the dose of diazepam needed to control the signs of alcohol withdrawal the day after admission (D1) or the signs of neurologic severity of alcohol withdrawal on D1 expressed by WEu2019s symptoms. They showed that plasmatic Tau, NFL and UCHL1 are biomarkers of alcohol use disorders in alcoholic patients notably after cessation. Thus the invention relates a method for predicting alcohol use disorders (AUD) and their complications in a subject in need thereof comprising i) determining in a sample obtained from the subject the expression levels of at least one biomarker selected from the group consisting of Tau, NFL and UCHL1.
[post_date] => 2023-03-06 10:05:17
[post_modified] => 2024-09-11 15:53:52
[ID] => 4893
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[date_application] => 21-06-2022
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO21348-D1
[keywords] => Alcohol Use Disorder, Diagnosis, Prognosis, Blood Biomarker, Alcohol Withdrawal
[pub_scient_inv_dispo] => Addict Biol, 2022 Nov 27, Clergue-Duval et al, Plasma tau, NfL, GFAP and UCHL1 as candidate biomarkers of alcohol withdrawal-associated brain damage: A pilot study, doi: 10.1111/adb.13232.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => VORSPAN Florence,CLERGUE-DUVAL Virgile,BELLIVIER Frank,QUESTEL Frank,PAQUET Claire
[number_application] => European Procedure (Patents) (EPA) - 21 Juin 2022 - 22 305 898.3
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
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[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
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[comteur] => 104
[terms] => Array
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[taxonomie] => Addiction, Alcohol addiction, Biomarker, Biomarker, Central Nervous System, Human POC, Immunoassay
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Addiction,
Alcohol addiction,
Biomarker,
Biomarker,
Central Nervous System,
Human POC,
Immunoassay
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[105] => stdClass Object
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[post] => stdClass Object
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[post_title] => NEW METHOD TO DIAGNOSE INFLAMMATORY DISEASES
[guid] => https://technology-offers.inserm-transfert.com/offer
ew-method-to-diagnose-inflammatory-diseases/
[post_content] => The present invention relates to the diagnostic of inflammatory diseases. The inventors described methods using NET biomarkers as diagnostic biomarkers for inflammatory diseases. COVID-19, Lupus or mCRC are used here as illustrative models for investigating an inflammatory disease. Examples in highlighting variation of the respective correlation of NET biomarkers in this invention rely on the determination of the NET main constituents: (i), DNA as determined by examining the amount of circulating DNA (cirDNA) that corresponds to the amount of NET as being degradation by-products that are released into the circulation; (ii) NE; and (iii), MPO; as well as the detection of a blood compound being indirectly associated to NET formation like the anti-cardiolipin auto-antibody. The invention provides threshold values of NE, MPO, cir-nDNA, and cir-mtDNA blood concentrations and of MNR that can be combined to diagnose/screen individuals. Thus the invention relates to a method for diagnosing a subject for an inflammatory disease comprising the steps of i) determining in a sample obtained from the subject the level of at least one marker selected in the group consisting in NET protein markers, cir-nDNA, cir-mtDNA and/or a cir-DNA fragmentation index.
[post_date] => 2023-03-03 19:15:02
[post_modified] => 2024-09-11 15:53:52
[ID] => 4892
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[application] =>
[idSugar] => 635af42c-f35f-1a1e-6418-64023a0de313
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[date_application] => 06-08-2021
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO20525-D1
[keywords] => Inflammatory disease, Diagnosis, Net protein marker, cf-DNA, cir-DNA fragmentation index, Neutrophil extracellular traps (NET)
[pub_scient_inv_dispo] => J Med Virol. 2023 Jan, Pisareva et al., Persistence of neutrophil extracellular traps and anticardiolipin auto?antibodies in post?acute phase COVID?19 patients, doi: 10.1002/jmv.28209Genome Med. 2022, Pisareva et al. Neutrophil extracellular traps have auto-catabolic activity and produce mononucleosome-associated circulating DNA ,doi: 10.1186/s13073-022-01125-8
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => THIERRY Alain,PISAREVA Ekaterina,PASTOR Brice
[number_application] => European Procedure (Patents) (EPA) - 06 Août 2021 - 21 306 103.9
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay,sequencing
[post_categoryname] => Diagnostic
[parent_category] => 195
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[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 105
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Human POC, Immunoassay, Immunology, Inflammation, Sequencing
[taxonomieurl] =>
Biomarker,
Biomarker,
Human POC,
Immunoassay,
Immunology,
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[106] => stdClass Object
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[post] => stdClass Object
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[post_title] => METHODS AND KITS FOR IDENTIFYING AND QUANTIFYING STORAGE-INDUCED MICROERYTHROCYTES
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-kits-for-identifying-and-quantifying-storage-induced-microerythrocytes/
[post_content] => Refrigerated storage of red cell concentrates (RCC) for transfusion is associated with the accumulation of various alterations to the red blood cells (RBCs). Among these, a subpopulation of small RBCs defined as storage-induced microerythrocytes (SMEs) accumulates during storage. The SMEs subpopulation correlates with transfusion recovery. Quantification of this morphologically-altered RBC subpopulation using flow cytometry would be a valuable tool to evaluate RCC quality. In the present invention, RBC obtained at the beginning or at the end of storage from RCC stored in SAGM in blood bank conditions were treated with a carboxyfluorescein diacetate succinimidyl ester (CFDA-SE) staining protocol and were finally analysed by flow cytometry to assess the intensity of CFSE staining. The inventors observed the accumulation of a CFDA-SEhigh subpopulation by flow cytometry that accounted for 0.8% and 36.3% at day 3 and 42 of storage, respectively. Images confirmed that the CFDA-SEhigh subpopulation mostly contains SMEs. Thus SMEs can now be simply quantified using a common fluorescent dye and a standard flow cytometer.
[post_date] => 2023-03-03 17:30:01
[post_modified] => 2024-09-11 15:53:49
[ID] => 4891
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[application] =>
[idSugar] => 2f545daf-b231-c294-bd6f-6402219fe7d4
[etat_fiche_online] => en_ligne
[date_application] => 14-12-2021
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO20517-D1
[keywords] => Red Blood Cell Concentrate, Transfusion, storage-induced microerythrocytes
[pub_scient_inv_dispo] => Front Physiol, 2022 Feb 23, Marin et al., Storage-Induced Micro-Erythrocytes Can Be Quantified and Sorted by Flow Cytometry, doi: 10.3389/fphys.2022.838138. eCollection 2022.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => AMIREAULT Pascal,BUFFET Pierre,ROUSSEL Camille,MARIN Mickaël,PELTIER Sandy,DUSSIOT Michaël
[number_application] => European Procedure (Patents) (EPA) - 14 Déc. 2021 - 21 306 765.5
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
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[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
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[first_name] => Inserm
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[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 106
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Hematological Disorders, Human POC, Method
[taxonomieurl] =>
Biomarker,
Biomarker,
Hematological Disorders,
Human POC,
Method
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[107] => stdClass Object
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[post] => stdClass Object
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[post_title] => IVIG Composition and Method of Treatment of Antibody Deficient Patients
[guid] => https://technology-offers.inserm-transfert.com/offer/ivig-composition-and-method-of-treatment-of-antibody-deficient-patients/
[post_content] => The invention is in the field of therapy of antibody deficiencies such as immune diseases and inflammatory disorders. The inventors demonstrate for the first time the convergence of intestinal IgA and serum IgG responses toward the same microbial targets, under homeostatic conditions. Private anti-microbiota IgG specificities are induced in IgA-deficient patients, but are not found in IgG pools from healthy donors, partially explaining why substitutive IgG (IVIG) cannot regulate antibody deficiency-associated gut dysbiosis and intestinal translocation. Finally, in both controls and IgA-deficient patients, systemic anti-microbiota IgG responses correlate with reduced inflammation suggesting that systemic IgG responses contribute to the gut microbiota confinement. Accordingly, the invention relates to IVIGs (Intravenous immunoglobulins) composition containing at least 1% of immunoglobulins (Ig) from SIgAd (Selective IgA deficiency) patient and their use in the treatment of antibody deficiency disorders such as immune diseases, inflammatory disorders and autoimmune disease.
[post_date] => 2023-03-03 10:35:02
[post_modified] => 2024-09-11 15:43:12
[ID] => 4890
)
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[idSugar] => a8686d96-5e02-ef05-8ae9-6401b92e86f3
[etat_fiche_online] => en_ligne
[date_application] => 28-10-2019
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO18376-T1
[keywords] => IgG, IgA, IVIG, Antibody deficiencies
[pub_scient_inv_dispo] => J Allergy Clin Immunol. 2019 Apr;143(4):1575-1585.e4. doi: 10.1016/j.jaci.2018.09.036. Epub 2018 Dec 13
[access_to_detailed_offer] => /wp-content/uploads/BIO18376-T1_Gorochov.pdf
[rare_disease] => false
[second_indication] => false
[inventors] => GOROCHOV Guy,FADLALLAH Jehane,LARSEN Martin,STERLIN Delphine
[number_application] => European Procedure (Patents) (EPA) - 29 Oct. 2018 - 18 306 409.6
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
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[last_name] => Transfert
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)
[wp_user_level] => 2
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 107
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Drug, Immunology, Target, Target, Validation in vivo
[taxonomieurl] =>
Drug,
Immunology,
Target,
Target,
Validation in vivo
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[post_title] => Use of IRAP Inhibitors for the Treatment of Inflammatory Diseases
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=4887
[post_content] => Upon activation, mast cells rapidly release preformed inflammatory mediators from large cytoplasmic granules via regulated exocytosis. This acute degranulation is followed by a late activation phase involving synthesis and secretion of cytokines, growth factors and other inflammatory molecules via the constitutive pathway that remains ill-defined. Here the inventors describe a role for an insulin-responsive vesicle-like endosomal compartment, marked by insulin-regulated aminopeptidase (IRAP), in the secretion of TNF-? and IL-6 in mast cells and macrophages. IRAP-deficient mice are protected from TNF-dependent kidney injury and inflammatory arthritis. In the absence of IRAP, TNF fails to be efficiently exported from the Golgi. Chemical targeting of IRAP+ endosomes reduced pro-inflammatory cytokine secretion thereby highlighting this compartment as a promising target for the therapeutic control of inflammation. Thus the present invention relates to the use of IRAP inhibitors for the treatment of inflammatory diseases.
[post_date] => 2024-06-07 11:32:27
[post_modified] => 2024-09-24 11:10:03
[ID] => 4887
)
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[idSugar] => 48831228-be8e-a547-3fc4-63ff57c3bcf0
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[date_application] =>
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO21469-T1
[keywords] => IRAP, Inflammatory diseases, Mast cells, Macrophages
[pub_scient_inv_dispo] => J Allergy Clin Immunol. 2023 Jan 25;S0091-6749(23)00090-8. doi: 10.1016/j.jaci.2023.01.014
[access_to_detailed_offer] => http://technology-offers.inserm-transfert.com/wp-content/uploads/BIO21469-T1_Hermine.pdf
[rare_disease] => 0
[second_indication] => 0
[inventors] => HERMINE Olivier,RIGNAULT-BRICARD Rachel,VAN ENDERT Peter,DUSSIOT Michaël,TROVATI MACIEL Thiago,WEIMERSHAUS Mirjana,CARVALHO Caroline
[number_application] => European Procedure (Patents) (EPA) - 01 Déc. 2021 - 21 306 677.2
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[tags_order_view] => stdClass Object
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[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
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[first_name] => Inserm
[last_name] => Transfert
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[author] => 1
[um_member] => 1
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[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 108
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Drug, Immunology, Rheumatoid Arthritis, Target, Target, Validation in vivo
[taxonomieurl] =>
Drug,
Immunology,
Rheumatoid Arthritis,
Target,
Target,
Validation in vivo
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[109] => stdClass Object
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[post] => stdClass Object
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[post_title] => METHODS AND COMPOSITIONS FOR MODULATING MACROPHAGES POLARIZATION
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-compositions-for-modulating-macrophages-polarization/
[post_content] => Inventors have surprisingly found that Emricasan is a much more potent inhibitor of monocyte differentiation compared to q-VD-OH by its ability to efficiently inhibit caspase-8, which is instrumental to this process. In addition, they have demonstrated that Emricasan alleviates the IL4-mediated M2-like polarization of human macrophages. Moreover, Emricasan also hampers bleomycin-induced pulmonary fibrosis in mice, a disease associated with an infiltration of M2-macrophages. Finally, caspase-8 deficient mice were found to be resistant to bleomycin-induced pulmonary fibrosis. As a whole, their findings indicate that the beneficial effect of Emricasan relies on its ability to inhibit caspase-8, and its capacity to prevent monocyte differentiation and M2 polarization of macrophages. Accordingly, the invention relates to a caspase 8 inhibitor for use in the polarization of macrophages.
[post_date] => 2023-02-23 17:05:20
[post_modified] => 2024-09-20 16:10:02
[ID] => 4881
)
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[application] =>
[idSugar] => 6fdd1ad6-e3c1-3723-2694-5f6d9adbd36f
[etat_fiche_online] => en_ligne
[date_application] => 2019-10-03
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO19407-T1
[keywords] =>
[pub_scient_inv_dispo] => Reprogramming monocyte-derived macrophages through caspase inhibition Chantreuil P et al. OncoImunology 2022 VOL 11 issue 1 Article: 2015859
[access_to_detailed_offer] => http://technology-offers.inserm-transfert.com/wp-content/uploads/BIO19407-T1_Auberger.pdf
[rare_disease] => 1
[second_indication] => 0
[inventors] => AUBERGER Patrick,JACQUEL Arnaud,CHANTREUIL Paul,ROBERT Guillaume
[number_application] => European Procedure (Patents) (EPA) - 03 Oct. 2019 - 19 306 276.7
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[thera_area] => Therapy Area
[type_of_patent] => Type of patent
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[last_name] => Transfert
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 109
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Drug, Idiopathic pulmonary fibrosis, Method, Respiratory Disease, Small Molecule, Target, Validation in vivo
[taxonomieurl] =>
Drug,
Idiopathic pulmonary fibrosis,
Method,
Respiratory Disease,
Small Molecule,
Target,
Validation in vivo
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[110] => stdClass Object
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[post_title] => METHODS AND COMPOSITIONS FOR TREATING PULMONARY ALVEOLAR PROTEINOSIS RELATED TO MARS MUTATIONS
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-compositions-for-treating-pulmonary-alveolar-proteinosis-related-to-mars-mutations/
[post_content] => The present invention relates to a method for treating pulmonary alveolar proteinosis related to MARS gene mutations in a subject in need thereof comprising a step of administering said subject with a therapeutically effective amount of supplementation of methionine and/or its derivatives. Pulmonary alveolar proteinosis related to mutations in the gene encoding the methionine tRNA synthetase is a severe, early-onset lung disease that also associates liver involvement, failure to thrive, and systemic inflammation. Inventors describe an infant affected by this disease who was successfully treated by oral methionine supplementation. After three months of treatment she was free of respiratory symptoms, inflammation and cholestasis resolved, and there was a catchup in growth. Her bronchoalveolar lavage fluid was free of extracellular lipoproteinaceous material. Functional assays on peripheral monocytes, initially altered, normalized. This study paves the way for similar strategies in other tRNA synthetase deficiencies.
[post_date] => 2023-02-23 16:45:05
[post_modified] => 2024-09-20 16:05:03
[ID] => 4880
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[pub_scient_inv_dispo] => Methionine supplementation for multi-organ dysfunction in MetRS-related pulmonary alveolarproteinosis Hadchouel A. et al. Eur Respir J. 2021 Sep 9:2101554.
