Sung Ig Cho, Ui Jin Park, Jun-Mo Chung, Byoung Joo Gwag
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引用次数: 38
摘要
在多种动物模型中,n -甲基- d -天冬氨酸(NMDA)受体和自由基的过度激活可引起缺氧缺血性脑损伤后神经细胞死亡。然而,在脑卒中患者中使用NMDA受体拮抗剂的临床试验未能显示出疗效,主要原因是神经保护的治疗时间窗口有限,治疗指数较窄。相比之下,抗氧化剂延长了缺血性脑卒中动物模型的神经保护时间窗口,在缺血性脑卒中的临床试验中显示出更大的治疗潜力。NMDA受体和自由基的过度激活介导中风中神经细胞死亡的两条独立途径,一种安全的多功能药物可以阻断大脑中的这两条途径,可能为中风患者提供更好的治疗结果。磺胺吡啶和阿司匹林的铅结构衍生物导致了一种新分子Neu2000的发现,该分子对NMDA和自由基诱导的细胞死亡具有出色的神经保护作用。Neu2000是一种选择性nr2b的中等NMDA受体拮抗剂,即使在纳摩尔浓度下也具有有效的细胞渗透性,自旋捕获抗氧化作用。非临床和人体I期研究表明,Neu2000可以转化为治疗脑卒中患者,具有更好的疗效和治疗时间窗。
Neu2000, an NR2B-selective, moderate NMDA receptor antagonist and potent spin trapping molecule for stroke.
Excess activation of ionotropic glutamate receptors, primarily N-methyl-D-aspartate (NMDA) receptors and free radicals, evoke nerve cell death following hypoxic-ischemic brain injury in various animal models. However, clinical trials in stroke patients using NMDA receptor antagonists have failed to show efficacy primarily due to the limited therapeutic time window for neuroprotection and a narrow therapeutic index. In comparison, antioxidants prolonged the time window for neuroprotection in animal models of ischemic stroke and showed greater therapeutic potential in clinical trials for ischemic stroke. Excess activation of NMDA receptors and free radicals mediate the two separate pathways of nerve cell death in stroke and a safe and multifunctional drug that can block both routes in the brain will likely provide a better therapeutic outcome in patients with stroke. Derivatives of the lead structures of sulfasalazine and aspirin have led to the discovery of a new molecule, Neu2000, that has demonstrated excellent neuroprotection against NMDA- and free radical-induced cell death. Neu2000 is an NR2B-selective, moderate NMDA receptor antagonist with potent cell-permeable, spin trapping antioxidant action even at nanomolar concentrations. Nonclinical and human phase I studies demonstrated that Neu2000 can be translated to treat patients with stroke with better efficacy and therapeutic time window.