Kirby Brian J, Symonds William T, Kearney Brian P, Mathias Anita A
Gilead Sciences Inc., 333 Lakeside Drive, Foster City, CA, 94404, USA.
Clin Pharmacokinet. 2015 Jul;54(7):677-90. doi: 10.1007/s40262-015-0261-7.
Sofosbuvir (SOVALDI(®)), a potent, once-daily, orally administered nucleotide analog prodrug inhibitor of the hepatitis C virus (HCV) NS5B polymerase is approved in the USA, EU, Canada, and other regions for the treatment of HCV infection as a component of an antiviral treatment regimen. Sofosbuvir undergoes intracellular activation to form GS-461203 (active triphosphate, not detected in plasma), and ultimately the inactive, renally eliminated metabolite GS-331007. GS-331007 was identified as the primary analyte of interest for clinical pharmacology studies as it accounted for >90 % of systemic drug-related material exposure, and provided comparable exposure-response relationships for viral kinetics as observed for sofosbuvir. GS-331007 and sofosbuvir exhibit linear pharmacokinetics with minimal accumulation upon multiple dosing. Compared to healthy subjects, HCV-infected patients had modestly lower (39 %) GS-331007 area under the plasma concentration-time curve (AUC) and higher sofosbuvir AUC (60 %). Sofosbuvir can be administered without dose modification in HCV-infected patients with any degree of hepatic impairment or mild to moderate renal impairment. Sofosbuvir has a low propensity for clinically significant drug interactions with common concomitant medications used by HCV-infected patients. Clinically significant alterations in GS-331007 or sofosbuvir exposures are limited to potent inducers of intestinal P-glycoprotein that may lower exposure. In HCV-infected patients, demographic variables do not significantly influence GS-331007 and sofosbuvir exposures and no consistent exposure-response relationships were observed for efficacy or safety. This review focuses on the clinical pharmacokinetics, pharmacodynamics, and pharmacokinetic-pharmacodynamic relationships of sofosbuvir, and summarizes a number of drug interaction studies with important concomitant medications commonly used by HCV-infected patients.
索磷布韦(商品名:索华迪(®))是一种强效的、每日一次口服的核苷酸类似物前药,为丙型肝炎病毒(HCV)NS5B聚合酶抑制剂,在美国、欧盟、加拿大及其他地区获批,作为抗病毒治疗方案的组成部分用于治疗HCV感染。索磷布韦在细胞内活化形成GS - 461203(活性三磷酸酯,在血浆中未检测到),最终形成无活性的、经肾脏消除的代谢产物GS - 331007。GS - 331007被确定为临床药理学研究的主要分析物,因为它占全身药物相关物质暴露量的90%以上,并且在病毒动力学方面提供了与索磷布韦观察到的相当的暴露-反应关系。GS - 331007和索磷布韦表现出线性药代动力学,多次给药后蓄积极少。与健康受试者相比,HCV感染患者的GS - 331007血浆浓度-时间曲线下面积(AUC)略低(39%),而索磷布韦的AUC较高(60%)。索磷布韦可在任何程度肝功能损害或轻度至中度肾功能损害的HCV感染患者中使用,无需调整剂量。索磷布韦与HCV感染患者常用的常见合并用药发生临床显著药物相互作用的可能性较低。GS - 331007或索磷布韦暴露的临床显著改变仅限于可能降低暴露的肠道P - 糖蛋白强效诱导剂。在HCV感染患者中,人口统计学变量对GS - 331007和索磷布韦的暴露没有显著影响,在疗效或安全性方面未观察到一致的暴露-反应关系。本综述重点关注索磷布韦的临床药代动力学、药效学以及药代动力学-药效学关系,并总结了一些与HCV感染患者常用重要合并用药的药物相互作用研究。