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[inventors] => HADCHOUEL-DUVERGE Alice,SCHIFF Manuel,PONTOIZEAU Clément
[number_application] => European Procedure (Patents) (EPA) - 26 Mai 2021 - 21 305 689.8
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[post_title] => USE OF B CELL DEPLETING AGENTS FOR THE TREATMENT OF RHEUMATIC HEART DISEASE
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[post_content] => Rheumatic heart disease (RHD) ranks as one of the most serious cardiovascular scourges of the past century and remains a force to be reckoned with in the developing world. Using the B-HOT panel, developed in part by our team, and based on heatmap analysis, we show two distinct transcriptomic profiles between inflammatory burden region of RHD valves patients (n=13) and control valves (without lesions, n=10). Our differential gene expression analysis between those 2 groups show several genes overexpressed in RHD group compared to control valves. Interestingly, and as potential therapeutic targets, genes related to CD20 (MS4A1, MS4A2) are among genes that are differentially expressed. Taken together, these results suggest a potential role for CD20 in inflammatory responses of RHD valves lesions. Anti-CD20 antibodies, like Rituximab (CD20), would be potential therapeutic molecules to be used on RHD patients.
[post_date] => 2023-02-23 15:15:03
[post_modified] => 2024-09-11 15:43:06
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[number_application] => European Procedure (Patents) (EPA) - 01 Juin 2021 - 21 305 727.6
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[post_title] => METHODS FOR IMPROVING RELAXATION OF STRIATED MYOCYTES
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-improving-relaxation-of-striated-myocytes/
[post_content] => The Inventors developed conditions allowing to efficiently detect differences in cardiomyocytes relaxation phases associated with increased cardiomyocytes stiffness. Theyused a library of patient-specific human induced pluripotent stem cells (hiPSC) either from healthy donors or carrying mutations (i.e., MYH7 and BRAF mutations) associated with hypertrophic cardiomyopathy, a condition typically associated with impaired diastolic function as well as an increase in cardiomyocytes passive stiffness. They performed a high throughput screening on hiPSC-derived cardiac cells to identify microRNAs capable of modifying the relaxation rates of cardiomyocytes. In particular, they set up a large-scale functional genomics using miRNAs screening. All identified miRNAs were tested for their impact on cardiac cells movement and calcium transient. miRNAs with the highest impact were in particular tested on ECTs and changes in diastolic function, were measured and compared to the results obtained at the cell level. They manipulated the most interesting u2019hitsu2019 in 3D models using similar readouts as in primary assays. They tested the impact of the positive u2019hitsu2019 in mechanical models (developed during the exploratory part) and establish physiological and biochemical mechanisms of action of the identified key proteins. They finally identified two promisingmiRNAs that could be used for improving striated myocytes relaxation and, more generally, to alleviate symptoms related to striated muscle stiffness, in particular in the context of heartfailure with a preserved ejection fraction (HFpEF).
[post_date] => 2023-02-23 15:05:19
[post_modified] => 2024-09-11 15:43:06
[ID] => 4878
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[bd_referent] => Aymeric EMPEREUR
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[inventors] => HULOT Jean-Sébastien,VERMERSCH Eva
[number_application] => European Procedure (Patents) (EPA) - 09 Juil. 2021 - 21 305 954.6
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[taxonomie] => Cardiovascular Diseases, Drug, Hit - validation in vivo, Left ventricular dysfunction, Oligonucleotide, Product, Product
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[post_title] => USE OF INHIBITORS OF PHOSPHATASE ACTIVITY OF SOLUBLE EPOXIDE FOR THE TREATMENT OF CARDIOMETABOLIC DISEASES
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-inhibitors-of-phosphatase-activity-of-soluble-epoxide-for-the-treatment-of-cardiometabolic-diseases/
[post_content] => The growing prevalence of obesity and type 2 diabetes complicates risk and clinical management by potentiating and/or exacerbating hypertension, hyperlipidemia, atherosclerosis and cardiomyopathy, leading to increasing use of the term u201ccardiometabolic diseaseu201d (CMD) to encompass the many facets of this complex syndrome. The inventors assessed the role of the soluble epoxide hydrolase (she) phosphatase domain in metabolism and cardiovascular system, by generating sEH phosphatase knock-in (KI) animals (rats). They unexpectedly revealed that inhibition of the phosphatase domain of sEH could improve cardiac systolic function, decrease body weight, increase insulin sensitivity. More over under high fat diet, the animals have a decreased body weight gain, were protected against the development of insulin resistance, hepatic steatosis and cardiac hypertrophy. Inhibition of the phosphatase domain of sEH could thus represent a new pharmacological target in the treatment of cardiometabolic diseases.
[post_date] => 2023-02-23 13:45:03
[post_modified] => 2024-09-11 15:44:14
[ID] => 4876
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[date] =>
[bd_referent] => Aymeric EMPEREUR
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[reference_online] => BIO18299-T1
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[pub_scient_inv_dispo] => Hydrolase activity) Varennes, Olivier et al. u201cThe Metabolism of Epoxyeicosatrienoic Acids by Soluble Epoxide Hydrolase Is Protective against the Development of Vascular Calcification.u201d International journal of molecular sciences vol. 21,12 4313. 17 Jun. 2020, doi:10.3390/ijms21124313
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[rare_disease] => false
[second_indication] => true
[inventors] => BELLIEN Jérémy,DJERADA Zoubir
[number_application] => European Procedure (Patents) (EPA) - 17 Sept. 2018 - 18 306 207.4
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[post_categoryname] => Therapeutic
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[taxonomie] => Cardiovascular Diseases, Drug, Target, Target, Validation in vivo
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Cardiovascular Diseases,
Drug,
Target,
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[post_title] => METHODS OF TREATMENT OF INFLAMMATORY BOWEL DISEASES
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=4875
[post_content] => Inventoru2019s general objective was to investigate the potential role of mucosal thrombin in intestinal inflammation and its mechanisms of action. First, they evaluated whether there is an increased presence of active thrombin in Crohnu2019s Disease (CD): both in patient tissues and in an animal models of IBD. Second, they investigated the effects on mucosal damage and tissue dysfunction resulting from the intracolonic administration of thrombin at a dose comparable to what was detected in the tissue of CD patients. Third, they demonstrated in IBD mouse model that pharmacological inhibition of mucosal thrombin activity is a new therapeutic approach to this debilitating condition, such inhibition, allows to significantly decrease all inflammatory parameters including the fecal bleeding score. Finally, inventors showed that human mucosa- associated commensal biofilms exposed to increasing concentrations of human thrombin exhibited increase in their virulent properties specifically, increased bacterial invasion into human epithelial cell line). So, the present invention relates to a method for preventing or treating inflammatory bowel diseases (IBD) such as Crohnu2019s disease (CD) and ulcerative colitis (UC) by targeting locally the mucosal Thrombin.
[post_date] => 2023-02-23 15:45:03
[post_modified] => 2024-09-20 15:05:04
[ID] => 4875
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[date_application] => 2021-09-06
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO20161-T1
[keywords] => Mucosal thrombin antagonist, PAR1 antagonist, Inflammatory bowel disease
[pub_scient_inv_dispo] => J Crohns Colitis. 2021 May 4;15(5):787-799. doi: 10.1093/ecco-jcc/jjaa229.Nat Commun. 2019 Jul 19;10(1):3224. doi: 10.1038/s41467-019-11140-w.Br J Pharmacol. 2018 Sep;175(18):3656-3668. doi: 10.1111/bph.14430. Epub 2018 Aug 7.
[access_to_detailed_offer] => /wp-content/uploads/BIO20161-T1_Vergnolles.pdf
[rare_disease] => 0
[second_indication] => 0
[inventors] => VERGNOLLE Nathalie,DERAISON Céline,MOTTA Jean-Paul
[number_application] => European Procedure (Patents) (EPA) - 07 Sept. 2020 - 20305988.6
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[post_categoryname] => Therapeutic
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[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
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[taxonomie] => Drug, Gastrointestinal Diseases, Inflammatory Bowel Disease / Crohn's Disease, Target, Target, Validation in vivo
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[post_title] => Safety and Efficacy of MAIT cells for Adoptive Cell Therapy Prevention of GvHD
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=4873
[post_content] => The inventors explored in an allogeneic situation the regulatory potential of Mucosal-Associated Invariant T cells (MAIT cells), a population of unconventional T cells that exhibit potent antibacterial activity, expressing a semi-invariant TCR which recognizes vitamin B2 derivatives of microbial origin presented by the MR1 molecule. In particular, the inventors used i) an allogenic reaction model in vitro (mixed lymphocyte reaction, MLR) and ii) murine model of xenogeneic aGvHD They first verified that human MAIT cells do not proliferate in response to allogeneic stimulation in vitro (MLR) or in vivo (immunodeficient mice) alone but require for their expansion both an inflammatory environment and TCR ligation by its ligand. In contrast, MAIT cells are able to inhibit the proliferation of allospecific LT in vitro in a dose-dependent manner. Furthermore, the adoptive transfer of MAIT cells in a mouse model of xeno-GVHD resulted in a delay in early or late GvHD development. Altogether, these data describe a new regulatory function of MAIT cells in an allogeneic context, allowing us to consider their use in cell therapy to limit GvHD.
[post_date] => 2024-06-07 11:32:26
[post_modified] => 2024-09-18 18:20:02
[ID] => 4873
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[date] =>
[bd_referent] => Nathan POMORSKI
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[contact_email] => nathan.pomorski@inserm-transfert.fr
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[reference_online] => BIO20499-T1
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[rare_disease] => 0
[second_indication] => 0
[inventors] => CAILLAT-ZUCMAN Sophie,TALVARD-BALLAND Nana
[number_application] => European Procedure (Patents) (EPA) - 10 Déc. 2020 - 20 306 528.9
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[post_categoryname] => Therapeutic
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[contact_email] => contact@inserm-transfert.fr
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[taxonomie] => Drug, Graft Versus Host Disease (GVHD), Immunology, Method, Transplantation
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Graft Versus Host Disease (GVHD),
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[post_title] => New Method to Treat Acidosis Related Diseases
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=4856
[post_content] => The present invention relates to the treatment of acidosis related diseases. In this study, the inventors have investigated how human monocytes adapt, survive and differentiate into macrophages under lactic acidosis. Experiments were conducted under atmospheric oxygen and in the presence of glucose, to rule out an effect of oxygen or glucose deprivation. Prolonged exposure to LA affected monocyte/macrophage metabolism. Extracellular acidosis induced mitochondrial membrane depolarization and significantly decreased nutrient consumption, resulting in a dependence of the macrophages on a transient phase of autophagy for survival. In fasting conditions, hepatocytes produce the ketone bodies acetoacetate (AcAc) and ?-hydroxybutyrate (?-OHB) that constitute alternative fuel for extrahepatic cells. The inventors found here that AcAc protected the mitochondria from acidosis-induced depolarization and mitophagy, allowing the cells to continue to metabolize nutrients, thereby avoiding the need for self-catabolism to survive. Acetoacetate therefore appears to be a crucial alternative fuel metabolite of potential therapeutic interest to increase tissue tolerance to lactic acidosis. Thus, the invention relates to the acetoacetate (AcAc) for use in the treatment of acidosis related diseases.
[post_date] => 2023-02-23 15:50:04
[post_modified] => 2024-09-18 19:00:02
[ID] => 4856
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[date_application] => 2022-07-07
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO19221-T1
[keywords] => Acetoacetate, Acidosis
[pub_scient_inv_dispo] => Nat Commun. 2021 Dec 8;12(1):7115. doi: 10.1038/s41467-021-27426-x
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[rare_disease] => 0
[second_indication] => 0
[inventors] => DELNESTE Yves,ASFAR Pierre,BEAUVILLAIN Céline,JEANNIN Pascale,PROCACCIO Vincent
[number_application] => European Procedure (Patents) (EPA) - 08 Juil. 2021 - 21305941.3
[technology_engineering] =>
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[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 116
[terms] => Array
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[taxonomie] => Drug, Hit - validation in vitro, Immunology, Method, Product, Small Molecule
[taxonomieurl] =>
Drug,
Hit - validation in vitro,
Immunology,
Method,
Product,
Small Molecule
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[post_title] => Targeting the Secreted IgE Poly-A Signal Allows Specific Inhibition of Allergen-Specific IgE Production
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=4854
[post_content] => Immunoglobulins (Ig) are expressed either on the surface of B cells or as secreted antibodies by plasma cells that represents the final stage of B cell differentiation. The present invention involves the use of antisense oligonucleotides (ASOs) for either reducing the production of the secreted form or either reducing the production of the membrane form. In particular, the inventors show that antisense oligonucleotides masking the secretory polyadenylation signal induce a decrease in the production of the secreted immunoglobulin. Inversely, antisense oligonucleotides masking the membrane polyadenylation signal induce a decrease in the production of the membrane-anchored immunoglobulin. The proof of concept has been obtained using an ASO hybridizing to the polyadenylation signal (PAS) sequence of the transcript encoding the secreted form of IgE. Indeed, the targeting of this PAS sequence induces a drastic decrease in IgE production. Thus the choice of the right antisense oligonucleotide would be suitable for the treatment of diseases associated to B-cell development (e.g. autoimmune diseases, inflammation or B-cell malignancies).
[post_date] => 2023-03-01 11:45:04
[post_modified] => 2024-09-11 15:43:09
[ID] => 4854
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[idSugar] => 2bccbaca-279c-4d92-e2bd-5e7cee46eee7
[etat_fiche_online] => en_ligne
[date_application] => 03-06-2020
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO19135-T1
[keywords] => Antisens oligonucleotide, Immunoglobulin, Allergy, B Cell Lymphomas
[pub_scient_inv_dispo] => J Allergy Clin Immunol. 2022 May;149(5):1795-1801. doi: 10.1016/j.jaci.2021.09.039. Epub 2021 Nov 2
[access_to_detailed_offer] => /wp-content/uploads/BIO19135-T1_Delpy.pdf
[rare_disease] => false
[second_indication] => false
[inventors] => DELPY Laurent,MARCHALOT Anne,COGNE Michel,LAFFLEUR Brice
[number_application] => European Procedure (Patents) (EPA) - 04 Juin 2019 - 19305716.3
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[parent_category] => 195
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[comteur] => 117
[terms] => Array
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[taxonomie] => Allergies, Antisense Oligonucleotide, Drug, Hit - validation in vivo, Immunology, Oligonucleotide, Product, Product
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Antisense Oligonucleotide,
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Hit - validation in vivo,
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Product
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[post_title] => New Vaccinal Strategy to Prevent or Treat Rheumatoid Arthritis
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=4852
[post_content] => The present invention relates to field of treatment of rheumatoid arthritis. The inventors propose that PAD4, one of the enzymes which convert arginine into citrulline, is a target antigen for T cells that help the production of ACPA. They recently demonstrated that PAD immunization triggers anti-citrullinated fibrinogen antibody production in normal mice. Here, they demonstrate that the risk (OR) to develop RA associated with each of 12 HLA-DRB1 genotype correlates with the likelihood for the two HLA-DR molecules encoded by each genotype to bind at least one random peptide from PAD4, but not from citrullinated or native fibrinogen. PBLs from patients wih RA, PsA and controls proliferate to PAD4 and they identify, notably, a peptide from PAD4, p8 (SEQ ID NO: 6), that stimulates T cells from RA patients and a few patients with PsA. Proliferative responses to p8 are associated with RA, shared epitope positive HLA-DR alleles and antibodies to PAD4. Thus the present invention relates to a peptide derived from the PAD4 protein and its use in the treatment and prevention of rheumatoid arthritis.
