Liu Rong, Curry Stephanie, McMonagle Patricia, Yeh Wendy W, Ludmerer Steven W, Jumes Patricia A, Marshall William L, Kong Stephanie, Ingravallo Paul, Black Stuart, Pak Irene, DiNubile Mark J, Howe Anita Y M
Merck Research Laboratories, Merck & Co., Inc., Kenilworth, New Jersey, USA
Merck Research Laboratories, Merck & Co., Inc., Kenilworth, New Jersey, USA.
Antimicrob Agents Chemother. 2015 Nov;59(11):6922-9. doi: 10.1128/AAC.01390-15. Epub 2015 Aug 24.
Elbasvir is an investigational NS5A inhibitor with in vitro activity against multiple HCV genotypes. Antiviral activity of elbasvir was measured in replicons derived from wild-type or resistant variants of genotypes 1a, 1b, and 3. The barrier to resistance was assessed by the number of resistant colonies selected by exposure to various elbasvir concentrations. In a phase 1b dose-escalating study, virologic responses were determined in 48 noncirrhotic adult men with chronic genotype 1 or 3 infections randomized to placebo or elbasvir from 5 to 50 mg (genotype 1) or 10 to 100 mg (genotype 3) once daily for 5 days. The NS5A gene was sequenced from plasma specimens obtained before, during, and after treatment. Elbasvir suppressed the emergence of resistance-associated variants (RAVs) in vitro in a dose-dependent manner. Variants selected by exposure to high elbasvir concentrations typically encoded multiple amino acid substitutions (most commonly involving loci 30, 31, and 93), conferring high-level elbasvir resistance. In the monotherapy study, patients with genotype 1b had greater reductions in HCV RNA levels than patients with genotype 1a at all elbasvir doses; responses in patients with genotype 3 were generally less pronounced than for genotype 1, particularly at lower elbasvir doses. M28T, Q30R, L31V, and Y93H in genotype 1a, L31V and Y93H in genotype 1b, and A30K, L31F, and Y93H in genotype 3 were the predominant RAVs selected by elbasvir monotherapy. Virologic findings in patients were consistent with the preclinical observations. NS5A-RAVs emerged most often at amino acid positions 28, 30, 31, and 93 in both the laboratory and clinical trial. (The MK-8742 P002 trial has been registered at ClinicalTrials.gov under identifier NCT01532973.).
艾尔巴韦是一种处于研究阶段的NS5A抑制剂,对多种丙肝病毒(HCV)基因型具有体外活性。在源自1a、1b和3型野生型或耐药变异体的复制子中测定了艾尔巴韦的抗病毒活性。通过暴露于不同浓度艾尔巴韦后筛选出的耐药菌落数量评估耐药屏障。在一项1b期剂量递增研究中,48名患有慢性1型或3型感染的非肝硬化成年男性被随机分配至安慰剂组或艾尔巴韦组,剂量为5至50毫克(1型)或10至100毫克(3型),每日一次,共5天,测定病毒学反应。从治疗前、治疗期间和治疗后的血浆标本中对NS5A基因进行测序分析。艾尔巴韦在体外以剂量依赖性方式抑制耐药相关变异体(RAV)的出现。暴露于高浓度艾尔巴韦后筛选出的变异体通常编码多个氨基酸替代(最常见的涉及位点30、31和93),赋予高水平的艾尔巴韦耐药性。在单药治疗研究中,在所有艾尔巴韦剂量下,1b型患者的HCV RNA水平下降幅度大于1a型患者;3型患者的反应通常不如1型患者明显,尤其是在较低剂量的艾尔巴韦治疗时。1a型中的M28T、Q30R、L31V和Y93H、1b型中的L31V和Y93H以及3型中的A30K、L31F和Y93H是艾尔巴韦单药治疗筛选出的主要RAV。患者的病毒学研究结果与临床前观察一致。在实验室和临床试验中,NS5A-RAV最常出现在氨基酸位置28、30、31和93处。(MK-8742 P002试验已在ClinicalTrials.gov上注册,标识符为NCT01532973。)