A phase 2, open-label study to assess the safety and efficacy of Bemnifosbuvir (bem) and Ruzasvir (rzr) in subjects with chronic hepatitis c virus (hcv) infection

开始日期2024-01-08

申办/合作机构

Atea Pharmaceuticals, Inc.

[+1]

NCT06204679

/ Completed临床1期

A Phase 1, Open-Label Study to Assess Comparative Bioavailability and Effect of Food on a Prototype Fixed-Dose Combination of Bemnifosbuvir and Ruzasvir Versus Individual Dosage Forms Taken Concomitantly in Healthy Adult Subjects

This study will assess comparative bioavailability and effect of food on a prototype fixed-dose combination (FDC) of Bemnifosbuvir (BEM) and Ruzasvir (RZR) in healthy subjects

开始日期2023-12-14

申办/合作机构

Atea Pharmaceuticals, Inc.

NCT05904470

/ Completed临床2期

A Phase 2, Open-label Study to Assess the Safety and Efficacy of Bemnifosbuvir (BEM) and Ruzasvir (RZR) in Subjects With Chronic Hepatitis C Virus (HCV) Infection

This is an open-label trial to evaluate safety and efficacy of treatment with BEM + RZR in subjects with chronic HCV infection.

开始日期2023-05-30

申办/合作机构

Atea Pharmaceuticals, Inc.

100 项与 Bemnifosbuvir 相关的临床结果

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100 项与 Bemnifosbuvir 相关的转化医学

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100 项与 Bemnifosbuvir 相关的专利（医药）

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项与 Bemnifosbuvir 相关的文献（医药）

2026-02-01·JOURNAL OF CLINICAL PHARMACOLOGY

In Vitro and Clinical Evaluation of Potential Interactions of Bemnifosbuvir with Drug Transporters

Article

作者: Hammond, Janet ; Agrawal, Nancy ; Belanger, Bruce ; Vo, Alex ; Montrond, Maureen ; Horga, Arantxa ; Lynch, Shannan ; Morelli, Gaetano ; Zhou, Xiao‐Jian ; Pietropaolo, Keith

Abstract:

Bemnifosbuvir is a novel oral guanosine nucleotide prodrug candidate for the treatment of chronic hepatitis C virus infection. Potential drug–drug interactions (DDIs) of bemnifosbuvir as a substrate or perpetrator with regard to ATP‐binding cassette (ABC) and solute carrier (SLC) transporters were evaluated in vitro and in clinical studies. Bemnifosbuvir was demonstrated in vitro as a substrate and inhibitor of the ABC transporters’ P‐glycoprotein (P‐gp), as an inhibitor of the breast cancer resistance protein (BCRP), as well as a weak inhibitor of SLC transporters, including organic anion transporting polypeptide 1B1 (OATP1B1). Phase 1 studies in healthy participants were subsequently conducted to assess the clinical significance of transporter‐mediated DDI potentials of bemnifosbuvir as a precipitant using digoxin and rosuvastatin as P‐gp and BCRP/OATP1B1 index substrates, respectively. A single dose of 0.25 mg digoxin or 10 mg rosuvastatin was administered alone and with 1100 mg bemnifosbuvir, either simultaneously or staggered. Simultaneous administration of a single dose of 1100 mg bemnifosbuvir increased total plasma exposure of both drugs by less than 20%, and transiently increased the peak plasma exposure of digoxin and rosuvastatin by 78% and 40%, respectively. Staggered dosing reduced the magnitude of changes in peak exposure to digoxin and rosuvastatin. No serious adverse events or drug discontinuations were observed. Dose adjustments are therefore unlikely for drugs that are substrates of P‐gp or BCRP/OAT1B1 when coadministered with bemnifosbuvir, and staggered dosing may further reduce any DDI risk.

2026-02-01·ANTIVIRAL RESEARCH

Substitutions M478K and A482G in the polymerase of yellow fever virus confer resistance to sofosbuvir and uprifosbuvir in vitro

Article

作者: Mikkelsen, Lotte ; Rosas, Ana Lucia Rosales ; Binderup, Alekxander ; Fahnøe, Ulrik ; Ramirez, Santseharay ; Delang, Leen ; Bukh, Jens ; Soto, Alina ; Elorz, Itsaso Ortigosa ; Ryberg, Line Abildgaard

