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瑞替加滨:从化学合成到临床应用

Retigabine: chemical synthesis to clinical application.

作者信息

Blackburn-Munro G, Dalby-Brown W, Mirza N R, Mikkelsen J D, Blackburn-Munro R E

机构信息

Department of Pharmacology, NeuroSearch A/S, Pederstrupvej 93, DK-2750 Ballerup, Denmark.

出版信息

CNS Drug Rev. 2005 Spring;11(1):1-20. doi: 10.1111/j.1527-3458.2005.tb00033.x.

Abstract

Retigabine [D23129; N-(2-amino-4-(4-fluorobenzylamino)-phenyl)carbamic acid ethyl ester] is an antiepileptic drug with a recently described novel mechanism of action that involves opening of neuronal K(V)7.2-7.5 (formerly KCNQ2-5) voltage-activated K(+) channels. These channels (primarily K(V)7.2/7.3) enable generation of the M-current, a subthreshold K(+) current that serves to stabilize the membrane potential and control neuronal excitability. In this regard, retigabine has been shown to have a broad-spectrum of activity in animal models of electrically-induced (amygdala-kindling, maximal electroshock) and chemically-induced (pentylenetetrazole, picrotoxin, NMDA) epileptic seizures. These encouraging results suggest that retigabine may also prove useful in the treatment of other diseases associated with neuronal hyperexcitability. Neuropathic pain conditions are characterized by pathological changes in sensory pathways, which favor action potential generation and enhanced pain transmission. Although sometimes difficult to treat with conventional analgesics, antiepileptics can relieve some symptoms of neuropathic pain. A number of recent studies have reported that retigabine can relieve pain-like behaviors (hyperalgesia and allodynia) in animal models of neuropathic pain. Neuronal activation within several key structures within the CNS can also be observed in various animal models of anxiety. Moreover, amygdala-kindled rats, which have a lowered threshold for neuronal activation, also display enhanced anxiety-like responses. Retigabine dose-dependently reduces unconditioned anxiety-like behaviors when assessed in the mouse marble burying test and zero maze. Early clinical studies have indicated that retigabine is rapidly absorbed and distributed, and is resistant to first pass metabolism. Tolerability is good in humans when titrated up to its therapeutic dose range (600-1200 mg/day). No tolerance, dependence or withdrawal potential has been reported, although adverse effects can include mild dizziness, headache, nausea and somnolence. Thus, retigabine may prove to be useful in the treatment of a diverse range of disease states in which neuronal hyperexcitability is a common underlying factor.

摘要

瑞替加滨[D23129;N-(2-氨基-4-(4-氟苄基氨基)-苯基)氨基甲酸乙酯]是一种抗癫痫药物,其作用机制新颖,涉及开启神经元K(V)7.2-7.5(原KCNQ2-5)电压激活的K(+)通道。这些通道(主要是K(V)7.2/7.3)可产生M电流,这是一种阈下K(+)电流,用于稳定膜电位并控制神经元兴奋性。在这方面,瑞替加滨在电诱导(杏仁核点燃、最大电休克)和化学诱导(戊四氮、印防己毒素、NMDA)癫痫发作的动物模型中已显示出广泛的活性。这些令人鼓舞的结果表明,瑞替加滨在治疗与神经元兴奋性过高相关的其他疾病中可能也有用。神经性疼痛病症的特征是感觉通路的病理变化,这有利于动作电位的产生和疼痛传递的增强。尽管有时用传统镇痛药难以治疗,但抗癫痫药可缓解神经性疼痛的一些症状。最近的一些研究报告称,瑞替加滨可缓解神经性疼痛动物模型中的疼痛样行为(痛觉过敏和异常性疼痛)。在各种焦虑动物模型中也可观察到中枢神经系统内几个关键结构内的神经元激活。此外,杏仁核点燃的大鼠神经元激活阈值降低,也表现出增强的焦虑样反应。在小鼠大理石埋藏试验和零迷宫试验中评估时,瑞替加滨剂量依赖性地减少无条件焦虑样行为。早期临床研究表明,瑞替加滨吸收和分布迅速,且对首过代谢有抗性。当滴定至其治疗剂量范围(600-1200毫克/天)时,人体耐受性良好。尽管不良反应可能包括轻度头晕、头痛、恶心和嗜睡,但尚未报道有耐受性、依赖性或戒断可能性。因此,瑞替加滨在治疗多种以神经元兴奋性过高为共同潜在因素的疾病状态中可能证明是有用的。

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Retigabine: chemical synthesis to clinical application.瑞替加滨:从化学合成到临床应用
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