METHODS AND COMPOSITIONS FOR MODULATING INSULIN SECRETION AND GLUCOSE METABOLISM
    6.
    发明申请
    METHODS AND COMPOSITIONS FOR MODULATING INSULIN SECRETION AND GLUCOSE METABOLISM 审中-公开
    用于调节胰岛素分泌和葡萄糖代谢的方法和组合物

    公开(公告)号:US20100204258A1

    公开(公告)日:2010-08-12

    申请号:US12450100

    申请日:2008-03-12

    摘要: The present invention relates to methods and compositions for treating or ameliorating the effects of diabetes. In addition, the present invention relates to methods and compositions for treating or preventing hyperglycemia, as well as modulating monoamine levels, islet β-cell insulin secretion, insulin and/or glucagon levels in a patient. In certain preferred embodiments, such methods include administering to a patient an effective amount of a vesicular monoamine transporter type 2 (VMAT2) antagonist, such as tetrabenazine (TBZ), dihydrotetrabenazine (DTBZ), tetrahydroberberine (THB), reserpine, emetine, Compound 6, or enantiomers, optical isomers, diastereomers, N-oxides, crystalline forms, hydrates, metabolites or pharmaceutically acceptable salts thereof.

    摘要翻译: 本发明涉及用于治疗或改善糖尿病的作用的方法和组合物。 此外,本发明涉及用于治疗或预防高血糖的方法和组合物,以及调节患者体内单胺水平,胰岛素和细胞胰岛素分泌,胰岛素和/或胰高血糖素水平。 在某些优选的实施方案中,这些方法包括向患者施用有效量的2型(VMAT2)囊泡单胺转运蛋白拮抗剂,如丁苯那嗪(TBZ),二氢丁苯那嗪(DTBZ),四氢小檗碱(THB),利血平, ,或对映体,旋光异构体,非对映异构体,N-氧化物,结晶形式,水合物,代谢物或药学上可接受的盐。

    NEURONAL PAIN PATHWAY
    7.
    发明申请
    NEURONAL PAIN PATHWAY 有权
    神经痛痛途径

    公开(公告)号:US20120295853A1

    公开(公告)日:2012-11-22

    申请号:US13569510

    申请日:2012-08-08

    摘要: The present invention relates to the discovery of a novel molecular pathway involved in long-term hyperexcitability of sensory neurons, which, in higher animals, is associated with persistent pain. It is based on the discovery that, following injury to an axon of a neuron, an increase in nitric oxide synthase activity results in increased nitric oxide production, which, in turn, activates guanylyl cyclase, thereby increasing levels of cGMP. Increased cGMP results in activation of protein kinase G (“PKG”), which then is retrogradely transported along the axon to the neuron cell body, where it phosphorylates MAPKerk.

    摘要翻译: 本发明涉及发现涉及感觉神经元的长期兴奋性的新型分子途径,其在高等动物中与持续性疼痛相关。 基于这样的发现,在神经元轴突损伤之后,一氧化氮合酶活性的增加导致一氧化氮产生增加,这反过来激活鸟苷酸环化酶,从而增加cGMP的水平。 增加的cGMP导致蛋白激酶G(PKG)的激活,其然后沿着轴突逆行转运到神经元细胞体,其中磷酸化MAPKerk。