The continuous re-emergence of yellow fever virus (YFV) poses a serious public health threat, with no approved specific antiviral drugs for treatment. Sofosbuvir and uprifosbuvir, developed for treatment of chronic hepatitis C, are nucleotide analogs with anti-YFV activity in vitro, and sofosbuvir has been used off-label in YFV-infected individuals. To study the barrier to resistance of these drugs, escape experiments were performed with the YFV 17D vaccine strain in human hepatoma Huh7.5 cells. Compared to the original virus, sofosbuvir and uprifosbuvir escape variants exhibited 8.6- to 10.7-fold increased 50% effective concentration (EC₅₀) values. Escape viruses developed putative resistance-associated-substitutions (RAS) M478K and A482G in the NS5 RNA-dependent RNA polymerase domain. Reverse-engineered YFV 17D mutants demonstrated that A482G was the primary determinant of drug resistance, resulting in 5.3- to 5.7-fold increased EC₅₀; however, the substitutions acted synergistically when combined, leading to 12.3- and 11.1-fold increased EC₅₀. A482G conferred slight cross-resistance to bemnifosbuvir, while no cross-resistance was observed for remdesivir, galidesivir, or NITD008. Escape and mutant viruses had slight delays in growth kinetics in Huh7.5 cells and were viable in C6/36 and Aag2-AF5 mosquito cells. Structural analysis of a predicted AlphaFold3 YFV NS5-RNA structure suggests that M478K and A482G induce conformational changes in RdRp motif F, which may reduce sofosbuvir and uprifosbuvir affinities. Sofosbuvir RAS described for other orthoflaviviruses did not substantially affect drug susceptibility in reverse-engineered YFV 17D. This study demonstrates that YFV can develop resistance to sofosbuvir and uprifosbuvir with only two NS5 substitutions that have slight impact on viral fitness.

2025-05-01·ANTIVIRAL RESEARCH

Bemnifosbuvir and ruzasvir in combination exhibit potent synergistic antiviral activity in vitro while maintaining a favorable nonclinical safety profile in vivo

Article

作者: Lin, Kai ; Good, Steven S ; Sommadossi, Jean-Pierre ; Luo, Shouqi ; Vo, Alex ; Agrawal, Nancy G B

Bemnifosbuvir (BEM), the orally available hemisulfate salt of the double prodrug of a guanosine nucleotide analog, is a potent, selective, and pan-genotypic inhibitor of HCV nonstructural protein 5B, an RNA-dependent RNA polymerase necessary for viral replication. Similarly, ruzasvir (RZR) is an orally available, highly potent, selective, and pan-genotypic inhibitor of HCV nonstructural protein 5A, an essential component of the viral replication complex. The antiviral effects of the combination of these two complementary direct-acting antivirals were determined in HCV GT1b Huh-7 replicon cells. Two independent in vitro evaluations suggested that BEM and RZR act synergistically to inhibit HCV replication without accompanying cytotoxicity. Additionally, the toxicity and toxicokinetic properties of BEM and RZR administered individually or in combination were investigated in rats given daily oral doses at 500 mg/kg of each drug for 13 weeks, with an interim analysis at 4 weeks. All doses were well tolerated with no test article-related adverse effects identified in either the separate or combined dose groups. Moreover, toxicokinetic analyses conducted on dose days 1, 28 and 84 indicated minimal pharmacokinetic interactions between the two drugs in rats, with AUC values for AT-511 (free base form of BEM), its major circulating metabolites, and RZR being similar, regardless of separate or co-administration.

