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    METHODS AND COMPOSITIONS FOR TREATING CELL SENESCENCE ACCUMULATION RELATED DISEASE
    1.
    发明公开
    METHODS AND COMPOSITIONS FOR TREATING CELL SENESCENCE ACCUMULATION RELATED DISEASE 审中-公开

    公开(公告)号：US20240158861A1

    公开(公告)日：2024-05-16

    申请号：US18556472

    申请日：2022-04-22

    Applicant: INSERM (INSTITUT NATIONAL DE LA SANTÉ ET DE LA RECHERCHE MÉDICALE) ,  CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE (CNRS) ,  UNIVERSITE COTE D'AZUR

    Inventor： Julien CHERFILS ,  Eric GILSON ,  Charlene ILTIS

    IPC: C12Q1/6883 ,  C12Q1/6851 ,  G01N33/68

    CPC classification number: C12Q1/6883 ,  C12Q1/6851 ,  G01N33/6893 ,  C12Q2600/158

    Abstract: 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 inventors' 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.

    METHODS AND COMPOSITIONS FOR MODULATING MACROPHAGES POLARIZATION
    4.
    发明申请
    METHODS AND COMPOSITIONS FOR MODULATING MACROPHAGES POLARIZATION 有权

    公开(公告)号：US20220354811A1

    公开(公告)日：2022-11-10

    申请号：US17764583

    申请日：2020-10-02

    Applicant: INSERM (INSTITUT NATIONAL DE LA SANTÉ ET DE LA RECHERCHE MÉDICALE) ,  UNIVERSITE COTE D'AZUR

    Inventor： Arnaud JACQUEL ,  Guillaume ROBERT ,  Patrick AUBERGER ,  Paul CHAINTREUIL

    IPC: A61K31/197 ,  A61P11/00 ,  A61K45/06

    Abstract: 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.

    METHODS AND COMPOSITIONS FOR TREATING MELANOMA
    10.
    发明公开
    METHODS AND COMPOSITIONS FOR TREATING MELANOMA 审中-公开

    公开(公告)号：US20240165094A1

    公开(公告)日：2024-05-23

    申请号：US18550352

    申请日：2022-03-16

    Applicant: INSTITUT NATIONAL DE LA SANTÉ ET DE LA RECHERCHE MÉDICALE ,  CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE (CNRS) ,  UNIVERSITE COTE D'AZUR

    Inventor： Marcel DECKERT ,  Sophie TARTARE-DECKERT ,  Bernard MARI ,  Serena DIAZZI

    IPC: A61K31/4523 ,  A61K31/437 ,  A61K31/496 ,  A61K31/506 ,  A61K31/519 ,  A61K45/06 ,  A61P35/00

    CPC classification number: A61K31/4523 ,  A61K31/437 ,  A61K31/496 ,  A61K31/506 ,  A61K31/519 ,  A61K45/06 ,  A61P35/00

    Abstract: The inventors' working hypothesis relies on the original observations that mesenchymal MAPKi resistant cells display markers of fibrosis, acquire a myofibroblast-like phenotype and extracellular matrix (ECM) remodelling activities. In addition to increased remodelling of the ECM, pro-fibrotic responses induced by MAPK-targeted therapy include enhanced actin cytoskeleton plasticity, high sensitivity to mechanical cues and the establishment of an inflammatory microenvironment that contribute to therapy escape. The inventor's reason that approaches aimed at manipulating this abnormal fibrotic-like response induced by targeted therapy may represent rationale combination strategies to normalize the fibrous stroma, enhance drug efficacy and overcome resistance in BRAE mutant melanoma. Here the inventors investigated the impact of Nintedanib, an EMA/FDA-approved anti-fibrotic drug, as a repurposed drus in combination with targeted therapy on melanoma cell viability and tumor growth. Their findings reveal that the triplet combination BRAFi/MEKi/Nintedanib is active in pre-clinical models of melanoma to normalize the fibrous ECM network, enhance the efficacy of MAPK-targeted therapy and delay tumor relapse. Accordingly, the 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 BRAE, ii) an inhibitor of MEK and iii) an anti-fibrotic agent.

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