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350 条记录 (耗时 0.034 秒)

    Platelet-specific chimeric 7E3 immunoglobulin
    52.
    发明授权
    Platelet-specific chimeric 7E3 immunoglobulin 失效
    血小板特异性嵌合7E3免疫球蛋白

    公开(公告)号：US5770198A

    公开(公告)日：1998-06-23

    申请号：US375074

    申请日：1995-01-17

    申请人： Barry S. Coller ,  David M. Knight

    发明人： Barry S. Coller ,  David M. Knight

    IPC分类号： A61K38/00 ,  A61P7/02 ,  C07K16/28 ,  C12N15/13 ,  A61K39/395

    CPC分类号： C07K16/2848 ,  A61K38/00 ,  C07K2317/24 ,  C07K2317/55 ,  C07K2319/00 ,  C07K2319/30 ,  C07K2319/33

    摘要： Platelet-specific, chimeric immunoglobulin and immunoglobulin fragments are described. The chimeric molecules are made up of a nonhuman antigen binding region and a human constant region. Preferred immunoglobulins are specific for glycoprotein IIb/IIIa receptor in its complexed form; they block ligand binding to the receptor and prevent platelet aggregation. The immunoglobulins are useful in anti-thrombotic therapy when administered alone or in conjunction with thrombolytic agents, as well as in thrombus imaging.

    摘要翻译： 描述血小板特异性，嵌合免疫球蛋白和免疫球蛋白片段。 嵌合分子由非人抗原结合区和人恒定区组成。 优选的免疫球蛋白对其复合形式的糖蛋白IIb / IIIa受体是特异性的; 它们阻断配体结合受体并防止血小板聚集。 当单独或联合溶栓剂以及血栓成像时，免疫球蛋白可用于抗血栓形成治疗。

    Characterization of platelet aggregation disorders
    53.
    发明授权
    Characterization of platelet aggregation disorders 失效
    血小板聚集障碍的表征

    公开(公告)号：US5656442A

    公开(公告)日：1997-08-12

    申请号：US264759

    申请日：1994-06-23

    申请人： Mark H. Ginsberg

    发明人： Mark H. Ginsberg

    IPC分类号： C12P21/08 ,  C07K16/28 ,  G01N33/49 ,  G01N33/53 ,  G01N33/569 ,  G01N33/577 ,  G01N33/567

    CPC分类号： C07K16/2848 ,  C07K16/2839 ,  G01N33/56966 ,  C07K2317/34 ,  Y10S435/975

    摘要： Methods are described for characterizing platelet aggregation defects. The defects are characterized as activation, ligand binding, or post-occupancy defects. In one embodiment of the invention a Cam variant of Glanzmann's thrombasthenia is characterized as having a ligand binding defect. In another embodiment, a patient with myelofibrosis is identified as having an activation defect. Rapid analysis are afforded using fluorescence-activated flow cytometry. Also, diagnostic kits are described which comprise antibodies suitable for characterizing the above defects.

    摘要翻译： 描述了描述血小板聚集缺陷的方法。 这些缺陷的特征在于激活，配体结合或后置缺陷。 在本发明的一个实施方案中，Glanzmann血栓形成症的凸轮变体的特征在于具有配体结合缺陷。 在另一个实施方案中，具有骨髓纤维化的患者被鉴定为具有活化缺陷。 使用荧光激活流式细胞仪进行快速分析。 此外，描述了包含适于表征上述缺陷的抗体的诊断试剂盒。

    Characterization of platelet aggregation disorders
    56.
    发明授权
    Characterization of platelet aggregation disorders 失效
    斑块聚集障碍的特征

    公开(公告)号：US5196309A

    公开(公告)日：1993-03-23

    申请号：US614723

    申请日：1990-11-15

    申请人： Mark H. Ginsberg

    发明人： Mark H. Ginsberg

    IPC分类号： C12P21/08 ,  C07K16/28 ,  G01N33/49 ,  G01N33/53 ,  G01N33/569 ,  G01N33/577

    CPC分类号： C07K16/2848 ,  C07K16/2839 ,  G01N33/56966 ,  C07K2317/34 ,  Y10S435/975

    摘要： Methods are described for characterizing platelet aggregation defects. The defects are characterized as activation, ligand binding, or post-occupancy defects. In one embodiment of the invention a Cam variant of Glanzmann's thrombasthenia is characterized as having a ligand binding defect. In another embodiment, a patient with myelofibrosis is identified as having an activation defect. Rapid analysis are afforded using fluorescence-activated flow cytometry. Also, diagnostic kits are described which comprise antibodies suitable for characterizing the above defects.

    摘要翻译： 描述了描述血小板聚集缺陷的方法。 这些缺陷的特征在于激活，配体结合或后置缺陷。 在本发明的一个实施方案中，Glanzmann血栓形成症的凸轮变体的特征在于具有配体结合缺陷。 在另一个实施方案中，具有骨髓纤维化的患者被鉴定为具有活化缺陷。 使用荧光激活流式细胞仪进行快速分析。 此外，描述了包含适于表征上述缺陷的抗体的诊断试剂盒。

    USE OF ALPHA-V-INTEGRIN (CD51) INHIBITORS FOR THE TREATMENT OF CARDIAC FIBROSIS
    59.
    发明公开
    USE OF ALPHA-V-INTEGRIN (CD51) INHIBITORS FOR THE TREATMENT OF CARDIAC FIBROSIS 审中-公开

    公开(公告)号：US20240165195A1

    公开(公告)日：2024-05-23

    申请号：US18460962

    申请日：2023-09-05

    申请人： INSERM (Institut National de la Santé et de la Recherche Médicale) ,  Université Paris Cité ,  Assistance Publique-Hôpitaux de Paris (APHP)

    发明人： Jean-Sébastien HULOT

    IPC分类号： A61K38/12 ,  A61P9/04 ,  C07K16/28

    CPC分类号： A61K38/12 ,  A61P9/04 ,  C07K16/2848

    摘要： Activated cardiac fibroblasts are essential for the production of extracellular matrix proteins that accumulate during cardiac fibrosis, and PW1+ cardiac adult stem cells were recently proposed as a cellular source of fibroblasts in the ischemic hearts. Here the inventors identify αV-integrin (or CD51) as an essential regulator of PW1+ cardiac adult stem cells fibrogenic behavior. Inhibition of αV-integrin reduce the profibrotic gene expression profile and the ability to differentiate into fibroblasts of cardiac PW1+ cells. The pharmacological blockade of αV-containing integrins improved cardiac function and survival after MI by reducing infarct size and attenuating the extension of reactive cardiac fibrosis. Notably, the total cardiac fibrotic area as well as interstitial fibrosis in the remote myocardial area are significantly reduced after pharmacological blockade of αV-containing integrins. These data identify a new mechanism that regulates cardiac fibrosis in response to an ischemic injury and suggest that pharmacological targeting of αV-integrin may provide clinical benefit in the treatment of cardiac fibrosis.