113

项与 Bemnifosbuvir 相关的新闻（医药）

2026-04-13

·知乎专栏

戊肝抗病毒研究的新进展：从复制体系创新到潜在治疗策略的重构

戊型肝炎病毒（HEV）是全球范围内急性病毒性肝炎的重要病原之一。HEV在传播方式和疾病谱上呈现出更加复杂的流行特征：一方面，HEV-1和HEV-2主要通过粪--口传播，在发展中国家流行；另一方面，HEV-3和HEV-4则具有明显的人畜共患特征，主要通过污染的肉制品传播，是发达国家急性戊肝的主要病因。图1. HEV全球感染病例的分布情况在多数免疫功能正常的个体中，HEV感染通常表现为自限性过程。然而，在免疫抑制人群（如器官移植受者）中，HEV-3和HEV-4可发展为慢性感染，进而导致肝纤维化甚至肝硬化。这一人群中的治疗问题，使HEV从“自限性病毒”转变为一个具有明确临床干预需求的研究对象。长期以来，HEV的基础机制研究、抗病毒药物研发进展缓慢，慢性戊肝感染始终缺乏获批的特异性靶向治疗药物。近日，国际顶级胃肠病学期刊《Gut》在线发表了北京大学、海德堡大学、波鸿鲁尔大学联合团队的重磅研究成果，该研究从模型系统构建与药物筛选策略两个层面同时推进，为HEV研究提供了新的技术路径，也带来了潜在的治疗突破。一、不止于新药发现：全新筛选体系重构HEV研究技术范式本研究中值得关注的一点是其建立的全长HEV荧光报告系统。传统HEV药物筛选主要依赖亚基因复制子（subgenomic replicon），这类系统通常删除了ORF2和ORF3结构蛋白区域，虽然操作简便，但存在一个关键问题——无法完整反映病毒生命周期，尤其是：• 缺失病毒装配与释放过程• 忽略结构蛋白参与宿主免疫调控• 对某些靶向结构蛋白的药物筛选能力不足本研究在ORF2衣壳蛋白C端引入split GFP标签，构建了一个可以覆盖完整复制周期的报告系统。这一改进带来的意义在于：• 将“复制”与“病毒结构功能”整合到同一筛选体系• 可以同步评估抗病毒活性与细胞毒性（通过荧光与核染信号）• 为后续靶向ORF2/ORF3的药物开发提供了直接实验基础图2. 基于ORF2的全长HEV荧光报告系统换句话说，这项工作实际上把HEV药物筛选，从“片段模型”推进到了“接近真实感染状态的系统级模型”。二、Bemnifosbuvir脱颖而出：为戊肝临床治疗提供全新候选方案基于该体系，研究对核苷（酸）类似物库进行了筛选，最终确定Bemnifosbuvir（BEM）为最具潜力的候选分子之一。从实验结果来看，这一分子的特点并不只是“有效”，而是具备几个对抗病毒研究尤为关键的属性：1. 抑制作用明确且稳定• 在体外细胞模型中表现出剂量依赖性抑制• IC50约为0.54 μM，优于部分已报道候选分子2. 跨模型一致性不仅在常规肝癌细胞系中有效，在以下系统中同样成立：• iPSC来源肝样细胞• 原代人肝细胞（PHHs）• 动物感染模型（沙鼠）这说明其抗病毒作用具有一定的生理相关性。3. 抗耐药潜力长期传代（>160天）后病毒仍保持对BEM敏感，提示其可能具有较高的耐药屏障，这一点在RNA病毒研究中尤为关键。4. 联合用药策略可行与RBV联用呈现加和效应（部分条件下协同），为未来治疗方案提供现实路径，而不是完全替代现有体系。三、一个更值得关注的信号：ORF2从“结构蛋白”走向“功能核心”该研究的价值不仅在于筛选出可快速推进临床的抗HEV候选药物，更在于为领域提供了标准化的新型研究模型，重新定义了ORF2衣壳蛋白在HEV研究中的核心地位，也催生了多个前沿研究方向。1. ORF2功能机制的深度研究该研究与近年多项成果共同证实，ORF2的生物学功能远超出传统认知的“结构蛋白”范畴，其在病毒免疫逃逸、跨物种传播、毒力调控、慢性感染维持等过程中均发挥关键作用。目前，不同基因型HEV ORF2的序列-功能差异、不同宿主来源（人、猪、禽类）HEV ORF2的跨物种感染机制、ORF2与宿主蛋白的互作网络、ORF2在病毒耐药中的调控作用等方向，均是领域内的研究热点。2. 新型HEV研究模型的构建与验证该研究构建的全长报告病毒为后续研究提供了范式。未来，不同基因型、不同宿主来源、不同突变株的全长报告病毒及感染性克隆的构建，均需要ORF2抗体作为核心工具，用于病毒感染效率定量、ORF2表达定位检测、病毒株鉴定等环节；同时需要重组ORF2蛋白作为实验体系的阳性对照。3. 下一代抗HEV药物的研发除靶向RdRp的核苷类似物外，靶向ORF2衣壳组装的抑制剂是下一代抗HEV药物的核心研发方向。这类药物的筛选与评价，需要重组ORF2蛋白开展体外衣壳组装实验、化合物结合实验，同时需要ORF2抗体评价化合物对病毒感染及ORF2功能的影响。4. 人畜共患HEV的防控研究HEV是典型的人兽共患病原体。除猪源HEV 3/4型外，禽类戊肝病毒（aHEV）不仅给家禽养殖业造成经济损失，还存在跨物种传播的潜在风险，是One Health理念下的重要研究方向。相关研究均需要对应的禽类HEV ORF2重组衣壳蛋白与特异性抗体作为核心支撑。四、结语本研究是HEV领域技术研发与药物探索的一次重要突破。研究团队以ORF2衣壳蛋白为核心，成功构建的全长HEV荧光报告病毒与成像型高通量筛选平台，为HEV基础机制探索、抗病毒药物高通量筛选建立了更贴合实际的技术体系，也为后续相关研究的开展提供了可借鉴的标准化实验范式。五、abinScience HEV研究工具为助力广大科研工作者开展HEV研究、抗病毒药物研发、人畜共患病防控、疫苗开发等相关工作，abinScience可提供多种HEV相关抗体与蛋白，产品聚焦ORF2靶点，覆盖人源、禽类等多物种。