[post_date] => 2024-09-20 14:55:07
[post_modified] => 2024-09-20 14:55:07
[ID] => 4852
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[etat_fiche_online] => en_ligne
[date_application] => 2020-03-06
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO19058-T1
[keywords] => Rheumatoid arthritis, Vaccine, PAD4
[pub_scient_inv_dispo] => Arthritis Rheumatol. 2020 Jun;72(6):903-911. doi: 10.1002/art.41189. Epub 2020 Apr 26Proc Natl Acad Sci USA. 2017 Nov 21;114(47):E10169-E10177. doi: 10.1073/pnas.1713112114. Epub 2017 Nov 6.
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[rare_disease] => 0
[second_indication] => 0
[inventors] => ROUDIER Jean,AUGER Isabelle,BALANDRAUD Nathalie
[number_application] => European Procedure (Patents) (EPA) - 07 Mars 2019 - 19 305 265.1
[technology_engineering] =>
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[post_categoryname] => Therapeutic
[parent_category] => 195
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[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
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[terms] => Array
(
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[taxonomie] => Biologic, Drug, Identification, Immunology, Rheumatoid Arthritis, Target, Target, Vaccine
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Biologic,
Drug,
Identification,
Immunology,
Rheumatoid Arthritis,
Target,
Target,
Vaccine
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[post] => stdClass Object
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[post_title] => Nanobody Against ELA2A to Treat Inflammatory Bowel Diseases (IBD) or Irritable Bowel Syndrome (IBS)
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=4844
[post_content] => The invention is in the field of therapy of gut inflammatory diseases such as Inflammatory Bowel Diseases (IBD) or Irritable Bowel Syndrome (IBS) including Gluten hypersensitivity. The inventors showed that ELA2A secreted by epithelial cells in the extracellular space is over-expressed in IBD conditions degrading tight junction proteins and controlling cytokines expression. Overexpression of ELA2A conferred a pro-inflammatory phenotype both in cell expression systems and in vivo in animal model of IBD. The inventors also showed that ELA2 over-expressing intestinal epithelial cells increase the release of CXCL8 protein compared to control cells. The increased CXCL-8 protein release observed in cells overexpressing ELA2A is inhibited by ELAFIN addition to the culture, in a dose-dependent manner. In particular, the invention relates to inhibitors of Elastase ELA2A, for use in the treatment of Inflammatory Bowel Diseases, such as Crohnu2019s Disease, Ulcerative Colitis, Celiac disease, and Pouchitis.
[post_date] => 2023-03-02 18:00:02
[post_modified] => 2024-09-20 15:05:05
[ID] => 4844
)
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[application] =>
[idSugar] => ff687fe5-66f8-4c70-afed-266b69a3dbd3
[etat_fiche_online] => en_ligne
[date_application] => 2017-06-16
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO1508601 -T1
[keywords] => Inflammatory Bowel Diseases, ELA2A
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => /wp-content/uploads/BIO1508601-T1_Vergnolles.pdf
[rare_disease] => 0
[second_indication] => 0
[inventors] => ROLLAND Corinne,DERAISON Céline
[number_application] => European Procedure (Patents) (EPA) - 16 Juin 2016 - 16 305 731.8
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 119
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Drug, Immunology, Target, Target, Validation in vivo
[taxonomieurl] =>
Drug,
Immunology,
Target,
Target,
Validation in vivo
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[120] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => Hepcidin Antagonists for Use in the Treatment of Inflammation
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=4840
[post_content] => The present invention relates to a hepcidin antagonist for use in the treatment of inflammatory diseases. TLR4-dependant intestinal hepcidin induces neutrophil migration and intestinal inflammation, and are expressed by lipopolysaccharides. The hepcidin is a proinflammatory molecule in macrophages which demonstrated its interest in inflammatory bowel diseases (IBDs).
[post_date] => 2024-10-08 18:20:02
[post_modified] => 2024-10-08 18:20:04
[ID] => 4840
)
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[application] =>
[idSugar] => e5e439de-495a-4d49-957e-11a2cb9e35e5
[etat_fiche_online] => en_ligne
[date_application] => 2016-03-14
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] => +33622908798
[reference_online] => BIO14455-T1
[keywords] => Hepcidin, Inflammatory Bowel Disease, Inflammation
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => /wp-content/uploads/BIO14455-Hepcidin-Antagonists-for-Use-in-the-Treatmet-Of-Inflammation.pdf
[rare_disease] => 0
[second_indication] => 0
[inventors] => ZUMERLE Sara,MATHIEU Jacques
[number_application] => European Procedure (Patents) (EPA) - 13 Mars 2015 - 15 159 033.8
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
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[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 120
[terms] => Array
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[taxonomie] => Drug, Identification, Immunology, Product, Target
[taxonomieurl] =>
Drug,
Identification,
Immunology,
Product,
Target
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[121] => stdClass Object
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[post] => stdClass Object
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[post_title] => UALH hAR cell line
[guid] => https://technology-offers.inserm-transfert.com/?p=4825
[post_content] => UALH were generated by transfection of osteocarcinoma cancer U2OS cells with the (ARE-RAD9)6-collagenase-Luciferase-SV40-hygromycin plasmid. UALH hAR cells were generated by co-transfection of UALH cells with the plasmids pSG5-hAR-puromycin and pSG5-hAR-Renilla-luciferase-(ARE-RAD9)6-collagenase-Luciferase-SV40-neomycin. The plasmid (ARE RAD9)6-Coll-Luc-SVNeo contains a luciferase gene driven by the mouse mammary tumor virus promoter and a neomycin phosphotransferase gene under the control of SV40 promoter. The pSG5-puro plasmid pSG5-human AR-puromycin enables to express the human androgen receptor (hAR). Puromycin N-acetyl transferase selection marker expression confers resistance to puromycin. The plasmid pSG5-hAR-Renilla-Neomycin contains the gene coding for hAR under the control of the SV40 promoter, the Renilla luciferase reporter gene under the control of the constitutive human cytomegalovirus (CMV), the firefly luciferase gene under the control of six androgen response elements (ARE) from the RAD9 gene promoter and placed upstream of the collagenase promoter, and the resistance gene to neomycin under the control of the SV40 promoter. This third plasmid has been included to over-express both AR and luciferase expression.
[post_date] => 2023-05-19 18:45:04
[post_modified] => 2024-09-11 16:06:53
[ID] => 4825
)
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[reference_online] => RT00586
[keywords] => hAR, luciferase, pharmaceutical and environmental androgens
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[access_to_detailed_offer] =>
[rare_disease] => false
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[number_application] =>
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[post_categoryname] => Cell Lines
[parent_category] => 215
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[first_name] => Patrick
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[comteur] => 121
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[taxonomie] => Industry Research (screening, tox.studies, bioreactor, ...), Oncology
[taxonomieurl] =>
Industry Research (screening, tox.studies, bioreactor, ...),
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[122] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => HAHLH (hAhR) cell line
[guid] => https://technology-offers.inserm-transfert.com/?p=4817
[post_content] => HAHLH were generated by transfection of cervical cancer HeLa cells with the XRE(TnGCGTG)3-TATA-Luciferase-SV40-Hygromycin plasmid. The plasmid XRE(TnGCGTG)3-TATA -Luc-SVHygro contains a luciferase gene driven by three AhR responsive elements and a hygromycin gene under the control of SV40 promoter.
[post_date] => 2023-05-19 18:45:02
[post_modified] => 2024-09-11 16:07:23
[ID] => 4817
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[date] =>
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[keywords] => hAhR, luciferase, pharmaceutical and environmental hAhR ligands
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[first_name] => Patrick
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[taxonomieurl] =>
Industry Research (screening, tox.studies, bioreactor, ...),
Oncology
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[post] => stdClass Object
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[post_content] => UALH were generated by transfection of osteocarcinoma cancer U2OS cells with the (ARE-RAD9)6-collagenase-Luciferase-SV40-hygromycin plasmid. The plasmid (ARE RAD9)6-Coll-Luc-SVNeo contains a luciferase gene driven by the mouse mammary tumor virus promoter and a neomycin phosphotransferase gene under the control of SV40 promoter.
[post_date] => 2023-05-19 18:45:04
[post_modified] => 2024-09-11 16:07:22
[ID] => 4816
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[first_name] => Patrick
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[bd_referent] =>
[contact_description] =>
[contact_email] =>
[contact_phone] =>
)
[comteur] => 123
[terms] => Array
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)
[taxonomie] => Industry Research (screening, tox.studies, bioreactor, ...), Oncology
[taxonomieurl] =>
Industry Research (screening, tox.studies, bioreactor, ...),
Oncology
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[124] => stdClass Object
(
[post] => stdClass Object
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[post_title] => UG5LN cell line
[guid] => https://technology-offers.inserm-transfert.com/?p=4811
[post_content] => UG5LN were generated by transfection of osteocarcinoma cancer U20S cells with the (GAL4RE)5-betaGlobin-Luciferase-SV40-Neomycin plasmid. The plasmid (GAL4RE)5-betaGlob-Luc-SVNeo contains a luciferase gene driven by a pentamer of yeast activator GAL4 binding sites in front of beta-globin promoter and a neomycin phosphotransferase gene under the control of SV40 promoter.
[post_date] => 2023-05-19 18:45:04
[post_modified] => 2024-09-11 16:07:21
[ID] => 4811
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[first_name] => Patrick
[last_name] => BALAGUER
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(
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[bd_referent] =>
[contact_description] =>
[contact_email] =>
[contact_phone] =>
)
[comteur] => 124
[terms] => Array
(
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)
[taxonomie] => Industry Research (screening, tox.studies, bioreactor, ...), Oncology
[taxonomieurl] =>
Industry Research (screening, tox.studies, bioreactor, ...),
Oncology
)
[125] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => UG5LN GAL4-hMR cell line
[guid] => https://technology-offers.inserm-transfert.com/?p=4810
[post_content] => UG5LN were generated by transfection of osteocarcinoma cancer U2OS cells with the (GAL4RE)5-betaGlobin-Luciferase-SV40-Neomycin plasmid.UG5LN GAL4-hMR cells were generated by transfection of UG5LN cells with the pSG5-puro plasmid pSG5-GAL4-human MR-puromycin.The plasmid (GAL4RE)5-betaGlob-Luc-SVNeo contains a luciferase gene driven by a pentamer of yeast activator GAL4 binding sites in front of beta-globin promoter and a neomycin phosphotransferase gene under the control of SV40 promoter.The pSG5-puro plasmid pSG5-human GAL4-hMR-puromycin enables to express the DNA binding domain of the yeast activator GAL4 (GAL4 DBD) followed by the ligand binding domain of the human mineralocorticoid receptor (hMR LBD). Puromycin N-acetyl transferase selection marker expression confers resistance to puromycin.
[post_date] => 2023-05-19 18:45:04
[post_modified] => 2024-09-11 16:07:22
[ID] => 4810
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[post_categoryname] => Cell Lines
[parent_category] => 215
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[comteur] => 125
[terms] => Array
(
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[taxonomie] => Industry Research (screening, tox.studies, bioreactor, ...), Oncology
[taxonomieurl] =>
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Oncology
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[126] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => HRLN (hRAR alpha) cell line
[guid] => https://technology-offers.inserm-transfert.com/?p=4809
[post_content] => HRLN were generated by transfection of cervical cancer HeLa cells with the (RARE)3-TK-Luciferase-SV40-Neomycin plasmid. The plasmid (RARE)3-TK-Luc-SVNeo contains a luciferase gene driven by three retinoid receptor responsive element (RARE) in front of thymidine kinase promoter and a neomycin phosphotransferase gene under the control of SV40 promoter.
[post_date] => 2023-05-19 18:45:04
[post_modified] => 2024-09-11 16:07:23
[ID] => 4809
)
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[post_title] => PrkcdG510S/G510S mice - Preclinical model of lupus
[guid] => https://technology-offers.inserm-transfert.com/?p=4736
[post_content] => We introduced the Prkcd G510S mutation that we previously associated to a Mendelian cause of SLE in the mouse genome, by means of CRISPR-Cas9 gene editing. PrkcdG510S/G510S mice recapitulate the human phenotype, presenting with glomerulonephritis, splenomegaly, and various serum autoantibodies, including anti-nuclear, and had reduced lifespan. We demonstrate that this phenotype is linked to a B cell autonomous role of PRKCD in immune regulation. The penetrance of the lupus phenotype is 100% in this mouse model.
[post_date] => 2023-01-04 18:55:01
[post_modified] => 2024-09-11 16:07:02
[ID] => 4736
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[keywords] => Lupus mouse model; autoimmunity mouse model; preclinical model of lupus
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[taxonomie] => Academic Research, Genomic variability, Immunology, Inflammation, Lupus nephritis, Proof of concept in vivo, Systemic Lupus Erythematosus
[taxonomieurl] =>
Academic Research,
Genomic variability,
Immunology,
Inflammation,
Lupus nephritis,
Proof of concept in vivo,
Systemic Lupus Erythematosus
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[post_title] => HG5LN GAL4-hPPAR beta/delta cell line
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=4722
[post_content] => HG5LN were generated by transfection of cervical cancer HeLa cells with the (GAL4RE)5-betaGlobin-Luciferase-SV40-Neomycin plasmid. HG5LN GAL4-hPPAR beta/delta cells were generated by transfection of HG5LN cells with the plasmid pSG5-GAL4-human PPAR beta/delta-puromycin. The plasmid (GAL4RE)5-betaGlob-Luc-SVNeo contains a luciferase gene driven by a pentamer of yeast activator GAL4 binding sites in front of beta-globin promoter and a neomycin phosphotransferase gene under the control of SV40 promoter. The pSG5-puro plasmid pSG5-human GAL4-hPPAR beta/delta -puromycin enables to express the DNA binding domain of the yeast activator GAL4 (GAL4 DBD) followed by the ligand binding domain of the human peroxisome proliferator activated receptor receptor beta/delta (hPPAR beta/delta LBD). Puromycin N-acetyl transferase selection marker expression confers resistance to puromycin.
[post_date] => 2023-05-19 18:45:03
[post_modified] => 2024-09-11 16:07:21
[ID] => 4722
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[taxonomie] => Industry Research (screening, tox.studies, bioreactor, ...), Oncology
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Industry Research (screening, tox.studies, bioreactor, ...),
Oncology
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[138] => stdClass Object
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[post_title] => METHODS AND COMPOSITIONS FOR TREATING CELL SENESCENCE ACCUMULATION RELATED DISEASE
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-compositions-for-treating-cell-senescence-accumulation-related-disease-2/
[post_content] => The inventors have surprisingly demonstrated that GD3 positive senescent cells inhibit NK cell in vitro and in vivo while GD3 negative senescent cells is associated with NK cell functionality, both with human or murine cells. The inventorsu2019 results bring the proof of concept that GD3 expression may represent a Senescence-associated Immune Checkpoint (SIC) that determines senescent cell immunogenicity and identify GD3 and more generally SIC as a multi-hit target for age-associated diseases. Thus, GD3 may be a major step forward in the development of efficient anti-senescence immunotherapies. In particular, the present invention relates to a method for identifying whether a cell is in senescence process comprising the steps of: i) measuring the co-expression level of ST8Sia1 (GD3) with a senescence marker in a biological sample; ii) comparing the co-expression level measured at step i) with its predetermined reference value, and iii) concluding that the cell is in senescence process when the co-expression level of GD3 with a senescence marker is higher than its predetermined reference value or concluding that cell is not in senescence process when the co-expression level of GD3 with a senescence marker is lower or similar than its predetermined reference value. The present invention also relates a method for treating senescent cells accumulation related disease in a subject in need thereof, comprising administering to said subject a therapeutically effective amount of a GD3 inhibitor.
