Wu Ruokun, Chen Wenfeng, Wang Xueyuan, Ye Xinran, Miao Hang, Shi Jingmiao, Lei Meng, Zhu Yongqiang
College of Science, Nanjing Forestry University, No. 159 Longpan Road, Nanjing, 210037, PR China.
College of Life Science, Nanjing Normal University, No. 1 Wenyuan Road, Nanjing, 210046, PR China.
Eur J Med Chem. 2025 Dec 5;299:118069. doi: 10.1016/j.ejmech.2025.118069. Epub 2025 Aug 25.
Chronic pain has become a major factor affecting the quality of human life. Nav1.7 is a subtype of neuronal voltage-gated sodium channel. Its mutation is closely related to pain syndrome. By inhibiting the function of Nav1.7, it can effectively relieve pain. As a result, it has been extensively researched as a hot target for pain management. In this manuscript, a series of new arylsulfonamide compounds based on Nav1.7 were designed and synthesized. The biological properties of these compounds were assessed through various experiments, including in vitro and in vivo evaluations, microsomal stability, selectivity, hERG and pharmacokinetic studies. Compound 50 was found to show favorable microsomal stability, in vivo safety, high selectivity and a low potential risk of cardiotoxicity. Further in vivo studies showed that compound 50 had a faster onset of action and better analgesic efficacy in several pain models than positive control. In addition, molecular docking results showed that compound 50 formed 2 hydrogen bonds and π-π stacking interactions with amino acid residues in the lipid exposed pocket of Nav1.7. These results suggested that compound 50 might be a potent candidate for the treatment of neuropathic pain.
慢性疼痛已成为影响人类生活质量的主要因素。Nav1.7是神经元电压门控钠通道的一种亚型。其突变与疼痛综合征密切相关。通过抑制Nav1.7的功能,可有效缓解疼痛。因此,它作为疼痛管理的热门靶点已被广泛研究。在本论文中,设计并合成了一系列基于Nav1.7的新型芳基磺酰胺化合物。通过各种实验评估了这些化合物的生物学特性,包括体外和体内评价、微粒体稳定性、选择性、hERG和药代动力学研究。发现化合物50具有良好的微粒体稳定性、体内安全性、高选择性和低心脏毒性潜在风险。进一步的体内研究表明,在几种疼痛模型中,化合物50比阳性对照起效更快且镇痛效果更好。此外,分子对接结果显示,化合物50与Nav1.7脂质暴露口袋中的氨基酸残基形成了2个氢键和π-π堆积相互作用。这些结果表明,化合物50可能是治疗神经性疼痛的有效候选药物。