Product NameCatalog No.InVivoMAb Anti-Hepatitis E virus/HEV pORF2 P domain Neutralizing Antibody (Iv0278)VK620020Anti-Hepatitis E virus/HEV pORF2 P domain Neutralizing Antibody (SAA2238)VK620023Anti-Hepatitis E virus/HEV pORF2 P domain Neutralizing Antibody (SAA2239)VK620033Anti-Hepatitis E virus/HEV pORF2 P domain Neutralizing Antibody (SAA2240)VK620043Anti-HEV Capsid protein Antibody (8G12)VK620013Anti-Avian HEV Capsid Polyclonal AntibodyVK620034Anti-Hepatitis E virus genotype 1/HEV-1 ORF2 Polyclonal AntibodyVK620014Anti-Hepatitis E virus genotype 1/HEV-1 ORF2 Polyclonal AntibodyVK620024Recombinant Avian HEV Capsid Protein, N-HisVK620032更多HEV相关研究产品欢迎发邮件给我们：References[1] Kamar N, Bendall R, Legrand-Abravanel F, Xia NS, Ijaz S, Izopet J, Dalton HR. Hepatitis E. Lancet. 2012 Jun 30;379(9835):2477-2488. doi: 10.1016/S0140-6736(11)61849-7. Epub 2012 Apr 30. Erratum in: Lancet. 2012 Aug 25;380(9843):730. PMID: 22549046.[2] Letafati A, Taghiabadi Z, Roushanzamir M, Memarpour B, Seyedi S, Farahani AV, Norouzi M, Karamian S, Zebardast A, Mehrabinia M, Ardekani OS, Fallah T, Khazry F, Daneshvar SF, Norouzi M. From discovery to treatment: tracing the path of hepatitis E virus. Virol J. 2024 Aug 23;21(1):194. doi: 10.1186/s12985-024-02470-3. Erratum in: Virol J. 2024 Sep 10;21(1):214. doi: 10.1186/s12985-024-02490-z. PMID: 39180020; PMCID: PMC11342613.[3] Debing Y, Moradpour D, Neyts J, Gouttenoire J. Update on hepatitis E virology: Implications for clinical practice. J Hepatol. 2016 Jul;65(1):200-212. doi: 10.1016/j.jhep.2016.02.045. Epub 2016 Mar 8. PMID: 26966047.[4] Guu TS, Liu Z, Ye Q, Mata DA, Li K, Yin C, Zhang J, Tao YJ. Structure of the hepatitis E virus-like particle suggests mechanisms for virus assembly and receptor binding. Proc Natl Acad Sci U S A. 2009 Aug 4;106(31):12992-7. doi: 10.1073/pnas.0904848106. Epub 2009 Jul 21. PMID: 19622744; PMCID: PMC2722310.[5] Hu J, Liu T, Klöhn M, Freistaedter A, Toprak E, Chi H, Gömer A, Pottkaemper L, Jordan P, Yang X, Zhang H, Becker J, Nkongolo S, Lohmann V, Steinmann E, Wang L, Dao Thi VL. Nucleotide analogue bemnifosbuvir inhibits hepatitis E virus replication in preclinical models. Gut. 2026 Mar 6:gutjnl-2025-336714. doi: 10.1136/gutjnl-2025-336714. Epub ahead of print. PMID: 41791851.本文所提供的所有产品与服务均仅供科研使用，不得用于人体诊断或治疗。For Research Use Only. Not for use in diagnostic or therapeutic procedures.

