Departments of Medicinal Chemistry, Merck Research Laboratories, Rahway, New Jersey 07065, USA.
J Med Chem. 2012 Nov 26;55(22):9847-55. doi: 10.1021/jm301056k. Epub 2012 Nov 12.
The voltage-gated calcium channel Ca(v)2.2 (N-type calcium channel) is a critical regulator of synaptic transmission and has emerged as an attractive target for the treatment of chronic pain. We report here the discovery of sulfonamide-derived, state-dependent inhibitors of Ca(v)2.2. In particular, 19 is an inhibitor of Ca(v)2.2 that is selective over cardiac ion channels, with a good preclinical PK and biodistribution profile. This compound exhibits dose-dependent efficacy in preclinical models of inflammatory hyperalgesia and neuropathic allodynia and is devoid of ancillary cardiovascular or CNS pharmacology at the doses tested. Importantly, 19 exhibited no efficacy in Ca(v)2.2 gene-deleted mice. The discovery of metabolite 26 confounds further development of members of this aminopiperidine sulfonamide series. This discovery also suggests specific structural liabilities of this class of compounds that must be addressed.
电压门控钙通道 Ca(v)2.2(N 型钙通道)是突触传递的关键调节因子,已成为治疗慢性疼痛的有吸引力的靶点。我们在此报告了磺酰胺衍生的、状态依赖性的 Ca(v)2.2 抑制剂的发现。特别是,19 是一种选择性作用于心脏离子通道的 Ca(v)2.2 抑制剂,具有良好的临床前 PK 和生物分布特征。该化合物在炎症性痛觉过敏和神经病理性痛觉过敏的临床前模型中表现出剂量依赖性疗效,并且在测试剂量下没有辅助心血管或中枢神经系统药理学作用。重要的是,19 在 Ca(v)2.2 基因缺失的小鼠中没有疗效。代谢产物 26 的发现进一步阻碍了这个氨基哌啶磺酰胺系列成员的开发。这一发现还表明,必须解决此类化合物的特定结构缺陷。