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    Agents for reducing injury to mammalian cells
    24.
    发明授权
    Agents for reducing injury to mammalian cells 有权
    降低哺乳动物细胞损伤的药剂

    公开(公告)号：US07846897B2

    公开(公告)日：2010-12-07

    申请号：US11894818

    申请日：2007-08-20

    申请人： Michael Tymianski

    发明人： Michael Tymianski

    IPC分类号： A61K38/04

    CPC分类号： A61K38/08 ,  A61K38/1709

    摘要： A method of inhibiting the binding between N-methyl-D-aspartate receptors and neuronal proteins in a neuron the method comprising administering to the neuron an effective inhibiting amount of a peptide replacement agent for the NMDA receptor or neuronal protein interaction domain that effect said inhibition of the NMDA receptor neuronal protein. The method is of value in reducing the damaging effect of injury to mammalian cells. Postsynaptic density-95 protein (PSD-95) couples neuronal N-methyl-D-aspartate receptors (NMDARs) to pathways mediating excitotoxicity and ischemic brain damage. This coupling was disrupted by transducing neurons with peptides that bind to modular domains on either side of the PSD-95/NMDAR interaction complex. This treatment attenuated downstream NMDAR signaling without blocking NMDAR activity, protected cultured cortical neurons from excitotoxic insults and dramatically reduced cerebral infarction volume in rats subjected to transient focal cerebral ischemia. The treatment was effective when applied either before, or one hour after, the onset of excitotoxicity in vitro and cerebral ischemia in vivo. This approach prevents negative consequences associated with blocking NMDAR activity and constitutes practical therapy for stroke.

    摘要翻译： 一种抑制神经元中N-甲基-D-天冬氨酸受体和神经元蛋白之间的结合的方法，包括向神经元施用有效抑制量的NMDA受体或神经元蛋白质相互作用区域的肽替代剂，其影响所述抑制 的NMDA受体神经元蛋白。 该方法在降低对哺乳动物细胞损伤的破坏作用方面是有价值的。 突触后密度-95蛋白（PSD-95）将神经元N-甲基-D-天冬氨酸受体（NMDAR）与介导兴奋性毒性和缺血性脑损伤的途径相结合。 通过用PSD-95 / NMDAR相互作用复合物的任一侧结合模块结构域的肽转导神经元，破坏了该偶联。 该治疗减弱下游NMDAR信号传导而不阻断NMDAR活性，保护培养的皮层神经元免受兴奋性毒性损伤，并显着降低大鼠脑梗死体积。 当在体外兴奋性毒性或体内脑缺血发生之前或之后1小时施用时，治疗是有效的。 这种方法可以预防与阻止NMDAR活动相关的负面后果，并构成中风的实际治疗。

    Method of reducing injury to mammalian cells
    25.
    发明申请
    Method of reducing injury to mammalian cells 有权

    公开(公告)号：US20090131321A1

    公开(公告)日：2009-05-21

    申请号：US11894818

    申请日：2007-08-20

    申请人： Michael Tymianski

    发明人： Michael Tymianski

    IPC分类号： A61K38/08 ,  C07K7/06 ,  A61P9/10

    CPC分类号： A61K38/08 ,  A61K38/1709

    摘要： A method of inhibiting the binding between N-methyl-D-aspartate receptors and neuronal proteins in a neuron the method comprising administering to the neuron an effective inhibiting amount of a peptide replacement agent for the NMDA receptor or neuronal protein interaction domain that effect said inhibition of the NMDA receptor neuronal protein. The method is of value in reducing the damaging effect of injury to mammalian cells. Postsynaptic density-95 protein (PSD-95) couples neuronal N-methyl-D-aspartate receptors (NMDARs) to pathways mediating excitotoxicity and ischemic brain damage. This coupling was disrupted by transducing neurons with peptides that bind to modular domains on either side of the PSD-95/NMDAR interaction complex. This treatment attenuated downstream NMDAR signaling without blocking NMDAR activity, protected cultured cortical neurons from excitotoxic insults and dramatically reduced cerebral infarction volume in rats subjected to transient focal cerebral ischemia. The treatment was effective when applied either before, or one hour after, the onset of excitotoxicity in vitro and cerebral ischemia in vivo. This approach prevents negative consequences associated with blocking NMDAR activity and constitutes practical therapy for stroke.

