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公开(公告)号:US20210128730A1
公开(公告)日:2021-05-06
申请号:US16628611
申请日:2018-07-04
申请人: NH THERAGUIX , Universite Claude Bernard Lyon 1 , Centre National de La Recherche Scientifique - CNRS - , INSERM (Institut National de la Sante et de la Recherche Médicale) , Institut Gustave Roussy
发明人: François LUX , Olivier TILLEMENT , Jean-Luc PERFETTINI , Eric DEUTSCH , Frédéric LAW , Awatef ALLOUCH
摘要: The invention relates to methods for treating tumors. In particular, the invention provides novel use of nanoparticles in combination with ionizing radiations for treating tumors, wherein the combined effect of nanoparticles induces senescence and/or cannibalism of the tumor cells.
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公开(公告)号:US20230218781A1
公开(公告)日:2023-07-13
申请号:US17753893
申请日:2020-09-18
申请人: NH THERAGUIX , INSTITUT GUSTAVE ROUSSY , INSERM (INSTITUT NATIONAL DE LA SANTÉ ET DE LA RECHERCHE MÉDICALE) , UNIVERSITE PARIS-SACLAY
CPC分类号: A61K49/1881 , A61K45/06
摘要: The present disclosure relates to the field of nanomedicine, in particular for treating cancers. The present disclosure more specifically provides new methods of treating undesirable M2-polarized macrophages and/or inducing M1 macrophage polarization in a subject in need thereof, comprising administering to said subject a therapeutically effective amount of nanoparticles containing metallic elements.
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公开(公告)号:US20200181714A1
公开(公告)日:2020-06-11
申请号:US16333409
申请日:2017-09-19
IPC分类号: C12Q1/6886 , C07K14/80
摘要: Although tumor-associated macrophages have been extensively studied in the control of response to radiotherapy, the molecular mechanisms involved in the ionizing radiation-mediated activation of macrophages remain elusive. Here the present inventors show that ionizing radiation induces the expression of interferon-regulatory factor 5 (IRF5) promoting thus macrophage activation toward a pro-inflammatory phenotype. They reveal that the activation of the Ataxia telangiectasia mutated (ATM) kinase is required for ionizing radiation-elicited macrophage activation, but also for macrophage reprogramming after treatments with γ-interferon, lipopolysaccharide or chemotherapeutic agent (such as cis-platin), underscoring the fact that the kinase ATM plays a central role during macrophage phenotypic switching toward a proinflammatory phenotype. They further demonstrate that NADPH oxidase 2 (NOX2)-dependent ROS production is upstream to ATM activation and is essential during this process. They also report that hypoxic conditions and the inhibition of any component of this signaling pathway (NOX2, ROS and ATM) impairs pro-inflammatory activation of macrophages and predicts a poor tumor response to preoperative radiotherapy in locally advanced rectal cancer. Altogether, these results identify a novel signaling pathway involved in macrophage activation that may enhance effectiveness of radiotherapy through the re-programming of tumor infiltrating macrophages.
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公开(公告)号:US20230302031A1
公开(公告)日:2023-09-28
申请号:US17928352
申请日:2021-06-01
发明人: Jean-Luc PERFETTINI , Deborah LECUYER , Desiree TANNOUS , Awatef ALLOUCH , Oliver DELELIS , Frederic SUBRA
IPC分类号: A61K31/7048 , A61K45/06 , A61P11/00 , A61P31/14 , A61K31/196 , A61K31/64 , A61K31/191
CPC分类号: A61K31/7048 , A61K45/06 , A61P11/00 , A61P31/14 , A61K31/196 , A61K31/64 , A61K31/191
摘要: The inventors herein show that purinergic receptors regulate the conversion of macrophage pro-inflammatory reprogramming into anti-inflammatory phenotype in patients suffering from COVID-19 disease. Moreover, they show that P2Y receptor agonists repress NLRP3 inflammasome-dependent IL-1b secretion, but also impair the replication and the cytopathogenic effects of SARS-CoV-2. These results therefore suggest that some purinergic receptors agonists can treat acute lung injury and respiratory disease that are associated with SARS-CoV-2 infection. In addition, their results show that antagonists of the purinergic receptors P2X impair the replication of said virus. The present invention therefore proposes to use purinergic receptors modulators and NLR3-P2Y2R immune checkpoint modulators to treat patients suffering from a virus-induced acute respiratory distress syndrome.
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公开(公告)号:US20220257709A1
公开(公告)日:2022-08-18
申请号:US17626360
申请日:2020-07-17
摘要: Identification of effective targets alleviating the programmed cell removal (PrCR) of tumor cells by macrophages is of very high interest. The present inventors have identified that the cyclin-dependent kinase inhibitor p21 protein is a strong regulator of the macrophage-mediated PrCR. Also, they showed that the adoptive transfer of p21 overexpressing monocytes induces macrophage PrCR and transition from an anti-inflammatory to a pro-inflammatory phenotype in vivo, delays cancer progression and increases significantly the overall survival of mice engrafted with cancer cells. The present invention therefore concerns therapeutic compositions comprising monocytes that over-express the cyclin-dependent kinase inhibitor p21 protein, and their use for treating mammals suffering from cancer, especially leukemia.
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公开(公告)号:US20170342411A1
公开(公告)日:2017-11-30
申请号:US15534321
申请日:2015-12-10
申请人: NSERM (Institut National de la Sante et la Recherc Medicale) , Universite Paris-Sud , Institut Gustave Roussy , Universite Paris Descartes , Universite Pierre et Marie Curie (Paris 6) , Institut Pasteur , Istituto Nazionale per Le Malattie Infettive IRCCS Lazzaro Spallanzani , Assistance Publique-Hopitaux de Paris (APHP)
IPC分类号: C12N15/113 , A61K31/713 , A61K31/17 , A61K31/395 , A61K31/165 , A61K31/683 , A61K31/5517 , C12Q1/18 , A61K45/06
CPC分类号: C12N15/113 , A61K31/165 , A61K31/17 , A61K31/395 , A61K31/5517 , A61K31/683 , A61K31/7088 , A61K31/713 , A61K45/06 , C12N15/1132 , C12N2310/14 , C12N2320/31 , C12Q1/18 , A61K2300/00
摘要: The present invention provides methods and pharmaceutical compositions for treating human immunodeficiency virus type 1 (HIV-1) infections. In particular, the present invention relates to a method for treating HIV-1 infection in a subject in need thereof comprising administering the subject with a therapeutically effective amount of an inhibitor of SGT1 activity or expression.
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