[post_date] => 2022-11-03 13:35:01
[post_modified] => 2024-09-11 15:53:38
[ID] => 4719
)
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[idSugar] => 9cf2f804-ee40-2efb-a29f-6363b88bd3f0
[etat_fiche_online] => en_ligne
[date_application] => 23-04-2021
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO19413-D1
[keywords] => Senescent cells, ageing, Scenescence-associated Immune Checkoint
[pub_scient_inv_dispo] => https:/doi.org/10.1101/2021.04.23.440408
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => CHERFILS Julien,GILSON Eric,ILTIS Charlène
[number_application] => United States Of America (PSP) - 23 Avr. 2021 - 63/178,738
[technology_engineering] =>
[multidisciplinary_field] => ageing
[technological_platform] => immunoassay,transcriptomics
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
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[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 138
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Ageing, Animal POC, Biomarker, Biomarker, Idiopathic pulmonary fibrosis, Immunoassay, Method, Respiratory Disease, Transcriptomics
[taxonomieurl] =>
Ageing,
Animal POC,
Biomarker,
Biomarker,
Idiopathic pulmonary fibrosis,
Immunoassay,
Method,
Respiratory Disease,
Transcriptomics
)
[139] => stdClass Object
(
[post] => stdClass Object
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[post_title] => NEW METHOD TO EVALUATE PANCREATIC PROGNOSIS
[guid] => https://technology-offers.inserm-transfert.com/offer
ew-method-to-evaluate-pancreatic-prognosis/
[post_content] => The present invention relates to the prediction of the survival time of a patient suffering of a pancreatic cancer. In this study, the inventors aimed to determine whether PDAC could be stratified on the basis of their GT gene expression profiles involved in the biosynthesis of glycoconjugates. By using bioinformatic analysis of RNA-seq data focused on 169 GT genes from patient-derived xenografts (PDX), they have identified a combination of 19 GT, which was able to discriminate 3 clusters of PDAC associated with specific molecular profiles and clinical features of patients. These GT genes were validated on public databases as a prognostic glyco-signature, which could allow best patient care in the future and also highlight new potential targets for diagnosis and prognosis of PDAC. Thus, the invention relates to a method for predicting the survival time of a patient suffering from a pancreatic cancer comprising i) determining in a sample obtained from the patient the expression level of at least one gene selected in the group consisting in GALNT9, A4GNT, B3GALT5, B3GNT6, C1GALT1, FUT2, FUT3, FUT4, FUT6, GALNT4, GALNT6, GALNT12, GCNT1, GYG2, LFNG, MGAT5, ST6GALNAC1, ST8SIA3 and XYLT.
[post_date] => 2022-10-19 14:20:02
[post_modified] => 2024-09-11 15:53:37
[ID] => 4709
)
[post_meta] => stdClass Object
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[object] =>
[application] =>
[idSugar] => 1c5f04b0-a0b9-4136-cada-634ffc218b81
[etat_fiche_online] => en_ligne
[date_application] => 29-03-2021
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO19060-D1
[keywords] => Pancreatic Cancer, RNA signatiure, RNA-Seq, Glycoprotein metabolism signature, Prognosis
[pub_scient_inv_dispo] => EBioMedicine, 2021 Sep, Abd-El-Halim et al. , A glycosyltransferase gene signature to detect pancreatic ductal adenocarcinoma patients with poor prognosis, doi: 10.1016/j.ebiom.2021.103541. Epub 2021 Aug 20.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => MAS Eric,SILVY Françoise,IOVANNA Juan-Lucio,DUSETTI Nelson,MOHAMED ABD-EL-HALIM Yousra
[number_application] => European Procedure (Patents) (EPA) - 29 Mars 2021 - 21 305 391.1
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => transcriptomics
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
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[type_of_patent] => Type of patent
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 139
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Human POC, Method, Oncology, Pancreatic Cancer, Transcriptomics
[taxonomieurl] =>
Biomarker,
Biomarker,
Human POC,
Method,
Oncology,
Pancreatic Cancer,
Transcriptomics
)
[140] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHODS FOR THE DIAGNOSIS AND TREATMENT OF T CELL-LYMPHOMAS CCR8
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-the-diagnosis-and-treatment-of-t-cell-lymphomas-ccr8/
[post_content] => T-cell lymphomas are a heterogeneous group of malignancies involving T lymphocytes and generally characterized by a poor prognosis. Among them, cutaneous T-cell lymphomas involve primarily the skin. Mycosis fungoides and Sézary syndrome are the most frequent cutaneous T-cell lymphomas. The inventors studied the regulatory T phenotype of Sézary cells and showed the expression of CCR8 (CD198) by Sézary cells and other T-cell lymphoma cell lines. CCR8 therefore appears as a useful diagnostic, prognostic and follow-up marker, and as a potential therapeutic target in T-cell lymphomas. Therapeutic depletion of CCR8-expressing cancer cells would eliminate tumor cells and also activate the anti-tumor immunity in T-cell lymphomas.
[post_date] => 2022-10-19 13:40:03
[post_modified] => 2024-09-11 15:53:36
[ID] => 4708
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => 589a57bb-131a-c004-478b-634ff3314d7c
[etat_fiche_online] => en_ligne
[date_application] => 23-03-2021
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO21120-D1
[keywords] => T-Cell Lymphoma, Diagnostic, Prognosis, CCR8, FACS based approach
[pub_scient_inv_dispo] => Blood Adv, 2022 Jun 14, Giustiniani et al., CCR8 is a new therapeutic target in cutaneous T-cell lymphomas, doi: 10.1182/bloodadvances.2021006512.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => BENSUSSAN Armand,DE MASSON Adele,BATTISTELLA Maxime,GIUSTINIANI Jérôme,BAGOT Martine,ORTONNE Nicolas,MARIE-CARDINE Anne
[number_application] => European Procedure (Patents) (EPA) - 23 Mars 2021 - 21 305 356.4
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 140
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Human POC, Immunoassay, Lymphoma, Method, Oncology, Sezary syndrome
[taxonomieurl] =>
Biomarker,
Biomarker,
Human POC,
Immunoassay,
Lymphoma,
Method,
Oncology,
Sezary syndrome
)
[141] => stdClass Object
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[post] => stdClass Object
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[post_title] => METHOD FOR DIAGNOSING PANCREATIC CANCER
[guid] => https://technology-offers.inserm-transfert.com/offer/method-for-diagnosing-pancreatic-cancer/
[post_content] => The present invention relates to the diagnostics of pancreatic cancer. The inventors engineered a novel biomarker discovery approach, tailored for PDAC, which is all-patient inclusive, termed PanEXPEL. This approach offers access to PDAC clinical material before any treatment is applied. The method benefits from clinical biopsy, yet does not interfere with that diagnostic procedure. It can be integrated seamlessly into clinical routine, and is compatible with any type of OMICS profiling. PanEXPEL relies on the interstitial tissue fluid released from the lesion during diagnostic biopsy by endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA). This is the first technique that allows both clinicians and researchers to analyze identical material in the field of proteomics biomarker research. Here, they demonstrate the potential of PanEXPEL methodology by identifying a PDAC early detection signature through proteomics and subsequent statistical learning. Thus, the present invention relates to a method for diagnosing a pancreatic cancer in a subject in need thereof comprising determining in a sample obtained from the subject the expression levels of at least one biomarker selected from the group consisting of AGR2, ANXA2, ANXA3, ANXA4, CECAM6, CYP2S1, DMBT1, KRT7, KRT8, KRT17, KRT18, KRT19, MAL2, MYH14, OLFM4, PIGR, SERPINB5, SERPINH1, and TIMP1.
[post_date] => 2022-10-19 10:05:16
[post_modified] => 2024-09-11 15:53:35
[ID] => 4707
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => 3079991a-090f-5093-3642-634fc1855a42
[etat_fiche_online] => en_ligne
[date_application] => 17-03-2021
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO20559-D1
[keywords] => Pancreatic Cancer, Machine learning, Protein Signature Score, Mass spectrometry, Preservcyte
[pub_scient_inv_dispo] => Endoscopy, 2022 May 5, Souche et al., Detection of soluble biomarkers of pancreatic cancer in endoscopic ultrasound-guided fine-needle aspiration samples, doi: 10.1055/a-1550-2503.Clinical Trial: NCT03791073.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => TURTOI Andrei,COLINGE Jacques,SOUCHE François Régis,TOSATO Guillaume
[number_application] => European Procedure (Patents) (EPA) - 17 Mars 2021 - 21 305 326.7
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => mass_spectrometry
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
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[user] => stdClass Object
(
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[first_name] => Inserm
[last_name] => Transfert
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(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 141
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Mass spectrometry, Oncology, Pancreatic Cancer, Pre-Analytic Validation
[taxonomieurl] =>
Biomarker,
Biomarker,
Mass spectrometry,
Oncology,
Pancreatic Cancer,
Pre-Analytic Validation
)
[142] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHOD FOR PRONOSIS AND TREATING A PATIENT SUFFERING FROM CANCER
[guid] => https://technology-offers.inserm-transfert.com/offer/method-for-pronosis-and-treating-a-patient-suffering-from-cancer/
[post_content] => Complement components form a plasma innate immune cascade but could also serve as multitasking proteins, as they have functions beyond this system. Here, we show that complement FH is locally expressed by multiple types of human tumors. We provide a paradigm shift for the impact of FH on cancer progression, showing a previously unrecognized, intracellular function of FH outside the complement cascade, while the canonical, complement-regulatory function had no effect. Int-FH served as a driver of the proliferation and migration of ccRCC and lung ADK cells but not of normal cells or lung SCC cells. The presence of int-FH staining in tumor cells indicated poor prognosis for ccRCC and lung ADK.Thus, the invention relates to a method for predicting the survival time of a patient suffering from a cancer, comprising i) determining in a sample obtained from the patient the expression level of int-FH ii) comparing the expression level determined at step i) with its predetermined reference value and iii) providing a prognosis when the expression level determined at step i) is modulated compared to its predetermined reference value.
[post_date] => 2022-10-19 08:15:02
[post_modified] => 2024-09-11 15:53:33
[ID] => 4705
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => bf18fd78-0b25-5f8e-e328-634fa6646948
[etat_fiche_online] => en_ligne
[date_application] => 12-02-2021
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO19289-D1
[keywords] => intracellular-FH, pronostic, companion diagnostic, Solid tumor, Kidney Cancer, Lung Cancer, Liver Cancer, IHC
[pub_scient_inv_dispo] => Cancer Immunol Res,Epub 2021 May 26, Daugan et a., Intracellular Factor H Drives Tumor Progression Independently of the Complement Cascade, doi: 10.1158/2326-6066.CIR-20-0787.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => ROUMENINA Lubka,REVEL Margot,CREMER Isabelle,DAUGAN Marie,SAUTES-FRIDMAN Catherine,FRIDMAN Wolf Herman (Hervé)
[number_application] => European Procedure (Patents) (EPA) - 12 Févr. 2021 - 21 305 187.3
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 142
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Immunoassay, Method, Oncology, Pre-Analytic Validation, Solid Tumors
[taxonomieurl] =>
Biomarker,
Biomarker,
Immunoassay,
Method,
Oncology,
Pre-Analytic Validation,
Solid Tumors
)
[143] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => BILE SALTS BACTOSENSOR AND USE THEREOF FOR DIAGNOSTIC AND THERAPEUTIC PURPOSES
[guid] => https://technology-offers.inserm-transfert.com/offer/bile-salts-bactosensor-and-use-thereof-for-diagnostic-and-therapeutic-purposes-2/
[post_content] => Bile salts are steroid acids derived from cholesterol in the liver, are released into the gastrointestinal tract to aid in digestion and are thoroughly modified by the resident gut microbiota. Bile acids act as versatile signaling molecules with a variety of endocrine functions and are linked to several diseases. In particular, serum and urinary bile salts represent biomarkers for early diagnostics of liver dysfunction, yet their current detection methods are impractical and hard to scale. Here the inventors engineered engineered synthetic bile salt receptors using VtrA as sensing domains connected to E. coli CadC system which activates transcription upon dimerization. The performance of the system was assayed for various selection of promoters and they can show that fine tunable response that may be reached by changing expression levels of the bile salt receptor. By performing multiple rounds of directed evolution of the VtrA sensor the inventors obtained a collection of variants with a lower limit of detection and a higher sensitivity. Finally, they show that their bactosensor can detect pathological bile-salt concentrations in samples from patients with liver dysfunction. The present invention thus relates to bile salts bactosensor and use thereof for diagnostic and therapeutic purposes.
[post_date] => 2022-10-11 15:20:01
[post_modified] => 2024-09-11 15:53:31
[ID] => 4696
)
[post_meta] => stdClass Object
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[object] =>
[application] =>
[idSugar] => 7a10898c-b241-39d6-73f2-63457fd48808
[etat_fiche_online] => en_ligne
[date_application] => 08-02-2021
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO20498-D1
[keywords] => Liver Dysfunctions, Bile Salts concentration, Synthetic Biology
[pub_scient_inv_dispo] => Nat Commun,2021 Sep 1, Chang et al., Programmable receptors enable bacterial biosensors to detect pathological biomarkers in clinical samples, doi: 10.1038/s41467-021-25538-y.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => BONNET Jérôme,CHANG Hung Ju
[number_application] => European Procedure (Patents) (EPA) - 08 Févr. 2021 - 21 305165.9
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[post_title] => METHODS OF ASSESSING THE RISK OF DEVELOPING PROGRESSIVEMULTIFOCAL LEUKOENCEPHALOPATHY IN PATIENTS TREATED WITHVLA-4 ANTAGONISTS
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-of-assessing-the-risk-of-developing-progressivemultifocal-leukoencephalopathy-in-patients-treated-withvla-4-antagonists/
[post_content] => Natalizumab a monoclonal antibody is associated with the risk of progressive multifocal leukoencephalopathy (PML), an infection caused by the John Cunningham (JC) virus. The inventors explored the hypothesis that bacteria should be involved in the onset of PML in connection to the HLA-DR haplotype in multiple sclerosis (MS) patients. Thus 625 MS patients starting Natalizumab therapy from the BIONAT study were followed prospectively. Among those patients, 12 developed a PML. Outside the BIONAT cohort, we included nine additional MS patients with PML who had been referred to our center. For each patient, blood metagenomics sequencing and sequencing-based typing for HLA-DRB1*15:01 ancestral haplotype were determined. HLA-DRB1*15:01 haplotype carriers show a protection against PML (p=0.03). Among blood taxa, at genus level, Phyllobacterium was only significantly associated in HLA-DRB1*15:01 haplotype carriers with an inflammatory marker (p2% have an odds ratio of 4.55 (95% confidence intervals 1.82-11.37; p=0.001) of developing or having PML under NTZ treatment. In conclusion, the inventors showed a relation between the HLA-DRB1*15:01 haplotype, the circulating microbiota and the risk of PML. The interaction between blood microbiota and the HLA-DRB1*15:01 haplotype may play a role in the virulence of the viruses.