2026-04-13

·搜狐新闻

戊肝抗病毒研究的新进展

戊型肝炎病毒（HEV）是全球范围内急性病毒性肝炎的重要病原之一。HEV在传播方式和疾病谱上呈现出更加复杂的流行特征：一方面，HEV-1和HEV-2主要通过粪--口传播，在发展中国家流行；另一方面，HEV-3和HEV-4则具有明显的人畜共患特征，主要通过污染的肉制品传播，是发达国家急性戊肝的主要病因。图1. HEV全球感染病例的分布情况在多数免疫功能正常的个体中，HEV感染通常表现为自限性过程。然而，在免疫抑制人群（如器官移植受者）中，HEV-3和HEV-4可发展为慢性感染，进而导致肝纤维化甚至肝硬化。这一人群中的治疗问题，使HEV从“自限性病毒”转变为一个具有明确临床干预需求的研究对象。长期以来，HEV的基础机制研究、抗病毒药物研发进展缓慢，慢性戊肝感染始终缺乏获批的特异性靶向治疗药物。近日，国际顶级胃肠病学期刊《Gut》在线发表了北京大学、海德堡大学、波鸿鲁尔大学联合团队的重磅研究成果，该研究从模型系统构建与药物筛选策略两个层面同时推进，为HEV研究提供了新的技术路径，也带来了潜在的治疗突破。一、不止于新药发现：全新筛选体系重构HEV研究技术范式本研究中值得关注的一点是其建立的全长HEV荧光报告系统。传统HEV药物筛选主要依赖亚基因复制子（subgenomic replicon），这类系统通常删除了ORF2和ORF3结构蛋白区域，虽然操作简便，但存在一个关键问题——无法完整反映病毒生命周期，尤其是：• 缺失病毒装配与释放过程• 忽略结构蛋白参与宿主免疫调控• 对某些靶向结构蛋白的药物筛选能力不足本研究在ORF2衣壳蛋白C端引入split GFP标签，构建了一个可以覆盖完整复制周期的报告系统。这一改进带来的意义在于：• 将“复制”与“病毒结构功能”整合到同一筛选体系• 可以同步评估抗病毒活性与细胞毒性（通过荧光与核染信号）• 为后续靶向ORF2/ORF3的药物开发提供了直接实验基础图2. 基于ORF2的全长HEV荧光报告系统换句话说，这项工作实际上把HEV药物筛选，从“片段模型”推进到了“接近真实感染状态的系统级模型”。二、Bemnifosbuvir脱颖而出：为戊肝临床治疗提供全新候选方案基于该体系，研究对核苷（酸）类似物库进行了筛选，最终确定Bemnifosbuvir（BEM）为最具潜力的候选分子之一。从实验结果来看，这一分子的特点并不只是“有效”，而是具备几个对抗病毒研究尤为关键的属性：1. 抑制作用明确且稳定• 在体外细胞模型中表现出剂量依赖性抑制• IC50约为0.54 μM，优于部分已报道候选分子2. 跨模型一致性不仅在常规肝癌细胞系中有效，在以下系统中同样成立：• iPSC来源肝样细胞• 原代人肝细胞（PHHs）• 动物感染模型（沙鼠）这说明其抗病毒作用具有一定的生理相关性。3. 抗耐药潜力长期传代（>160天）后病毒仍保持对BEM敏感，提示其可能具有较高的耐药屏障，这一点在RNA病毒研究中尤为关键。4. 联合用药策略可行与RBV联用呈现加和效应（部分条件下协同），为未来治疗方案提供现实路径，而不是完全替代现有体系。三、一个更值得关注的信号：ORF2从“结构蛋白”走向“功能核心”该研究的价值不仅在于筛选出可快速推进临床的抗HEV候选药物，更在于为领域提供了标准化的新型研究模型，重新定义了ORF2衣壳蛋白在HEV研究中的核心地位，也催生了多个前沿研究方向。1. ORF2功能机制的深度研究该研究与近年多项成果共同证实，ORF2的生物学功能远超出传统认知的“结构蛋白”范畴，其在病毒免疫逃逸、跨物种传播、毒力调控、慢性感染维持等过程中均发挥关键作用。目前，不同基因型HEV ORF2的序列-功能差异、不同宿主来源（人、猪、禽类）HEV ORF2的跨物种感染机制、ORF2与宿主蛋白的互作网络、ORF2在病毒耐药中的调控作用等方向，均是领域内的研究热点。2. 新型HEV研究模型的构建与验证该研究构建的全长报告病毒为后续研究提供了范式。未来，不同基因型、不同宿主来源、不同突变株的全长报告病毒及感染性克隆的构建，均需要ORF2抗体作为核心工具，用于病毒感染效率定量、ORF2表达定位检测、病毒株鉴定等环节；同时需要重组ORF2蛋白作为实验体系的阳性对照。3. 下一代抗HEV药物的研发除靶向RdRp的核苷类似物外，靶向ORF2衣壳组装的抑制剂是下一代抗HEV药物的核心研发方向。这类药物的筛选与评价，需要重组ORF2蛋白开展体外衣壳组装实验、化合物结合实验，同时需要ORF2抗体评价化合物对病毒感染及ORF2功能的影响。4. 人畜共患HEV的防控研究HEV是典型的人兽共患病原体。除猪源HEV 3/4型外，禽类戊肝病毒（aHEV）不仅给家禽养殖业造成经济损失，还存在跨物种传播的潜在风险，是One Health理念下的重要研究方向。