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    INHIBITION OF REPERFUSION INJURY WITH A PSD-95 INHIBITOR
    2.
    发明公开
    INHIBITION OF REPERFUSION INJURY WITH A PSD-95 INHIBITOR 审中-公开

    公开(公告)号：US20230285504A1

    公开(公告)日：2023-09-14

    申请号：US17800883

    申请日：2021-02-19

    申请人： NONO INC.

    发明人： Michael TYMIANSKI

    IPC分类号： A61K38/10 ,  A61K38/48 ,  A61P25/28 ,  A61P7/02 ,  A61P9/10

    CPC分类号： A61K38/10 ,  A61K38/482 ,  A61P25/28 ,  A61P7/02 ,  A61P9/10

    摘要： The peptide inhibitor of PSD-95, Tat-NR2B9c, and related peptides can inhibit reperfusion injury when administered before blood flow is restored. This role is in addition to the role of active agent that inhibits PSD-95 inhibiting damage resulting from ischemia and resulting excitotoxicity. The relative timing of administering an active agent that inhibits PSD-95 and reperfusion by thrombolytic agents is additionally influenced by degradation of plasmin-sensitive active agent that inhibits PSD-95 by plasmin induced by thrombolytic agents if the active agent that inhibits PSD-95 and plasmin are co-resident in the plasma. Plasmin-degradation can be reduced or avoided and the benefit of inhibiting reperfusion injury obtained by administering an active agent that inhibits PSD-95 before restoration of blood flow by reperfusion, preferably at least 10, 15, 20, 22, 25, 30, 40, 50 or 60 minutes before restoration of blood flow by reperfusion.

    Therapy for subarachnoid hemorrhage and ischemia
    3.
    发明授权
    Therapy for subarachnoid hemorrhage and ischemia 有权

    公开(公告)号：US11338015B2

    公开(公告)日：2022-05-24

    申请号：US16381757

    申请日：2019-04-11

    申请人： NoNO, Inc.

    发明人： Michael Tymianski

    IPC分类号： A61K38/16 ,  A61K38/10 ,  A61K45/06 ,  A61K49/00 ,  A61K38/08 ,  G01N33/68 ,  C07K14/705 ,  C07K14/47 ,  C12N7/00 ,  A61K38/00

    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 benefitting 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.

    Combination therapy for ischemia
    4.
    发明授权
    Combination therapy for ischemia 有权

    公开(公告)号：US10967041B2

    公开(公告)日：2021-04-06

    申请号：US16051971

    申请日：2018-08-01

    申请人： NONO INC.

    发明人： Michael Tymianski

    IPC分类号： A61K38/10 ,  A61K38/49 ,  A61K38/17

    摘要： The invention provides a combination treatment for ischemia conditions in or otherwise affecting the CNS, such as stroke. The treatment involves administration of a PSD-95 inhibitor and performing reperfusion therapy (e.g., by administration of tPA). Administering a PSD-95 inhibitor in combination with reperfusion therapy increases the efficacy of the reperfusion therapy and/or slows the decline in efficacy of reperfusion therapy with time after onset of ischemia thus extending the window in which reperfusion therapy can be administered.

    Therapy for subarachnoid hemorrhage and ischemia
    5.
    发明授权
    Therapy for subarachnoid hemorrhage and ischemia 有权

    公开(公告)号：US10300110B2

    公开(公告)日：2019-05-28

    申请号：US14965694

    申请日：2015-12-10

    申请人： NoNO Inc.

    发明人： Michael Tymianski ,  Jonathan David Garman

    IPC分类号： G01N33/68 ,  A61K38/16 ,  A61K38/10 ,  A61K45/06 ,  A61K49/00 ,  A61K38/08 ,  C07K14/705 ,  C07K14/47 ,  C12N7/00 ,  A61K38/00

    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.

    Combination therapy for ischemia
    8.
    发明授权
    Combination therapy for ischemia 有权

    公开(公告)号：US11878044B2

    公开(公告)日：2024-01-23

    申请号：US17177970

    申请日：2021-02-17

    申请人： NoNO Inc.

    发明人： Michael Tymianski

    IPC分类号： A61K38/10 ,  A61K38/49 ,  A61K38/17

    CPC分类号： A61K38/10 ,  A61K38/1787 ,  A61K38/49 ,  A61K38/1787 ,  A61K2300/00 ,  A61K38/49 ,  A61K2300/00

    摘要： The invention provides a combination treatment for ischemia conditions in or otherwise affecting the CNS, such as stroke. The treatment involves administration of a PSD-95 inhibitor and performing reperfusion therapy (e.g., by administration of tPA). Administering a PSD-95 inhibitor in combination with reperfusion therapy increases the efficacy of the reperfusion therapy and/or slows the decline in efficacy of reperfusion therapy with time after onset of ischemia thus extending the window in which reperfusion therapy can be administered.

    CHLORIDE SALT OF TAT-NR2B9C
    9.
    发明申请
    CHLORIDE SALT OF TAT-NR2B9C 审中-公开

    公开(公告)号：US20190175689A1

    公开(公告)日：2019-06-13

    申请号：US16128423

    申请日：2018-09-11

    申请人： NONO INC.

    发明人： Jonathan David Garman

    IPC分类号： A61K38/16 ,  C07K14/005 ,  A61K9/00 ,  A61K38/10 ,  C07K14/16 ,  C07K19/00 ,  C07K7/08 ,  C07K7/06 ,  C07K14/705 ,  A61K9/19 ,  A61K47/26 ,  A61K47/18 ,  A61K47/12

    摘要： The present invention provides lyophilized formulations of active agents, particularly of TAT-NR2B9c, as chloride salts. TAT-NR2B9c has shown promise for treating stroke, aneurysm, subarachnoid hemorrhage and other neurological or neurotraumatic conditions. The chloride salt of TAT-NR2B9c shows improved stability compared with the acetate salt form of prior formulations. Formulations of the chloride salt of TAT-NR2B9c are stable at ambient temperature thus facilitating maintenance of supplies of such a formulation in ambulances for administration at the scene of illness or accident or in transit to a hospital.

    Method of Reducing Injury to Mammalian Cells
    10.
    发明申请
    Method of Reducing Injury to Mammalian Cells 审中-公开

    公开(公告)号：US20180369319A1

    公开(公告)日：2018-12-27

    申请号：US15956563

    申请日：2018-04-18

    申请人： NONO, INC.

    发明人： Michael Tymianski

    IPC分类号： A61K38/08 ,  A61K38/17

    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.