[post_date] => 2022-10-07 17:15:01
[post_modified] => 2024-09-11 15:53:30
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[bd_referent] => Pierre MAZOT
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[keywords] => Natalizumab; progressive multifocal leukoencephalopathy (PML); multiple sclerosis (MS) patients; HLA-DR haplotype; Microbiota
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[rare_disease] => false
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[inventors] => AMAR Jacques,BRASSAT David,PIGNOLET Béatrice
[number_application] => European Procedure (Patents) (EPA) - 29 Janv. 2021 - 21305115.4
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[post_content] => HG5LN were generated by transfection of cervical cancer HeLa cells with the (GAL4RE)5-betaGlobin-Luciferase-SV40-Neomycin plasmid. HG5LN GAL4-hPPAR gamma cells were generated by transfection of HG5LN cells with the plasmid pSG5-GAL4-human PPAR gamma-puromycin. The plasmid (GAL4RE)5-betaGlob-Luc-SVNeo contains a luciferase gene driven by a pentamer of yeast activator GAL4 binding sites in front of beta-globin promoter and a neomycin phosphotransferase gene under the control of SV40 promoter. The pSG5-puro plasmid pSG5-human GAL4-hPPAR gamma-puromycin enables to express the DNA binding domain of the yeast activator GAL4 (GAL4 DBD) followed by the ligand binding domain of the human peroxisome proliferator activated receptor receptor gamma (hPPAR gamma LBD). Puromycin N-acetyl transferase selection marker expression confers resistance to puromycin.
[post_date] => 2023-05-19 18:45:03
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[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=4693
[post_content] => HG5LN were generated by transfection of cervical cancer HeLa cells with the (GAL4RE)5-betaGlobin-Luciferase-SV40-Neomycin plasmid. HG5LN GAL4-hPPAR alpha cells were generated by transfection of HG5LN cells with the plasmid pSG5-GAL4-human PPAR alpha-puromycin. The plasmid (GAL4RE)5-betaGlob-Luc-SVNeo contains a luciferase gene driven by a pentamer of yeast activator GAL4 binding sites in front of beta-globin promoter and a neomycin phosphotransferase gene under the control of SV40 promoter. The pSG5-puro plasmid pSG5-human GAL4-hPPAR alpha-puromycin enables to express the DNA binding domain of the yeast activator GAL4 (GAL4 DBD) followed by the ligand binding domain of the human peroxisome proliferator activated receptor receptor alpha hPPAR alpha LBD. Puromycin N-acetyl transferase selection marker expression confers resistance to puromycin.
[post_date] => 2023-05-19 18:45:03
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[post_title] => METHODS FOR INCREASING FETAL HEMOGLOBIN CONTENT IN EUKARYOTIC CELLS AND USES THEREOF FOR THE TREATMENT OF HEMOGLOBINOPATHIES
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-increasing-fetal-hemoglobin-content-in-eukaryotic-cells-and-uses-thereof-for-the-treatment-of-hemoglobinopathies/
[post_content] => The clinical severity of ?-hemoglobinopathies is alleviated by the co-inheritance of genetic mutations causing a sustained fetal ?-globin chain production at adult age, a condition termed hereditary persistence of fetal hemoglobin (HPFH). Here, the inventors have compared the extent of fetal hemoglobin (HbF) de-repression following CRISPR/Cas9-mediated targeting of different regions of the HBG1 and HBG2 promoters in an adult erythroid cell line (HUDEP-2). They achieved a potent and pancellular HbF re-activation upon disruption of binding sites for ?-globin repressors located in both HBG1 and HBG2 genes. They validated these findings in Red Blood Cells (RBCs) derived from genome edited Sickle Cell Disease (SCD) patient hematopoietic stem/progenitor cells. Overall, this study identified a binding site for an HbF repressor as a novel and potent target for the treatment of ?-hemoglobinopathies. Accordingly, the present invention relates to a method for increasing fetal hemoglobin content in a eukaryotic cell comprising the step of disrupting the binding site for Leukemia/lymphoma-related factor (LRF) in the HBG1 or HBG2 promoter.
[post_date] => 2022-09-29 12:45:01
[post_modified] => 2024-09-11 15:43:46
[ID] => 4674
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[date] =>
[bd_referent] => Aymeric EMPEREUR
[bd_referent_id] =>
[contact_email] => aymeric.empereur@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO18215-T1
[keywords] => CRISPR
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http:/
[rare_disease] => true
[second_indication] => false
[inventors] => MICCIO Annarita,WEBER Leslie
[number_application] => European Procedure (Patents) (EPA) - 11 Sept. 2018 - 18 306 191.0
[technology_engineering] => gene_therapy
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[taxonomie] => Biologic, Candidate drug, Drug, Gene Therapy, Gene therapy, Hematological Disorders, Product, Thalassemia
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Biologic,
Candidate drug,
Drug,
Gene Therapy,
Gene therapy,
Hematological Disorders,
Product,
Thalassemia
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[148] => stdClass Object
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[post_title] => Transgenic mouse model for myotonic dystrophy: DM300 carrying 300 CTG repeats
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=4651
[post_content] => Transgenic mouse model carrying the myotonic dystrophy type 1 (DM1) locus (45kb of human sequences) with the DMPK gene and about 300 unstable CTG repeats.
[post_date] => 2022-12-01 16:25:01
[post_modified] => 2024-09-11 16:06:55
[ID] => 4651
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[date] =>
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[keywords] => Myotonic dystrophy; Trinucleotide repeat instability
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[nickname] => Geneviève GOURDON
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[taxonomie] => Academic Research, Central Nervous System, Genetic Disorders, Industry Research (screening, tox.studies, bioreactor, ...), Musculoskeletal, Proof of concept in vivo
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Academic Research,
Central Nervous System,
Genetic Disorders,
Industry Research (screening, tox.studies, bioreactor, ...),
Musculoskeletal,
Proof of concept in vivo
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[post_title] => NANOPARTICLES FOR TREATING OR PREVENTING A CARDIOMYOPATHY AND ANTHRACYCLINE-CYTOTOXICITY, AND THEIR ADMINISTRATION AS AN AEROSOL
[guid] => https://technology-offers.inserm-transfert.com/offer
anoparticles-for-treating-or-preventing-a-cardiomyopathy-and-anthracycline-cytotoxicity-and-their-administration-as-an-aerosol/
[post_content] => Anthracyclines such as doxorubicin are chemotherapeutic molecules are also widely incorporated in many chemotherapy protocols. However, their clinical use is still limited by time- and dose-dependent cardiotoxicity. Herein the inventors have determined the therapeutic potential of acidic nanoparticles (NPs) in doxo-treated cardiac cells. In particular, they have identified a set of grafted nanoparticles as non-toxic and which rapidly internalize into lysosomes in cardiac cells. Such NPs improve lysosomal acidification and autophagic flux blockade caused by bafilomycin A1, chloroquine and doxorubicin, resulting in reduced oxidative stress, preserved mitochondrial integrity and improved cell survival. Thus, the invention relates to a biocompatible and biodegradable nanoparticle having a diameter of 100 nm or less, wherein the nanoparticle is selected from: a poly(lactic-co-glycolic acid) (PLGA) nanoparticle, a poly(lactic acid) (PLA) nanoparticle, a poly(glutamic acid) (PGA) nanoparticle, a polycaprolactone (PCL) nanoparticle, and/or a polyester nanoparticle; for use in a method for treating or preventing a cardiomyopathy or anthracycline cytotoxicity.
[post_date] => 2022-09-22 16:10:01
[post_modified] => 2024-09-11 15:44:19
[ID] => 4647
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[idSugar] => 71ec5824-9107-5022-8029-632c7ec6e1f5
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[date_application] => 26-08-2019
[date] =>
[bd_referent] => Aymeric EMPEREUR
[bd_referent_id] =>
[contact_email] => aymeric.empereur@inserm-transfert.fr
[contact_phone] =>
[reference_online] => CHIM1902901-T1
[keywords] =>
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => PEREZ Jeanne,LECHEVALLIER Séverine,SANTIN Yohan,VERELST Marc Raoul Joseph
[number_application] => European Procedure (Patents) (EPA) - 10 Sept. 2020 - 20 306 004.1
[technology_engineering] =>
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[post_categoryname] => Therapeutic
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[terms] => Array
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[taxonomie] => Cardiomyopathy, Cardiovascular Diseases, Drug, Method, Target, Validation in vitro
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Cardiomyopathy,
Cardiovascular Diseases,
Drug,
Method,
Target,
Validation in vitro
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[150] => stdClass Object
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[post_title] => METHODS AND PHARMACEUTICAL COMPOSITIONS FOR INDUCING IMMUNE TOLERANCE BY MUCOSAL VACCINATION WITH FC-COUPLED ANTIGENS
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-pharmaceutical-compositions-for-inducing-immune-tolerance-by-mucosal-vaccination-with-fc-coupled-antigens/
[post_content] => The present invention relates to methods and pharmaceutical compositions of inducing immune tolerance by mucosal vaccination with Fc-coupled antigens. In particular, the present invention relates to a method for inducing tolerance to one antigen of interest in a subject in need thereof, comprising the mucosal administration to the subject of a therapeutically effective amount of a recombinant chimeric construct comprising a FcRn targeting moiety and an antigen-containing moiety.
[post_date] => 2022-09-22 15:50:01
[post_modified] => 2024-09-11 15:43:36
[ID] => 4646
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[idSugar] => e2ee384e-4ba7-4c8b-9078-7a3b6b0f65ac
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[date_application] => 17-07-2015
[date] =>
[bd_referent] => Aymeric EMPEREUR
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[contact_email] => aymeric.empereur@inserm-transfert.fr
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[reference_online] => BIO15274-T1
[keywords] =>
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => /wp-content/uploads/Licensing-opportunity-Immunology-Therapeutic-June2018_Mallone.pdf
[rare_disease] => false
[second_indication] => false
[inventors] => GUPTA Nimesh,CULINA Slobodan,LACROIX-DESMAZES Sébastien
[number_application] => European Procedure (Patents) (EPA) - 17 Juil. 2015 - 15 306 169.2
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[terms] => Array
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[taxonomie] => Biologic, Diabetes, Drug, Metabolic Disorders, Product, Type 1 Diabetes (Juvenile Diabetes), Vaccine
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Biologic,
Diabetes,
Drug,
Metabolic Disorders,
Product,
Type 1 Diabetes (Juvenile Diabetes),
Vaccine
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[151] => stdClass Object
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[post_title] => ANTIGENIC PEPTIDES DERIVING FROM UROCORTIN 3 AND USES THEREOF FOR THE DIAGNOSIS AND TREATMENT OF TYPE 1 DIABETES
[guid] => https://technology-offers.inserm-transfert.com/offer/antigenic-peptides-deriving-from-urocortin-3-and-uses-thereof-for-the-diagnosis-and-treatment-of-type-1-diabetes/
[post_content] => Despite the notion that human CD8+ T cells are the final mediators of autoimmune ?- cell destruction in type 1 diabetes (T1D), none of their target epitopes has been demonstrated to be naturally processed and presented by ? cells. The inventors therefore performed an epitope discovery study combining HLA Class I peptidomics and transcriptomics strategies.Inflammatory cytokines increased ?-cell peptide presentation in vitro, paralleling upregulation of HLA Class I expression. Peptide sources included known ?-cell antigens and several insulin granule proteins. Urocortin 3 was identified as a novel ?-cell antigen, which was processed into HLA-A2- and HLA-A3-restricted epitopes recognized by circulating naïve CD8+ T cells in type 1 diabetic and healthy donors. Accordingly, the present invention relates to antigenic peptides derived from urocortin-3 and uses thereof for the diagnosis and treatment of T1D.
[post_date] => 2022-09-22 15:45:01
[post_modified] => 2024-09-11 15:43:34
[ID] => 4645
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[date] =>
[bd_referent] => Aymeric EMPEREUR
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[access_to_detailed_offer] => http:/
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[inventors] => MALLONE Roberto,GONZALEZ-DUQUE Sergio,AFONSO Georgia,VINH Joëlle,VERDIER Yann,AZOURY Marie Eliane
[number_application] => European Procedure (Patents) (EPA) - 16 Mars 2018 - 18 305 288.5
[technology_engineering] =>
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[technological_platform] =>
[post_categoryname] => Therapeutic
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[taxonomie] => Biologic, Diabetes, Drug, Metabolic Disorders, Product, Target, Type 1 Diabetes (Juvenile Diabetes)
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Biologic,
Diabetes,
Drug,
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Product,
Target,
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[post_title] => ANTIGENIC PEPTIDES DERIVING FROM PCSK2 AND USES THEREOF FOR THE DIAGNOSIS AND TREATMENT OF TYPE 1 DIABETES
[guid] => https://technology-offers.inserm-transfert.com/offer/antigenic-peptides-deriving-from-pcsk2-and-uses-thereof-for-the-diagnosis-and-treatment-of-type-1-diabetes/
[post_content] => Despite the notion that human CD8+ T cells are the final mediators of autoimmune ?-cell destruction in type 1 diabetes (T1D), none of their target epitopes has been demonstrated to be naturally processed and presented by ? cells. The inventors therefore performed an epitope discovery study combining HLA Class I peptidomics and transcriptomics strategies. Inflammatory cytokines increased ?-cell peptide presentation in vitro, paralleling upregulation of HLA Class I expression. Peptide sources included known ?-cell antigens and several insulin granule proteins. PCSK2 was identified as a novel ?-cell antigen, which was processed into HLA-A2-restricted epitopes recognized by circulating naïve CD8+ T cells in type 1 diabetic and healthy donors. Accordingly, the present invention relates to antigenic peptides derived from PCSK2 and uses thereof for the diagnosis and treatment of T1D.
[post_date] => 2022-09-22 15:45:01
[post_modified] => 2024-09-11 15:43:34
[ID] => 4644
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[number_application] => European Procedure (Patents) (EPA) - 16 Mars 2018 - 18 305 287.7
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[taxonomie] => Biologic, Diabetes, Drug, Metabolic Disorders, Product, Target, Type 1 Diabetes (Juvenile Diabetes)
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Biologic,
Diabetes,
Drug,
Metabolic Disorders,
Product,
Target,
Type 1 Diabetes (Juvenile Diabetes)
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[post_title] => ANTIGENIC PEPTIDES DERIVING FROM SECRETOGRANIN V AND USES THEREOF FOR THE DIAGNOSIS AND TREATMENT OF TYPE 1 DIABETES
[guid] => https://technology-offers.inserm-transfert.com/offer/antigenic-peptides-deriving-from-secretogranin-v-and-uses-thereof-for-the-diagnosis-and-treatment-of-type-1-diabetes/
[post_content] => Despite the notion that human CD8+ T cells are the final mediators of autoimmune ?- cell destruction in type 1 diabetes (T1D), none of their target epitopes has been demonstrated to be naturally processed and presented by ? cells. The inventors therefore performed an epitope discovery study combining HLA Class I peptidomics and transcriptomics strategies.Inflammatory cytokines increased ?-cell peptide presentation in vitro, paralleling upregulation of HLA Class I expression. Peptide sources included known ?-cell antigens and several insulin granule proteins. Secretogranin V (SCG5/7B2) was identified as a novel ?-cell antigen, which was processed into HLA-A2- and HLA-A3-restricted epitopes recognized by circulating naïve CD8+ T cells in type 1 diabetic and healthy donors. HLA-A2-bound neo-epitopes were also represented and originated from an alternative SCG5-009 mRNA splice isoform. Accordingly, the present invention relates to antigenic peptides derived from secretogranin V and uses thereof for the diagnosis and treatment of T1D.