相关研究均需要对应的禽类HEV ORF2重组衣壳蛋白与特异性抗体作为核心支撑。四、结语本研究是HEV领域技术研发与药物探索的一次重要突破。研究团队以ORF2衣壳蛋白为核心，成功构建的全长HEV荧光报告病毒与成像型高通量筛选平台，为HEV基础机制探索、抗病毒药物高通量筛选建立了更贴合实际的技术体系，也为后续相关研究的开展提供了可借鉴的标准化实验范式。五、abinScience HEV研究工具为助力广大科研工作者开展HEV研究、抗病毒药物研发、人畜共患病防控、疫苗开发等相关工作，abinScience可提供多种HEV相关抗体与蛋白，产品聚焦ORF2靶点，覆盖人源、禽类等多物种。更多HEV相关研究产品欢迎发邮件给我们： support@abinscience.com References[1] Kamar N, Bendall R, Legrand-Abravanel F, Xia NS, Ijaz S, Izopet J, Dalton HR. Hepatitis E. Lancet. 2012 Jun 30;379(9835):2477-2488. doi: 10.1016/S0140-6736(11)61849-7. Epub 2012 Apr 30. Erratum in: Lancet. 2012 Aug 25;380(9843):730. PMID: 22549046.[2] Letafati A, Taghiabadi Z, Roushanzamir M, Memarpour B, Seyedi S, Farahani AV, Norouzi M, Karamian S, Zebardast A, Mehrabinia M, Ardekani OS, Fallah T, Khazry F, Daneshvar SF, Norouzi M. From discovery to treatment: tracing the path of hepatitis E virus. Virol J. 2024 Aug 23;21(1):194. doi: 10.1186/s12985-024-02470-3. Erratum in: Virol J. 2024 Sep 10;21(1):214. doi: 10.1186/s12985-024-02490-z. PMID: 39180020; PMCID: PMC11342613.[3] Debing Y, Moradpour D, Neyts J, Gouttenoire J. Update on hepatitis E virology: Implications for clinical practice. J Hepatol. 2016 Jul;65(1):200-212. doi: 10.1016/j.jhep.2016.02.045. Epub 2016 Mar 8. PMID: 26966047.[4] Guu TS, Liu Z, Ye Q, Mata DA, Li K, Yin C, Zhang J, Tao YJ. Structure of the hepatitis E virus-like particle suggests mechanisms for virus assembly and receptor binding. Proc Natl Acad Sci U S A. 2009 Aug 4;106(31):12992-7. doi: 10.1073/pnas.0904848106. Epub 2009 Jul 21. PMID: 19622744; PMCID: PMC2722310.[5] Hu J, Liu T, Klöhn M, Freistaedter A, Toprak E, Chi H, Gömer A, Pottkaemper L, Jordan P, Yang X, Zhang H, Becker J, Nkongolo S, Lohmann V, Steinmann E, Wang L, Dao Thi VL. Nucleotide analogue bemnifosbuvir inhibits hepatitis E virus replication in preclinical models. Gut. 2026 Mar 6:gutjnl-2025-336714. doi: 10.1136/gutjnl-2025-336714. Epub ahead of print. PMID: 41791851.本文所提供的所有产品与服务均仅供科研使用，不得用于人体诊断或治疗。For Research Use Only. Not for use in diagnostic or therapeutic procedures.返回搜狐，查看更多

