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    Cell Permeable Inhibitors Of The Scaffold Protein Plenty Of SH3 Domains (POSH) Or Sh3Rfl
    6.
    发明申请
    Cell Permeable Inhibitors Of The Scaffold Protein Plenty Of SH3 Domains (POSH) Or Sh3Rfl 有权
    支架蛋白的细胞可渗透抑制剂大量SH3结构域（POSH）或Sh3Rfl

    公开(公告)号：US20160193292A1

    公开(公告)日：2016-07-07

    申请号：US14911939

    申请日：2014-08-08

    申请人： THE CURATORS OF THE UNIVERSITY OF MISSOURI

    发明人： Mark A. DANIELS

    IPC分类号： A61K38/17 ,  A61K47/48 ,  C12N7/00 ,  C07K14/47 ,  C07K14/005

    CPC分类号： A61K38/1709 ,  A61K38/00 ,  A61K47/64 ,  C07K7/08 ,  C07K14/005 ,  C07K14/47 ,  C07K2319/00 ,  C07K2319/10 ,  C12N7/00 ,  C12N2740/16322 ,  C12N2740/16371

    摘要： Plenty of SII3 (POSH) and INK-interacting protein 1 (JIP-1) function as a multi-protein scaffold network for TCR-mediated JNK1 activation in CD8+ T-cells. Disruption of the POSH/JIP-1 complex led to profound defects in the activation of JNK1, as well as deficient activation or induction of the transcription factors c-Jun, T-bet and Eomesodermin Furthermore, disruption of the POSH/JIP complex in CD8+T-cells resulted in impaired proliferation, decreased cytokine expression and the inability to control tumors. Collectively, these data identify a mechanism for the specific regulation of TCR-dependent JNK1 activation and function that is key for CD8+ T-cell responses. The disclosure describes a group of compounds that individually or in concert target a common set of biological pathways important in T cell function, activation of innate inflammation, ischemic reperfusion injury, HIV release and oncogenesis.

    摘要翻译： SII3（POSH）和INK相互作用蛋白1（JIP-1）作为CD8 + T细胞中TCR介导的JNK1激活的多蛋白质支架网络发挥作用。 POSH / JIP-1复合物的破坏导致JNK1激活的深刻缺陷，以及转录因子c-Jun，T-bet和Eomesodermin的活化或诱导缺陷。此外，CD8 / JIP复合物在CD8中的破坏 + T细胞导致增殖受损，细胞因子表达降低，无法控制肿瘤。 总的来说，这些数据确定了TCR依赖性JNK1激活和功能的特异性调节机制，这是CD8 + T细胞应答的关键。 本公开描述了一组化合物，其单独或一致地靶向在T细胞功能中重要的常见生物学途径，激活先天性炎症，缺血再灌注损伤，HIV释放和肿瘤形成。

    Therapy for subarachnoid hemorrhage and ischemia
    8.
    发明授权
    Therapy for subarachnoid hemorrhage and ischemia 有权
    蛛网膜下腔出血和局部缺血的治疗

    公开(公告)号：US09241970B2

    公开(公告)日：2016-01-26

    申请号：US13774053

    申请日：2013-02-22

    申请人： NoNO Inc.

    发明人： Michael Tymianski

    IPC分类号： A61K38/00 ,  A61K38/08 ,  A61K38/10 ,  G01N33/68 ,  C07K14/47 ,  A61K45/06 ,  A61K49/00 ,  C07K14/705

    CPC分类号： A61K38/162 ,  A61K38/00 ,  A61K38/08 ,  A61K38/10 ,  A61K45/06 ,  A61K49/00 ,  C07K14/47 ,  C07K14/70571 ,  C07K2319/10 ,  C12N7/00 ,  C12N2740/16311 ,  C12N2740/16322 ,  C12N2740/16371 ,  G01N33/6893 ,  G01N2800/2871

    摘要： The application provides data from a clinical trial of a PSD-95 inhibitor in subjects undergoing endovascular repair of an aneurysm in or otherwise affecting the CNS. The subjects were stratified by whether the aneurysm ruptured before performing the endovascular surgery. Rupture is associated with higher mortality or increased debilitation if a subject survives. The trial provided evidence of significant benefit in subjects with and without aneurysm rupture before endovascular was surgery performed. Surprisingly, the subjects benefiting most from treatment as judged both by pathology and neurocognitive outcome were those in which the aneurysm had ruptured causing a subarachnoid hemorrhage. These data constitute evidence that a PSD-95 inhibitor is beneficial not only in ischemic and hemorrhagic stroke but in forms of hemorrhage in or affecting the CNS, particularly, subarachnoid hemorrhage.

    摘要翻译： 该应用程序提供来自在经历血管内修复动脉瘤或以其他方式影响CNS的受试者中的PSD-95抑制剂的临床试验的数据。 受试者是否在进行血管内手术之前是否将动脉瘤破裂分层。 如果受试者存活，破裂与更高的死亡率或增加的衰弱有关。 该试验提供证据显示，在进行血管内手术前有和无动脉瘤破裂的受试者。 令人惊讶的是，受病理学和神经认知结果判断的治疗受益最大的受试者是动脉瘤破裂引起蛛网膜下腔出血的受试者。 这些数据构成了PSD-95抑制剂不仅在缺血性和出血性中风中有益，而且对出血或影响CNS，特别是蛛网膜下腔出血的形式有益。