[post_date] => 2022-09-22 15:40:01
[post_modified] => 2024-09-11 15:43:35
[ID] => 4643
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[inventors] => MALLONE Roberto,GONZALEZ-DUQUE Sergio,VINH Joëlle,COLLI Maikel Luis,AFONSO Georgia,VERDIER Yann,LAKS EIZIRIK Decio
[number_application] => European Procedure (Patents) (EPA) - 16 Mars 2018 - 18 305 286.9
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[terms] => Array
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[taxonomie] => Biologic, Diabetes, Drug, Metabolic Disorders, Product, Target, Type 1 Diabetes (Juvenile Diabetes)
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Biologic,
Diabetes,
Drug,
Metabolic Disorders,
Product,
Target,
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[154] => stdClass Object
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[post_title] => USE OF AGENTS CAPABLE OF INDUCING LC3-ASSOCIATED PHAGOCYTOSIS FOR TREATING SUSTAINED INFLAMMATION IN PATIENTS SUFFERING FROM CHRONIC LIVER DISEASE
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-agents-capable-of-inducing-lc3-associated-phagocytosis-for-treating-sustained-inflammation-in-patients-suffering-from-chronic-liver-disease/
[post_content] => Sustained hepatic and systemic inflammation, in particular originating from monocyte/macrophages, is a driving force for chronic liver disease progression to cirrhosis and underlies the development of multiorgan failure. Therefore, reprogramming monocyte/macrophage phenotype has emerged as an interesting strategy to limit inflammation during chronic liver injury. The inventors report here that a non-canonical form of autophagy, LC3-associated phagocytosis (LAP), is endogenously enhanced in blood and liver monocytes from cirrhotic patients and is negatively correlated to the levels of inflammatory markers in these patients. Pharmacological inhibition of LAP components or genetic disruption of LAP (Rubicon-deficient mice in myeloid cells), exacerbates the inflammatory signature in isolated human cirrhotic monocytes and the hepatic inflammatory profile in mice with chronic liver injury, resulting in enhanced liver fibrosis. Mice overexpressing human Fc?RIIA in CD11b+ cells show enhanced LAP in response to chronic liver injury, and are protected against inflammation and liver fibrosis. Finally, endogenous activation of LAP is lost in monocytes from severe cirrhotic patients with massive systemic inflammation, and restored upon exposure to intravenous monomeric Immunoglobulin (IVIg). These data shed light on a novel role for LAP in the protection against inflammation during cirrhosis and its progression to severe stages and thus suggest that agents capable of inducing LAP are suitable for treating sustained inflammation in patients suffering from chronic liver disease
[post_date] => 2022-09-22 15:35:01
[post_modified] => 2024-09-11 15:43:45
[ID] => 4642
)
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[date] =>
[bd_referent] => Aymeric EMPEREUR
[bd_referent_id] =>
[contact_email] => aymeric.empereur@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO18182-T1
[keywords] =>
[pub_scient_inv_dispo] => Autophagy. 2020 Aug;16(8):1526-1528. doi: 10.1080/15548627.2020.1770979. Epub 2020 May 31.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => LOTERSZTAJN Sophie,BEN MKADDEM Sanae,WAN JingHong,MONTEIRO-COSTA Renato,WEISS Emmanuel,CODOGNO Patrice,SAVEANU Loredana
[number_application] => European Procedure (Patents) (EPA) - 16 Janv. 2019 - 19 305 050.7
[technology_engineering] =>
[multidisciplinary_field] => fibrosis
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
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[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
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[first_name] => Aymeric
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[comteur] => 154
[terms] => Array
(
[0] => Therapeutic
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[taxonomie] => Drug, Fibrosis, Gastrointestinal Diseases, Liver Disease, Method, Non-Alcoholic Steatohepatitis, Target
[taxonomieurl] =>
Drug,
Fibrosis,
Gastrointestinal Diseases,
Liver Disease,
Method,
Non-Alcoholic Steatohepatitis,
Target
)
[155] => stdClass Object
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[post] => stdClass Object
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[post_title] => GDF3 AS BIOMARKER AND BIOTARGET IN POST-ISCHEMIC CARDIAC REMODELING
[guid] => https://technology-offers.inserm-transfert.com/offer/gdf3-as-biomarker-and-biotarget-in-post-ischemic-cardiac-remodeling-2/
[post_content] => Markers of an intense scarring process in the early phase post- myocardial infarction (MI) are still undetermined, and the identification of patients at higher risk of developing large adverse fibrotic remodeling and heart failure remains challenging. Here, the inventors demonstrate the modulation in the paracrine behavior of resident PW1+ cells in scarring cardiac tissue post-MI and the differential abundance of 12 candidate markers in their secretome. Of these, growth differentiation factor 3 (GDF3), a member of transforming growth factor-? family, upregulates proliferation of cardiac fibroblasts, which are instrumental in fibrosis. GDF3 is upregulated in the scarred tissue and plasma of mice and humans post-MI, with the highest plasma levels predicting higher fibrotic cardiac remodeling and cardiac dilation. The inventors thus reveal the previously unidentified function of GDF3 in predicting adverse fibrotic cardiac remodeling post-MI. Thus the present invention relates to the use of GDF3 as biomarker and biotarget in post-ischemic cardiac remodeling.
[post_date] => 2022-09-20 17:00:02
[post_modified] => 2024-09-11 15:43:57
[ID] => 4633
)
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[date] =>
[bd_referent] => Aymeric EMPEREUR
[bd_referent_id] =>
[contact_email] => aymeric.empereur@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO20319-T1
[keywords] =>
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => HULOT Jean-Sébastien
[number_application] => European Procedure (Patents) (EPA) - 05 Oct. 2020 - 20 306 156.9
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[first_name] => Aymeric
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[contact_description] =>
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)
[comteur] => 155
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Biomarker, Cardiovascular Diseases, Chronic Heart Failure, Drug, Target, Target, Validation in vitro
[taxonomieurl] =>
Biomarker,
Cardiovascular Diseases,
Chronic Heart Failure,
Drug,
Target,
Target,
Validation in vitro
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[156] => stdClass Object
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[post_title] => Intestinal Cathelicidin Antimicrobial Peptide Shapes the Gut Microbiota to Educate the Immune System and Prevent Pancreatic Autoimmunity
[guid] => https://technology-offers.inserm-transfert.com/?post_type=inserm_forms&p=4610
[post_content] => The present invention relates to the treatment of autoimmune diseases. The inventors determined that the cathelicidin related antimicrobial peptide (CRAMP) expression was defective in the colon of newborn NOD mice and that this defect was responsible for early dysbiosis. Dysbiosis stimulated the colonic epithelium to produce type I IFNs that pathologically imprinted the local immune system during the pre-weaning period. This miseducation of the immune system promoted the pancreatic autoimmune response and the development of diabetes. Increasing colonic CRAMP expression in newborn NOD mice, by local CRAMP treatment or by CRAMP-expressing probiotic, restored colonic homeostasis, and halted the diabetogenic response preventing autoimmune diabetes. Thus, they identified whether a defective colonic expression in the CRAMP antimicrobial peptide promotes autoimmunity in the pancreas. The use of CRAMP-expressing probiotic can be very helpful to treat autoimmune diseases and particularly autoimmune type 1 diabetes or obesity. Thus, the present invention relates to a recombinant CRAMP-expressing food-grade bacterium and its use in the treatment of autoimmune diseases.
[post_date] => 2024-06-07 11:32:26
[post_modified] => 2024-09-19 14:30:02
[ID] => 4610
)
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[object] =>
[application] =>
[idSugar] => 346378e8-7ff7-ce01-d6ff-62ff97a46016
[etat_fiche_online] => en_ligne
[date_application] => 2021-08-06
[date] =>
[bd_referent] => Nathan POMORSKI
[bd_referent_id] =>
[contact_email] => nathan.pomorski@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO21500-T1
[keywords] => Probiotic, antimicrobial peptide, autoimmune diseases, type 1 diabete
[pub_scient_inv_dispo] => Intestinal Cathelicidin Antimicrobial Peptide Shapes a Protective Neonatal Gut Microbiota Against Pancreatic Autoimmunity. Liang and al. Gastroenterology. 2022.https://doi.org/10.1053/j.gastro.2021.12.272
[access_to_detailed_offer] =>
[rare_disease] => 0
[second_indication] => 0
[inventors] => DIANA Julien,SUN Jia
[number_application] => European Procedure (Patents) (EPA) - 06 Août 2021 - 21 306 102.1
[technology_engineering] => peptides
[multidisciplinary_field] => microbiota
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[type_of_patent] => Type of patent
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[first_name] => Inserm
[last_name] => Transfert
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[author] => 1
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[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 156
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Drug, Immunology, Inflammation, Microbiota, Others, Peptides, Product, Product
[taxonomieurl] =>
Drug,
Immunology,
Inflammation,
Microbiota,
Others,
Peptides,
Product,
Product
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[157] => stdClass Object
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[post] => stdClass Object
(
[post_title] => USE OF ALARMINS AS BIOMARKERS FOR ASSESSING ISCHEMIAREPERFUSION INJURY SEVERITY AFTER SOLID ORGAN TRANSPLANTATION
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-alarmins-as-biomarkers-for-assessing-ischemiareperfusion-injury-severity-after-solid-organ-transplantation/
[post_content] => The inventors aim to assess IL-33 and HMGB1 contributions as alarmins to I injury following solid organ transplantation in particular liver transplantation. This study was conducted from a prospective biological collection and a clinical database of 40 liver transplant recipients in Tours hospital center. Serum IL-33 and HMGB1 levels were determined at graft reperfusion, at the end of the liver transplantation and at postoperative day 1 and 3. A post-reperfusion liver biopsy was systematic. Serum IL-33 increase is associated with: i) severe-moderate liver lesions; ii) an early allograft dysfunction; iii) a post-reperfusion syndrome occurrence; iv) a post liver transplantation acute kidney injury occurrence. Serum HMGB1 increase is associated with: i) an early allograft dysfunction; ii) a post-reperfusion syndrome occurrence. IL-33 and HMGB1 thus contribute as alarmins to I injury in human liver transplantation. Their serum levels are predictive of I injury severity and its clinical impact. Serum assay for IL-33 and HMGB1 upon graft reperfusion could be used as early biomarkers of early allograft function in solid organ transplantation, in particular in liver transplantation.
[post_date] => 2022-08-16 15:40:01
[post_modified] => 2024-09-11 15:53:29
[ID] => 4609
)
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[object] =>
[application] =>
[idSugar] => 6f3e4c0b-a3d7-9edc-cee4-62fbb0713572
[etat_fiche_online] => en_ligne
[date_application] => 16-12-2020
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO20448-D1
[keywords] => Liver Transplant, Alarmin, Ischemia-reperfusion injury assessment, Immunoassay
[pub_scient_inv_dispo] => Front Immunol, 2021 Sep 21, Barbier L, Endogenous Interleukin-33 Acts as an Alarmin in Liver Ischemia-Reperfusion and Is Associated With Injury After Human Liver Transplantation, doi: 10.3389/fimmu.2021.744927. eCollection 2021.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => HERBELIN André,ROBIN Aurelie,BARBIER Louise,SALAME Ephrem,SINDAYIGAYA Remy,GOMBERT Jean-Marc
[number_application] => European Procedure (Patents) (EPA) - 16 Déc. 2020 - 20 306 584.2
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
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[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 157
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Human POC, Immunoassay, Immunology, Liver transplantation, Method, Transplantation
[taxonomieurl] =>
Biomarker,
Biomarker,
Human POC,
Immunoassay,
Immunology,
Liver transplantation,
Method,
Transplantation
)
[158] => stdClass Object
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[post] => stdClass Object
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[post_title] => METHODS AND COMPOSITIONS FOR TREATING SKIN AFFLICTIONS
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-compositions-for-treating-skin-afflictions/
[post_content] => The present invention relates to a method for treating skin afflictions in a subject comprising a step of administering said subject with a therapeutically effective amount of small extracellular vesicles (sEV) comprising CD98hc. Inventors have demonstrated that healthy dermal fibroblasts produced and secreted EVs bearing characteristic of exosome-like small EVs (sEVs). They have shown that CD98hc was present at the surface of sEVs, transferred and stabilized at the plasma membrane of recipient cells. They observed that the transferred protein was functional both in vitro and in vivo. Furthermore, injection of sEVs in epidermal CD98hcKO mice exhibiting wound healing defect rescued wound closure in vivo. Thus, their findings reveal that CD98hc contained in EVs could potentially be used in vivo to treat and improve multiple skin afflictions by allowing protein rescue.
[post_date] => 2022-08-03 09:35:01
[post_modified] => 2024-09-11 15:43:39
[ID] => 4606
)
[post_meta] => stdClass Object
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[object] =>
[application] =>
[idSugar] => 110518f9-c5aa-9781-343e-5b35e8f276fa
[etat_fiche_online] => en_ligne
[date_application] =>
[date] =>
[bd_referent] => Aymeric EMPEREUR
[bd_referent_id] =>
[contact_email] => aymeric.empereur@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO17663-T1
[keywords] => Exosomes; CD98; Wound healing
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => FERAL Chloé,ESTRACH Soline,TISSOT Floriane,CAILLETEAU Laurence
[number_application] => European Procedure (Patents) (EPA) - 02 Mai 2018 - 18 170 458.6
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
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[type_of_patent] => Type of patent
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[first_name] => Aymeric
[last_name] => Empereur
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[um_admin-inserm-transfert] => 1
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[wp_user_level] => 0
[dismissed_wp_pointers] =>
[role] =>
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[contact_description] =>
[contact_email] =>
[contact_phone] =>
)
[comteur] => 158
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Dermatology, Drug, Method, Others, Product, Wounds
[taxonomieurl] =>
Dermatology,
Drug,
Method,
Others,
Product,
Wounds
)
[159] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHOD TO TREAT AND STRATIFICATE A PATIENT SUFFERINGFROM A CANCER
[guid] => https://technology-offers.inserm-transfert.com/offer/method-to-treat-and-stratificate-a-patient-sufferingfrom-a-cancer/
[post_content] => The present invention relates to the stratification and treatment of patients suffering of cancer. Due to the fact that anti-PD1 therapy targets lymphocytes and the efficiency of anti-cancer therapy is measured by the impact on the tumor cells, the inventors postulated that studying the molecular mechanisms of resistance of anti-PD1 therapy should take into consideration existing intercellular communication between lymphocytes and tumor cells. As exosomes are the carriers for the intercellular transfer of the miRNA responsible of chemoresistance, they herein investigated whether exposure of T cells to anti-PD1 therapy might promote the expression of exosomal miRNA (exomiR) causing the chemoresistance of cancer cells. Surprisingly, they found that anti-PD1 exposure of T-cell promotes an enrichment of exosomal miRNA-4315. They also noted that exosomal miRNA-4315 induced a phenomenon of apopto-resistance to conventional chemotherapies in cancer cells receiving exosomal miRNA-4315. At molecular level, they discern that the apopto-resistance phenomenon was associated with the miRNA-4315-mediated down-regulation of Bim, a pro-apoptotic protein. In cellular and mice models, they observed that the BH3 mimetic agent ABT263 circumvented this resistance. Thus, the invention relates to methods of stratification using exosomal miRNA-4315 and method of treatment of patients suffering of cancer using BH3 mimetic agent.