2026-04-06

·Science Daily

A drug already in trials may finally stop hepatitis E

Scientists have identified a potential new weapon against hepatitis E, a virus with no approved treatment and tens of thousands of deaths each year. The drug bemnifosbuvir, currently in trials for hepatitis C, was found to block the virus from replicating by disrupting its genetic machinery. Tests in cells and animals showed strong effectiveness without harming healthy tissue. If ongoing trials succeed, the drug could soon be repurposed for hepatitis E.A drug currently being tested to treat hepatitis C may also work against hepatitis E by stopping the virus from reproducing. Hepatitis E infects millions of people worldwide and leads to about 70,000 deaths each year. Despite its impact, there is still no approved vaccine or targeted treatment. That situation may soon change with the discovery of bemnifosbuvir, a compound that shows strong activity against hepatitis E viruses (HEV). An international team of researchers from Bochum and Heidelberg in Germany and Beijing in China identified the drug while screening a collection of antiviral compounds. Bemnifosbuvir belongs to a class of molecules known as nucleotide/nucleoside analogues. Because it is already being tested in clinical trials for hepatitis C, scientists are hopeful it could be repurposed more quickly as a treatment for hepatitis E. Their findings were published in the journal Gut on March 6, 2026. How the Drug Blocks Viral Replication The researchers began by analyzing a commercially available library of nucleotide/nucleoside analogues, which are designed to mimic the building blocks of genetic material. "These synthetically produced molecules are constructed similarly to the building blocks of our genetic material and likewise to that of viruses," explains Dr. Mara Klöhn from Ruhr University Bochum. To identify promising candidates, the team tested about 500 compounds using a specially engineered hepatitis E virus that produces a fluorescent signal. They infected cell cultures with this modified virus and then treated the cells with different compounds. By tracking the fluorescence, they could quickly determine whether the virus continued to replicate. "With bemnifosbuvir we were able to see that the virus no longer replicated, while the treated cells remained healthy," reports Jungen Hu from Heidelberg University. Follow-up studies in animals confirmed that the drug reduced both viral activity and liver inflammation. "If the ongoing clinical trials of bemnifosbuvir against hepatitis C are successful, the drug could soon also be available for off label use against hepatitis E," say Dr. Viet Loan Dao Thi and Professor Eike Steinmann. Hepatitis E Risks and Lack of Treatments The hepatitis E virus (HEV) is a leading cause of acute viral hepatitis. Although many infections resolve on their own in people with healthy immune systems, the virus can become chronic in individuals with weakened immunity, including organ transplant recipients and people living with HIV. It also poses a serious risk during pregnancy. The disease was first documented in a major outbreak between 1955 to 1956, but it took decades before it became a major focus of scientific research. Even today, there is still no vaccine or specific antiviral therapy available. International Collaboration and Research Support This research involved the Department of Molecular and Medical Virology at Ruhr University Bochum, the Dao Thi Lab at the Center for Integrative Infectious Disease Research (CIID) of Heidelberg University Hospital, and the Lin Wang Lab at Peking University in China. The study received support from multiple funding sources, including the National Key Research and Development Program of China (2023YFC2306900), the research program "Antiviral Therapies" of the Baden-Württemberg Stiftung, the German Research Foundation within Collaborative Research Center 1129 (project number 240245660), the German Center for Infection Research -- TTU Hepatitis Project 05.823, the Beijing Municipal Natural Science Foundation (L244032), and the National Natural Science Foundation of China (82522053).

siRNA疫苗临床结果临床研究

100 项与 Bemnifosbuvir 相关的药物交易

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KEGG	Wiki	ATC	Drug Bank
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研发状态

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适应症	最高研发状态	国家/地区	公司	日期
新型冠状病毒感染	临床3期	日本	Atea Pharmaceuticals, Inc.	2021-04-28
新型冠状病毒感染	临床3期	日本	Hoffmann-La Roche, Inc.	2021-04-28
新型冠状病毒感染	临床3期	阿根廷	Atea Pharmaceuticals, Inc.	2021-04-28
新型冠状病毒感染	临床3期	阿根廷	Hoffmann-La Roche, Inc.	2021-04-28
新型冠状病毒感染	临床3期	比利时	Hoffmann-La Roche, Inc.	2021-04-28
新型冠状病毒感染	临床3期	比利时	Atea Pharmaceuticals, Inc.	2021-04-28
新型冠状病毒感染	临床3期	巴西	Atea Pharmaceuticals, Inc.	2021-04-28
新型冠状病毒感染	临床3期	巴西	Hoffmann-La Roche, Inc.	2021-04-28
新型冠状病毒感染	临床3期	哥伦比亚	Atea Pharmaceuticals, Inc.	2021-04-28
新型冠状病毒感染	临床3期	丹麦	Hoffmann-La Roche, Inc.	2021-04-28