    Method of reducing injury to mammalian cells
    28.
    发明申请
    Method of reducing injury to mammalian cells 有权
    降低哺乳动物细胞损伤的方法

    公开(公告)号：US20050059597A1

    公开(公告)日：2005-03-17

    申请号：US10930192

    申请日：2004-08-31

    申请人： Michael Tymianski

    发明人： Michael Tymianski

    IPC分类号： A61K38/08 ,  A61K38/17

    CPC分类号： A61K38/08 ,  A61K38/1709

    摘要： A method of inhibiting the binding between N-methyl-D-aspartate receptors and neuronal proteins in a neuron is disclosed. The method comprises administering to the neuron an effective inhibiting amount of a peptide replacement agent for the NMDA receptor or neuronal protein interaction domain that effect said inhibition of the NMDA receptor—neuronal protein interaction. The method is of value in reducing the damaging effect of injury to mammalian cells. Postsynaptic density-95 protein (PSD-95) couples neuronal N-methyl-D-aspartate receptors (NMDARs) to pathways mediating excitotoxicity, ischemic and traumatic brain damage. This coupling was disrupted by transducing neurons with peptides that bind to modular domains on either side of the PSD-95/NMDAR interaction complex. This treatment attenuated downstream NMDAR signaling without blocking NMDAR activity, protected cultured cortical neurons from excitotoxic insults, dramatically reduced cerebral infarction volume in rats subjected to transient focal cerebral ischemia, and traumatic brain injury (TBI) in rats.

    摘要翻译： 公开了抑制神经元中N-甲基-D-天冬氨酸受体和神经元蛋白之间结合的方法。 该方法包括向神经元施用有效抑制量的NMDA受体或神经元蛋白相互作用区域的肽置换剂，其影响NMDA受体 - 神经元蛋白相互作用的所述抑制。 该方法在降低对哺乳动物细胞损伤的破坏作用方面是有价值的。 突触后密度-95蛋白（PSD-95）将神经元N-甲基-D-天冬氨酸受体（NMDAR）与介导兴奋性毒性，缺血性和创伤性脑损伤的途径相结合。 通过用PSD-95 / NMDAR相互作用复合物的任一侧结合模块结构域的肽转导神经元，破坏了该偶联。 这种治疗减弱下游NMDAR信号，而不阻断NMDAR活性，保护培养的皮质神经元免受兴奋性毒性损伤，大大减少了大鼠局部脑缺血大鼠脑损伤的体积，大鼠外伤性脑损伤（TBI）。

    Method Of Reducing Injury To Mammalian Cells
    29.
    发明申请
    Method Of Reducing Injury To Mammalian Cells 审中-公开
    减少哺乳动物细胞损伤的方法

    公开(公告)号：US20120302504A1

    公开(公告)日：2012-11-29

    申请号：US13286071

    申请日：2011-10-31

    申请人： Michael Tymianski

    发明人： Michael Tymianski

    IPC分类号： A61K38/08 ,  A61P9/10 ,  A61P25/00

    CPC分类号： A61K38/08 ,  A61K38/1709

    摘要： A method of inhibiting the binding between N-methyl-D-aspartate receptors and neuronal proteins in a neuron is disclosed. The method comprises administering to the neuron an effective inhibiting amount of a peptide replacement agent for the NMDA receptor or neuronal protein interaction domain that effect said inhibition of the NMDA receptor-neuronal protein interaction. The method is of value in reducing the damaging effect of injury to mammalian cells. Postsynaptic density-95 protein (PSD-95) couples neuronal N-methyl-D-aspartate receptors (NMDARs) to pathways mediating excitotoxicity, ischemic and traumatic brain damage. This coupling was disrupted by transducing neurons with peptides that bind to modular domains on either side of the PSD-95/NMDAR interaction complex. This treatment attenuated downstream NMDAR signaling without blocking NMDAR activity, protected cultured cortical neurons from excitotoxic insults, dramatically reduced cerebral infarction volume in rats subjected to transient focal cerebral ischemia, and traumatic brain injury (TBI) in rats.

    摘要翻译： 公开了抑制神经元中N-甲基-D-天冬氨酸受体和神经元蛋白之间结合的方法。 该方法包括向神经元施用有效抑制量的NMDA受体或神经元蛋白相互作用区域的肽置换剂，其影响NMDA受体 - 神经元蛋白相互作用的所述抑制。 该方法在降低对哺乳动物细胞损伤的破坏作用方面是有价值的。 突触后密度-95蛋白（PSD-95）将神经元N-甲基-D-天冬氨酸受体（NMDAR）与介导兴奋性毒性，缺血性和创伤性脑损伤的途径相结合。 通过用PSD-95 / NMDAR相互作用复合物的任一侧结合模块结构域的肽转导神经元，破坏了该偶联。 这种治疗减弱下游NMDAR信号，而不阻断NMDAR活性，保护培养的皮质神经元免受兴奋性毒性损伤，大大减少了大鼠局部脑缺血大鼠脑损伤的体积，大鼠外伤性脑损伤（TBI）。