[post_date] => 2022-07-15 15:20:01
[post_modified] => 2024-09-11 15:53:28
[ID] => 4601
)
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[application] =>
[idSugar] => dc20c299-0ed8-f858-29c8-6156d830761e
[etat_fiche_online] => en_ligne
[date_application] => 14-09-2020
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO20408-D1
[keywords] => Exoxome, PD1 treatment response prediction, Pan-Cancer
[pub_scient_inv_dispo] => Cell Death Dis. 2020 Dec 11;11(12):1048. Guyon et al. Anti-PD1 therapy induces lymphocyte-derived exosomal miRNA-4315 release inhibiting Bim-mediated apoptosis of tumor cells doi: 10.1038/s41419-020-03224-z.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => CARTRON Pierre-François,BOUGRAS-CARTRON Gwenola
[number_application] => European Procedure (Patents) (EPA) - 14 Sept. 2020 - 20306025.6
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => transcriptomics
[post_categoryname] => Diagnostic
[parent_category] => 195
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)
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[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 159
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Human POC, Oncology, Solid Tumors, Transcriptomics
[taxonomieurl] =>
Biomarker,
Biomarker,
Human POC,
Oncology,
Solid Tumors,
Transcriptomics
)
[160] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => GDF3 AS BIOMARKER AND BIOTARGET IN POST-ISCHEMIC CARDIAC REMODELING
[guid] => https://technology-offers.inserm-transfert.com/offer/gdf3-as-biomarker-and-biotarget-in-post-ischemic-cardiac-remodeling/
[post_content] => Markers of an intense scarring process in the early phase post- myocardial infarction (MI) are still undetermined, and the identification of patients at higher risk of developing large adverse fibrotic remodeling and heart failure remains challenging. Here, the inventors demonstrate the modulation in the paracrine behavior of resident PW1+ cells in scarring cardiac tissue post-MI and the differential abundance of 12 candidate markers in their secretome. Of these, growth differentiation factor 3 (GDF3), a member of transforming growth factor-? family, upregulates proliferation of cardiac fibroblasts, which are instrumental in fibrosis. GDF3 is upregulated in the scarred tissue and plasma of mice and humans post-MI, with the highest plasma levels predicting higher fibrotic cardiac remodeling and cardiac dilation. The inventors thus reveal the previously unidentified function of GDF3 in predicting adverse fibrotic cardiac remodeling post-MI. Thus the present invention relates to the use of GDF3 as biomarker and biotarget in post-ischemic cardiac remodeling.
[post_date] => 2022-07-15 15:20:01
[post_modified] => 2024-09-11 15:53:27
[ID] => 4600
)
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[date_application] => 05-10-2020
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO20319-D1
[keywords] => Prognosis, Risk Prediction, Myocardial Infarction, GDF3, Fibrotic cardiac remodeling
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => HULOT Jean-Sébastien
[number_application] => European Procedure (Patents) (EPA) - 05 Oct. 2020 - 20 306 156.9
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
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[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
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[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 160
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Cardiovascular Diseases, Immunoassay, Method, Myocardial Infarction, Pre-Analytic Validation, Target
[taxonomieurl] =>
Biomarker,
Biomarker,
Cardiovascular Diseases,
Immunoassay,
Method,
Myocardial Infarction,
Pre-Analytic Validation,
Target
)
[161] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHODS FOR THE DIAGNOSIS AND THETREATMENT OF GRAFT-VERSUS-HOSTDISEASE
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-the-diagnosis-and-thetreatment-of-graft-versus-hostdisease/
[post_content] => The invention relates to methods for the prediction and the treatment of risk of acute graft versus host disease. The inventors demonstrated that an alteration of CD73-mediated regulatory function of DP8? Tregs could contribute to the acute GvHD pathophysiology. In particular, the present invention relates to method of determining whether a subject has or is at a risk of developing graft-versus-host disease (GvHD) comprising the steps of: i) determining the level of CD73 expression by DP8? TREGS in a sample obtained from the subject, ii) comparing the level determined at step i) with a predetermined reference value wherein detecting differential between the level of CD73 expression by DP8? TREGS determined at step i) and the predetermined reference value is indicative of whether a subject has or is at a risk of developing graft-versus-host disease (GvHD).
[post_date] => 2022-07-15 15:15:01
[post_modified] => 2024-09-11 15:53:25
[ID] => 4598
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => bf9f08f4-aad6-7851-b8f2-6229cca9f520
[etat_fiche_online] => en_ligne
[date_application] => 04-11-2020
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO20418-D1
[keywords] => Graft-versus-host disease, Prognosis, CD73 expression on Treg cells, hematological malignancies, allogeneic hematopoietic stem cell transplantation
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => GODEFROY Emmanuelle,CHEVALLIER Patrice,ALTARE Frédéric,JOTEREAU Francine
[number_application] => European Procedure (Patents) (EPA) - 04 Nov. 2020 - 20 306 320.1
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
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(
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)
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[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 161
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Graft Versus Host Disease (GVHD), Human POC, Immunoassay, Immunology, Method, Transplantation
[taxonomieurl] =>
Biomarker,
Biomarker,
Graft Versus Host Disease (GVHD),
Human POC,
Immunoassay,
Immunology,
Method,
Transplantation
)
[162] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHODS AND COMPOSITIONS FOR PREDICTING AND TREATING UVEAL MELANOMA
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-compositions-for-predicting-and-treating-uveal-melanoma-2/
[post_content] => Here, in multi-scale analyses using single-cell RNA sequencing of six different primary uveal melanomas, inventors uncover a previously unrecognized intratumor heterogeneity at the genetic and transcriptomic level. They identify distinct transcriptional cell states and diverse tumor-associated populations in a subset of primary uveal melanomas.
[post_date] => 2022-07-15 15:10:01
[post_modified] => 2024-09-11 15:53:25
[ID] => 4597
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => d2dac1d7-258e-3d5b-2a89-61572a588ca5
[etat_fiche_online] => en_ligne
[date_application] => 16-11-2020
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO20429-D1
[keywords] => RNA signature, Prognosis, Uveal Melanoma, Intratumor heterogeneity
[pub_scient_inv_dispo] => Cell Death Differ., 2021 Jun 28, Pandiani et al, Single-cell RNA sequencing reveals intratumoral heterogeneity in primary uveal melanomas and identifies HES6 as a driver of the metastatic disease., DOI: 10.1038/s41418-020-00730-7Prog Retin Eye Res, 2021 Apr 13, Strub et al, Translation of single-cell transcriptomic analysis of uveal melanomas to clinical oncology, DOI: 10.1016/j.preteyeres.2021.100968
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => BERTOLOTTO Corine,BALLOTTI Robert,STRUB Thomas,PANDIANI Charlotte
[number_application] => European Procedure (Patents) (EPA) - 16 Nov. 2020 - 20 306 384.7
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => transcriptomics
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 162
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Human POC, Melanoma, Oncology, Transcriptomics
[taxonomieurl] =>
Biomarker,
Biomarker,
Human POC,
Melanoma,
Oncology,
Transcriptomics
)
[163] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => METHODS AND COMPOSITIONS FOR PREDICTING AND TREATING UVEAL MELANOMA
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-and-compositions-for-predicting-and-treating-uveal-melanoma/
[post_content] => Here, in multi-scale analyses using single-cell RNA sequencing of six different primary uveal melanomas, inventors uncover a previously unrecognized intratumor heterogeneity at the genetic and transcriptomic level. They identify distinct transcriptional cell states and diverse tumor-associated populations in a subset of primary uveal melanomas. They also decipher a gene regulatory network underlying an invasive and poor prognosis state driven in part by the transcription factor HES6, a member of the NOTCH signaling pathway. HES6 heterogenous expression has been validated by RNAscope assays within primary uveal melanomas, which unveils the existence of these cells conveying a dismal prognosis in tumors diagnosed with a favorable outcome using bulk analyses. Depletion of HES6 impairs growth, migration and metastatic dissemination, demonstrating essential roles of HES6 in uveal melanoma progression.
[post_date] => 2022-07-15 15:10:01
[post_modified] => 2024-09-11 15:53:24
[ID] => 4596
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => 8017a2c5-7783-edb1-0876-615720179f66
[etat_fiche_online] => en_ligne
[date_application] => 16-11-2020
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO19426-D2
[keywords] => Uveal Melanoma, RNA Signatures, Prognosis, Intratumoral heterogeneity
[pub_scient_inv_dispo] => Cell Death Differ., 2021 Jun 28, Pandiani et al, Single-cell RNA sequencing reveals intratumoral heterogeneity in primary uveal melanomas and identifies HES6 as a driver of the metastatic disease., DOI: 10.1038/s41418-020-00730-7Prog Retin Eye Res, 2021 Apr 13, Strub et al, Translation of single-cell transcriptomic analysis of uveal melanomas to clinical oncology, DOI: 10.1016/j.preteyeres.2021.100968
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => BERTOLOTTO Corine,PANDIANI Charlotte,BALLOTTI Robert,STRUB Thomas
[number_application] => European Procedure (Patents) (EPA) - 16 Nov. 2020 - 20 306 385.4
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => transcriptomics
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 163
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Human POC, Melanoma, Oncology, Transcriptomics
[taxonomieurl] =>
Biomarker,
Biomarker,
Human POC,
Melanoma,
Oncology,
Transcriptomics
)
[164] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => USE OF THE EMM ANTIGEN AS A BIOMARKER OF INHERITED GPI DEFICIENCIES
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-the-emm-antigen-as-a-biomarker-of-inherited-gpi-deficiencies/
[post_content] => Glycosylphosphatidylinositol (GPI) is a glycolipid that anchors more than 150 proteins to the cell surface. Pathogenic variants in several genes that participate in GPI biosynthesis cause inherited GPI deficiency (IGD) disorders. Here, the inventors reported that homozygous null alleles of PIGG, a gene involved in GPI modification, are responsible for the rare Emm-negative blood phenotype. Using a panel of K562 cells defective in both the GPI-transamidase and GPI remodeling pathways, they demonstrate that the Emm antigen, whose molecular basis has remained unknown for decades, is carried only by free GPI and that its epitope is composed of the second and third ethanolamine of the GPI backbone. Importantly, the inventors show that the decrease in Emm expression in several IGD patients is indicative of GPI defects. Overall, our findings establish Emm as a novel blood group system and have important implications for understanding the biological function of human free GPI.
[post_date] => 2022-07-15 14:50:02
[post_modified] => 2024-09-11 15:53:23
[ID] => 4594
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => 90558cf5-74b9-a44d-5f5f-62d174f466a7
[etat_fiche_online] => en_ligne
[date_application] => 09-12-2020
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO20561-D1
[keywords] => Emm antigen, Inherited GPI deficiency, paroxysmal nocturnal hemoglobinuria
[pub_scient_inv_dispo] => Blood, 2021 Jul 1, Duval R et al., Inherited glycosylphosphatidylinositol defects cause the rare Emm-negative blood phenotype and developmental disorders ,doi: 10.1182/blood.2020009810.
[access_to_detailed_offer] => http:/
[rare_disease] => true
[second_indication] => false
[inventors] => PEYRARD Thierry,DUVAL Romain,HERMINE Olivier,COLIN-ARONOVICZ Yves,AZOUZI Slim,LE VAN KIM Caroline
[number_application] => European Procedure (Patents) (EPA) - 09 Déc. 2020 - 20 306 520.6
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => Inserm Transfert
[first_name] => Inserm
[last_name] => Transfert
[wp_capabilities] => stdClass Object
(
[author] => 1
[um_member] => 1
)
[wp_user_level] => 2
[dismissed_wp_pointers] => pll_lgt
[role] => member
[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 164
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Anemia, Biomarker, Biomarker, Hematological Disorders, Human POC, Immunoassay
[taxonomieurl] =>
Anemia,
Biomarker,
Biomarker,
Hematological Disorders,
Human POC,
Immunoassay
)
[165] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => USE OF RETINOIC ACID RECEPTOR (RAR) AGONISTS FORREVERSIN G, PREVENTING, OR DELAYING CALCIFICATION OF AORTICVALVE
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-retinoic-acid-receptor-rar-agonists-forreversin-g-preventing-or-delaying-calcification-of-aorticvalve/
[post_content] => Aortic valve calcification is a condition in which calcium deposits form on the aortic valve in the heart. These deposits can cause narrowing at the opening of the aortic valve. This narrowing can become severe enough to reduce blood flow through the aortic valve - a condition called aortic valve stenosis. The inventors have shown that retinoic acid decreases calcification and osteoblast-like phenotype in valvular interstitial cells (VICs). More particularly, RAR? activation reduces calcification and osteoblast-like phenotype in VIC. On the contrary, ALDH1A1 inhibition increases calcification and osteoblast-like phenotype in VIC. Thus the results prompt to consider that use or retinoic acid receptor (RAR) agonists would be suitable for the reversing, preventing or delaying calcification of the aortic valve.
[post_date] => 2022-06-21 09:25:01
[post_modified] => 2024-09-11 15:43:31
[ID] => 4589
)
[post_meta] => stdClass Object
(
[object] =>
[application] =>
[idSugar] => 9e50d4c1-3b66-460d-8f21-5df8ac71932f
[etat_fiche_online] => en_ligne
[date_application] => 02-10-2019
[date] =>
[bd_referent] => Aymeric EMPEREUR
[bd_referent_id] =>
[contact_email] => aymeric.empereur@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO17543-T1
[keywords] => Calcification
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => SUSEN Sophie,SOTTEJEAU Yoann,CORSEAUX Delphine,SOQUET Jérôme,VAN BELLE Eric,STAELS Bart,DUPONT Annabelle,ROSA Mickael
[number_application] => European Procedure (Patents) (EPA) - 02 Oct. 2019 - 19 306 256.9
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] =>
[post_categoryname] => Therapeutic
[parent_category] => 195
[inserm_tags_to_put] =>
[tags_order_view] => stdClass Object
(
[field_of_development] => Field of development
[thera_area] => Therapy Area
[type_of_patent] => Type of patent
)
)
[user] => stdClass Object
(
[nickname] => aymeric.empereur@inserm-transfert.fr
[first_name] => Aymeric
[last_name] => Empereur
[wp_capabilities] => stdClass Object
(
[um_admin-inserm-transfert] => 1
)
[wp_user_level] => 0
[dismissed_wp_pointers] =>
[role] =>
[bd_referent] =>
[contact_description] =>
[contact_email] =>
[contact_phone] =>
)
[comteur] => 165
[terms] => Array
(
[0] => Therapeutic
)
[taxonomie] => Aortic valve diseases, Cardiovascular Diseases, Drug, Method, Target, Validation in vivo
[taxonomieurl] =>
Aortic valve diseases,
Cardiovascular Diseases,
Drug,
Method,
Target,
Validation in vivo
)
[166] => stdClass Object
(
[post] => stdClass Object
(
[post_title] => USE OF MAST CELL STABILIZER FOR THE TREATMENT OF HEART FAILURE WITH PRESERVED EJECTION FRACTION
[guid] => https://technology-offers.inserm-transfert.com/offer/use-of-mast-cell-stabilizer-for-the-treatment-of-heart-failure-with-preserved-ejection-fraction/
[post_content] => Heart failure with preserved ejection fraction (HFpEF) which results from diastolic dysfunction is a growing epidemiologic problem. However, the pathophysiology of this disease is poorly understood. Our goal is to investigate whether microvessel disease may promote HFpEF. To do so we have used Leptin receptor deficient (Leprdb/db) female mice as a model of HFpEF and performed a transcriptomic analysis via RNA sequencing of the cardiac vascular fraction of both these mice and their control Leprdb/+littermates. In Leprdb/db female mice, end diastolic pressure (EDP) signing diastolic dysfunction is significantly increased from 3 month of age. It is correlated with a cardiac and cardiomayocyte hypertrophy, vascular leakage, endothelial cell activation and leucocyte infiltration. As expected, the RNA sequencing analysis confirmed endothelial dysfunction. Besides, it also revealed a strong increase in several mast cell markers. We confirmed, via histology, an accumulation of mast cells in the heart of Leprdb/db mice. Importantly, it was associated with increased levels of circulating IgE. Leprdb/db mice were then treated or not with Cromolyn sodium, an inhibitor of mast cell degranulation. After a month treatment, EDP was significantly reduced in Leprdb/db mice demonstrating the critical role of mast cell in the development of diastolic dysfunction in diabetic obese mice.
