Nonclinical Drug Safety and Pharmacokinetics Dynamics Metabolism and Bioanalysis, Preclinical Development, Merck & Co. Inc., Rahway, NJ 07065, United States.
Toxicol Sci. 2024 Dec 1;202(2):278-290. doi: 10.1093/toxsci/kfae112.
Molnupiravir is registered or authorized in several countries as a 5-d oral coronavirus disease 2019 treatment for adults. Molnupiravir is a prodrug of the antiviral ribonucleoside β-D-N4-hydroxycytidine (NHC) that distributes into cells, where it is phosphorylated to its pharmacologically active ribonucleoside triphosphate (NHC-TP) form. NHC-TP incorporates into severe acute respiratory syndrome coronavirus 2 RNA by the viral RNA-dependent RNA polymerase, resulting in an accumulation of errors in the viral genome, leading to inhibition of viral replication and loss of infectivity. The potential of molnupiravir to induce genomic mutations and DNA damage was comprehensively assessed in several in vitro and in vivo genotoxicity assays and a carcinogenicity study, in accordance with international guideline recommendations and expert opinion. Molnupiravir and NHC induced mutations in vitro in bacteria and mammalian cells but did not induce chromosome damage in in vitro or in vivo assays. The in vivo mutagenic and carcinogenic potential of molnupiravir was tested in a series of in vivo mutagenicity studies in somatic and germ cells (Pig-a Assay and Big Blue® TGR Mutation Assay) and in a carcinogenicity study (transgenic rasH2-Tg mouse), using durations of exposure and doses exceeding those used in clinical therapy. In vitro genotoxicity results are superseded by robustly conducted in vivo studies. Molnupiravir did not increase mutations in somatic or germ cells in the in vivo animal studies and was negative in the carcinogenicity study. The interpretation criteria for each study followed established regulatory guidelines. Taken together, these data indicate that molnupiravir use does not present a genotoxicity or carcinogenicity risk for patients.
莫努匹韦在多个国家注册或批准用于治疗成人的 5 天口服冠状病毒疾病 2019。莫努匹韦是抗病毒核苷 β-D-N4-羟基胞嘧啶(NHC)的前药,分布到细胞内,在细胞内被磷酸化为其具有药理活性的核苷三磷酸(NHC-TP)形式。NHC-TP 通过病毒 RNA 依赖性 RNA 聚合酶掺入严重急性呼吸系统综合征冠状病毒 2 RNA,导致病毒基因组中积累错误,从而抑制病毒复制并丧失感染力。根据国际指南建议和专家意见,在几项体外和体内遗传毒性试验和致癌性研究中,全面评估了莫努匹韦诱导基因组突变和 DNA 损伤的潜力。莫努匹韦和 NHC 在体外细菌和哺乳动物细胞中诱导突变,但在体外或体内试验中不诱导染色体损伤。在一系列体内体细胞和生殖细胞(Pig-a 测定和 Big Blue®TGR 突变测定)和致癌性研究(转基因 rasH2-Tg 小鼠)中的体内致突变和致癌潜力研究中,测试了莫努匹韦的体内致突变和致癌潜力,使用的暴露持续时间和剂量超过了临床治疗中使用的剂量。体外遗传毒性结果被进行良好的体内研究所取代。莫努匹韦在体内动物研究中未增加体细胞或生殖细胞中的突变,并且致癌性研究为阴性。每个研究的解释标准均遵循既定的监管指南。总而言之,这些数据表明莫努匹韦的使用不会对患者造成遗传毒性或致癌性风险。