[post_date] => 2022-06-21 09:05:17
[post_modified] => 2024-09-11 15:44:15
[ID] => 4588
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[date_application] => 12-11-2019
[date] =>
[bd_referent] => Aymeric EMPEREUR
[bd_referent_id] =>
[contact_email] => aymeric.empereur@inserm-transfert.fr
[contact_phone] =>
[reference_online] => BIO19459-T1
[keywords] => Cardiology, cadiovascular diseases, Heart Failure,
[pub_scient_inv_dispo] => Arterioscler Thromb Vasc Biol. 2021 Apr;41(4):e193-e207. doi: 10.1161/ATVBAHA.121.315900. Epub 2021 Feb 11.
[access_to_detailed_offer] => http:/
[rare_disease] => false
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[inventors] => RENAULT Marie-Ange,GUIMBAL Sarah,COUFFINHAL Thierry,CHAPOULY Candice
[number_application] => European Procedure (Patents) (EPA) - 12 Nov. 2019 - 19208649.4
[technology_engineering] =>
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[taxonomie] => Cardiovascular Diseases, Chronic Heart Failure, Drug, Method, Small Molecule, Target, Validation in vivo
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Cardiovascular Diseases,
Chronic Heart Failure,
Drug,
Method,
Small Molecule,
Target,
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[post_title] => METHODS FOR DIAGNOSIS AND MONITORING OF TOXIC EPIDERMAL NECROLYSIS
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-diagnosis-and-monitoring-of-toxic-epidermal-necrolysis-2/
[post_content] => In the present invention, inventors investigate the representation of T cell subsets in Toxic epidermal necrolysis (TEN) a life-threatening cutaneous adverse drug reaction (cADR), characterized by massive epidermal necrosis. To better understand why skin symptoms are so severe in TEN disease, inventors conducted a prospective immunophenotyping study on skin samples and blood from 18 TEN patients, using mass cytometry and next generation TCR sequencing. Deep sequencing of the T cell receptor CDR3 repertoire revealed massive expansion of unique CDR3 clonotypes in blister cells. Over-represented clonotypes were mainly effector memory CD8+CD45RA-CCR7- T cells, and expressed high levels of cytotoxic (Granulysin and Granzymes A & B) and activation (CD38) markers. Thus present invention relates to non-invasive, specific and rapid methods for diagnostic and monitoring Toxic Epidermal Necrolysis. More specifically present invention relates to methods for diagnosis and/or monitoring of Toxic Epidermal Necrolysis through detection of a specific population of T ymphocytes in a subject. The present invention also relates to a method of preventing or treating a Toxic Epidermal Necrolysis in a subject in need thereof.
[post_date] => 2022-06-10 15:00:01
[post_modified] => 2024-09-11 15:53:17
[ID] => 4586
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[date] =>
[bd_referent] => Pierre MAZOT
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[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO19417-D1
[keywords] => Toxic epiderm necrolysis (TEN), cutaneous adverse drug reaction (cADR), T cell subsets
[pub_scient_inv_dispo] => Sci Adv, 2021 Mar 19, Villani et al, Massive clonal expansion of polycytotoxic skin and blood CD8 + T cells in patients with toxic epidermal necrolysis , doi: 10.1126/sciadv.abe0013. Print 2021 Mar.
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => VOCANSON Marc,NOSBAUM Audrey,VILLANI Axel,ROZIERES Aurore
[number_application] => European Procedure (Patents) (EPA) - 27 Nov. 2020 - 20 306 460.5
[technology_engineering] =>
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[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
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[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 167
[terms] => Array
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[taxonomie] => Biomarker, Biomarker, Dermatology, Human POC, Immunoassay, Target
[taxonomieurl] =>
Biomarker,
Biomarker,
Dermatology,
Human POC,
Immunoassay,
Target
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[post_title] => METHOD FOR PREDICTING THE RESPONSE TO TNF INHIBITORS
[guid] => https://technology-offers.inserm-transfert.com/offer/method-for-predicting-the-response-to-tnf-inhibitors/
[post_content] => Rheumatoid arthritis (RA) is the most prevalent chronic autoimmune inflammatory rheumatism. Its pathophysiology is largely dependent on TNF. Severe RA as well as several other inflammatory and autoimmune diseases are treated with TNF inhibitors (TNFi). However, to date only 30-50% achieve low disease activity or remission with this treatment regimen and some patients experience secondary non-response or relapse. Herein, the inventors evaluated by RT-qPCR the mRNA expression of CD36, which was already described to be regulated by TNFi5, some specific NRF2 target genes (FBX030, GABARA, LBR, MAFG, OSGIN1, HMOX1), which play a role in the anti-oxidative stress response or anti-inflammatory pathway, and the expression of CSMD1, an anti-inflammatory gene that we observed as up-regulated by all TNFi. Interestingly, they observed 2 different subsets of healthy donors: (i) donors in which TNFi stimulation increased mRNA of target genes in macrophages and (ii) conversely donors with no significant upregulation in transcription of these target genes. Then they classified donors two different status, u201cactivatorsu201d or u201cnon-activatorsu201d of tmTNF reverse signaling after TNFi stimulation, which correlates to clinically responder and non-responders to TNFi. Thus, based on all these observations, they developed an in vitro method for predicting the response to TNF inhibitors in patient in need thereof.
[post_date] => 2022-05-25 13:55:01
[post_modified] => 2024-09-11 15:53:26
[ID] => 4582
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[idSugar] => 3416c253-412f-3f44-634e-6229f2c67c1a
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[date_application] => 20-10-2020
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO19272-D1
[keywords] => Treatment Response Prediction, Rhumatoid Arthritis, TNFinhibitor treatments, CD36
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => DAVIGNON Jean-Luc,DEGBOE Yannick,CONSTANTIN Arnaud,DIALLO Katy,BARON Michel,RAUWEL Benjamin,BOYER Jean-Frédéric
[number_application] => European Procedure (Patents) (EPA) - 20 Oct. 2020 - 20 306 247.6
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => transcriptomics
[post_categoryname] => Diagnostic
[parent_category] => 195
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[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 168
[terms] => Array
(
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[taxonomie] => Biomarker, Biomarker, Human POC, Immunology, Method, Rheumatoid Arthritis, Transcriptomics
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Biomarker,
Biomarker,
Human POC,
Immunology,
Method,
Rheumatoid Arthritis,
Transcriptomics
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[169] => stdClass Object
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[post] => stdClass Object
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[post_title] => Vaccine model based on recombinant hydrophobic protein and saponin
[guid] => https://technology-offers.inserm-transfert.com/?p=4560
[post_content] => The Bd37 is an erythrocyte binding protein anchored at the surface of the parasite Babesia divergens. B. divergens is an Apicomplexa parasite, mostly of veterinary importance but able to infect humans after tick-bites. The lab model of bovine and human babesiosis is provided by the gerbils Meriones unguiculatus infected by Babesia divergens.Recombinant hydrophobic Bd37 is able to induce complete protective immune response when mixed with saponin, in contrast to hydrophilic Bd37 which only induce non-protective antibodies.
[post_date] => 2022-04-21 16:24:07
[post_modified] => 2024-09-11 16:07:17
[ID] => 4560
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[date] =>
[bd_referent] =>
[bd_referent_id] =>
[contact_email] =>
[contact_phone] =>
[reference_online] => RT00511
[keywords] => POC in vivo, vaccine, Apicomplexa, parasite, adjuvant,
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] =>
[rare_disease] => false
[second_indication] =>
[inventors] =>
[number_application] =>
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[post_categoryname] => Others
[parent_category] => 215
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[contact_email] =>
[contact_phone] =>
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[comteur] => 169
[terms] => Array
(
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[taxonomie] => Academic Research, Immunology, Industry Research (screening, tox.studies, bioreactor, ...), Infectious Diseases
[taxonomieurl] =>
Academic Research,
Immunology,
Industry Research (screening, tox.studies, bioreactor, ...),
Infectious Diseases
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[170] => stdClass Object
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[post] => stdClass Object
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[post_title] => METHODS FOR DETECTING THE PRESENCE OF PEMPHIGUS-SPECIFIC AUTOANTIBODIES IN A SAMPLE
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-detecting-the-presence-of-pemphigus-specific-autoantibodies-in-a-sample/
[post_content] => Pemphigus is a group of rare autoimmune diseases that causes blistering of the skin and mucous membranes, and includes pemphigus vulgaris (PV) and pemphigus foliaceus (PF). Patients with pemphigus have various combinations of autoantibodies to keratinocyte muscarinic acetylcholine receptor subtype M3 (CHRM3), the secretory pathway Ca2+/Mn2+-ATPase isoform 1 (SPCA1), and desmocollin 3 (DSC3). However, there is still a need to characterize these autoantibodies and optimize their detection for diagnosis and disease monitoring. The inventors now developed an ALBIA for the 3 proteins and successfully detected and quantified the presence of auto-antibodies directed against each of these antigens in pemphigus patients. Furthermore, they showed that detection and quantification of anti-SPCA1 and/or anti-CHRM3 were also associated to a risk of relapse in the first year following the treatment using rituximab as a first-line agent. The present invention thus relates to methods for detecting the presence of said pemphigus-specific autoantibodies.
[post_date] => 2022-03-07 15:14:56
[post_modified] => 2024-09-11 15:53:06
[ID] => 4551
)
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[date_application] => 27-08-2020
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO20361-D1
[keywords] => PEMPHIGUS, Diagnostic, ALBIA ELISA
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => BOYER Olivier,JOLY Pascal,LEMIEUX Alexandre,GOLINSKI Marie-Laure
[number_application] => European Procedure (Patents) (EPA) - 27 Août 2020 - 20 305 958.9
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
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[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 170
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Immunoassay, Immunology, Method, Pre-Analytic Validation
[taxonomieurl] =>
Biomarker,
Biomarker,
Immunoassay,
Immunology,
Method,
Pre-Analytic Validation
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[171] => stdClass Object
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[post] => stdClass Object
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[post_title] => METHODS FOR PROGNOSIS AND MONITORING OF CRITICAL FORM OF CORONAVIRUS INFECTION
[guid] => https://technology-offers.inserm-transfert.com/offer/methods-for-prognosis-and-monitoring-of-critical-form-of-coronavirus-infection/
[post_content] => In the present invention, inventors investigate the representation of neutrophil subsets in severe and critical COVID-19 patients based on Intensive Care Units (ICU) and non-ICU admission. The results show that 80% of ICU patients develop strong myelemia with CD10-CD64+ immature neutrophils. Cellular profiling revealed two distinct neutrophil subsets expressing either the LOX?1 or CD123 marker, both overrepresented in ICU patients compared to non-ICU patients. The proportion of LOX-1-expressing immature neutrophils positively correlated with clinical severity, with the cytokine storm (IL-1?, IL-6, IL-8, TNF?), and with intravascular coagulation. Importantly, high proportions of LOX-1+-immature neutrophils are associated with higher risk of severe thrombosis. The present invention relates to non-invasive, specific and rapid methods for prognostic and monitoring the severe / critical form of coronavirus infection. More specifically present invention relates to methods for prognosis and/or monitoring of the critical form of coronavirus infection through detection of a specific population of neutrophils in a covid patient. The present invention also relates to a method of preventing or treating a coronavirus infection in a subject in need thereof
[post_date] => 2022-03-07 15:14:55
[post_modified] => 2024-09-11 15:53:05
[ID] => 4550
)
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[idSugar] => c44167c0-7fc8-71a1-889c-6050c1a342e0
[etat_fiche_online] => en_ligne
[date_application] => 23-07-2020
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO20308-D1
[keywords] => COVID19, Severe form Prognosis, Lox1+ immature neutrophils
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => COMBADIERE Christophe,COMBADIERE Béhazine
[number_application] => European Procedure (Patents) (EPA) - 23 Juil. 2020 - 20 305 847.4
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => immunoassay
[post_categoryname] => Diagnostic
[parent_category] => 195
[inserm_tags_to_put] =>
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[type_of_patent] => Type of patent
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[bd_referent] => Inserm Transfert
[contact_description] =>
[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 171
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Human POC, Immunoassay, Infectious Diseases, Target
[taxonomieurl] =>
Biomarker,
Biomarker,
Human POC,
Immunoassay,
Infectious Diseases,
Target
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[172] => stdClass Object
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[post] => stdClass Object
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[post_title] => METHOD FOR PREDICTING SURVIVAL TIME IN PATIENTS SUFFERING FROM CANCER
[guid] => https://technology-offers.inserm-transfert.com/offer/method-for-predicting-survival-time-in-patients-suffering-from-cancer/
[post_content] => The inventors found that metabolic gene signatures of human pan-tumor associated myeloid cells correlate with patient survival and cancer cell mitotic index. Indeed by crossing i) metabolic genes expression from single cell RNA-seq data of myeloid cell subsets, and ii) their functional metabolism by SCENITH, a method to determine in parallel the phenotype and metabolic state of the immune, stromal and tumor cells, the inventors identified glycolytic and respiratory metabolic gene signatures which predict survival time in patients. They found that in different human tumors, the glycolytic signature was associated with significantly reduced patient survival, while a respiratory gene signature correlated with increased survival. Moreover they demonstrated that the presence of glycolytic myeloid cells in the tumor correlates with malignancy.Thus the present invention relates to new gene signatures that are suitable for predicting survival time in patients suffering from cancer and for diagnosing malignancy tumor.
[post_date] => 2022-03-07 15:14:55
[post_modified] => 2024-09-11 15:53:04
[ID] => 4548
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[idSugar] => daeff71f-3333-ec0a-e33c-622231ae51cf
[etat_fiche_online] => en_ligne
[date_application] => 22-07-2020
[date] =>
[bd_referent] => Pierre MAZOT
[bd_referent_id] =>
[contact_email] => pierre.mazot@inserm-transfert.fr
[contact_phone] => +33 (0) 155030136
[reference_online] => BIO20108-D1
[keywords] => Metabolic gene expression signature, Solid Tumors, Prognosis
[pub_scient_inv_dispo] =>
[access_to_detailed_offer] => http:/
[rare_disease] => false
[second_indication] => false
[inventors] => ARGUELLO Rafael José,SAMAD Bushra,COMBES Alexis,PIERRE Philippe,KRUMMEL Matthew
[number_application] => European Procedure (Patents) (EPA) - 22 Juil. 2020 - 20 305 841.7
[technology_engineering] =>
[multidisciplinary_field] =>
[technological_platform] => transcriptomics
[post_categoryname] => Diagnostic
[parent_category] => 195
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[contact_email] => contact@inserm-transfert.fr
[contact_phone] => +33 1 55 03 01 00
)
[comteur] => 172
[terms] => Array
(
[0] => Diagnostic
)
[taxonomie] => Biomarker, Biomarker, Method, Oncology, Pre-Analytic Validation, Solid Tumors, Transcriptomics
[taxonomieurl] =>
Biomarker,
Biomarker,
Method,
Oncology,
Pre-Analytic Validation,