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临床结果

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分期

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT05904470 (AT-01B-004, CTgov)	临床2期	肝硬化 \| 慢性丙型肝炎 \| 代偿期肝硬化	275	BEM+Bemnifosbuvir+RZR	鹹齋觸鏇遞憲齋糧餘鏇 = 獵築齋窪積繭襯齋觸製顧簾繭範選餘齋淵顧鹽 (餘餘蓋簾糧簾醖遞簾夢, 遞衊憲築選夢願觸憲鏇 ~ 壓鏇選構積廠齋獵鹽製) 更多	-	2025-10-21
NCT05629962 (CTgov)	临床3期	新型冠状病毒感染	2,285	BEM (BEM - SCO Stratum)	網顧範窪遞獵廠餘願糧 = 構壓鹽觸膚鑰醖積艱淵餘鑰構願製鹹壓淵鹽齋 (醖願網製網艱製壓顧觸, 觸鹹膚壓夢觸鬱鹹襯餘 ~ 鑰鑰繭憲鹹艱網壓壓網) 更多	-	2025-06-13
				BEM (PBO - SCO Stratum)	網顧範窪遞獵廠餘願糧 = 憲蓋醖獵鬱淵網餘遞製餘鑰構願製鹹壓淵鹽齋 (醖願網製網艱製壓顧觸, 繭繭範範壓膚觸製鹹壓 ~ 選遞糧夢網齋鹽鬱齋簾) 更多
NCT05904470 (AT-01B-004, GlobeNewswire) 人工标引	临床2期	丙型肝炎	275	Bemnifosbuvir 550 mg + Ruzasvir 180 mg	齋壓襯蓋選膚積淵製糧(醖鏇餘廠願積積製遞選) = 鹹淵憲廠蓋鹽齋襯築夢觸窪遞衊構衊簾範壓艱 (淵艱蓋鹹蓋艱窪夢鹽壓 ) 达到	积极	2024-12-04
				Bemnifosbuvir 550 mg + Ruzasvir 180 mg (non-cirrhotic and infected with genotypes 1-4)	齋壓襯蓋選膚積淵製糧(醖鏇餘廠願積積製遞選) = 築鏇鑰艱衊夢繭醖構繭觸窪遞衊構衊簾範壓艱 (淵艱蓋鹹蓋艱窪夢鹽壓 ) 达到
NCT05629962 (SUNRISE-3, GlobeNewswire) 人工标引	临床3期	新型冠状病毒感染	-	bemnifosbuvir	簾艱顧顧壓鹹鏇艱構遞(齋壓範繭夢鏇醖齋艱範) = did not meet 鬱網積餘製積顧顧顧鬱 (鑰醖遞築顧襯繭簾鬱範 ) 更多	不佳	2024-09-13
				placebo
NCT05905484 (Biospace) 人工标引	临床1期	-	42	Bemnifosbuvir	糧窪鹽壓獵選顧夢鏇齋(膚憲醖願齋範壓鹽窪襯) = The results presented at ESCMID further support the favorable safety profile for bemnifosbuvir by demonstrating the lack of cardiotoxicity in healthy participants. 積餘憲築襯鑰齋簾積範 (網範選繭鑰鹹窪繭壓齋 )	积极	2024-04-29
				Placebo
NCT04396106 (CTgov)	临床2期	新型冠状病毒感染	83	AT-527 (AT-527 - 550 mg BID)	鹽簾膚餘觸獵築鹹鬱壓 = 壓鹹膚餘醖壓齋蓋廠鏇範觸齋窪廠顧鏇壓繭獵 (繭簾衊壓夢選夢繭鹹繭, 餘製齋壓築顧遞願簾網 ~ 簾壓糧壓鹹餘餘製鹽鏇) 更多	-	2023-03-09
				Placebo (Placebo for 550 mg BID)	鹽簾膚餘觸獵築鹹鬱壓 = 簾繭繭願構顧繭夢襯製範觸齋窪廠顧鏇壓繭獵 (繭簾衊壓夢選夢繭鹹繭, 鑰構築衊齋遞繭構糧顧 ~ 襯廠願膚顧構鹽製遞鑰) 更多
NCT04709835 (MOONSONG Study, CTgov)	临床2期	新型冠状病毒感染	104	AT-527 (AT-527 550 mg (1x550 mg))	觸顧壓膚網夢鬱網遞淵(築製衊齋顧鬱簾糧鹹壓) = 觸餘廠選憲淵醖構淵糧蓋襯襯艱廠積齋廠襯醖 (醖艱鹹觸積窪襯願憲簾, 0.206) 更多	-	2022-10-13
				AT-527 (AT-527 1100 mg (4x275 mg))	築遞壓選鬱膚鑰網壓獵(廠獵鹹鏇醖構鑰膚淵獵) = 蓋醖選淵製遞蓋廠窪繭窪鏇構艱夢製遞齋製膚 (淵膚憲膚衊觸蓋醖網製, 0.223) 更多
NCT04711187 (Corporate Publications) 人工标引	临床1期	机会致病菌感染	20	AT-527	簾鏇構觸構網網醖網願(窪憲積醖鑰蓋鏇餘製願) = The study results showed AT-527 was well tolerated with a favorable safety profile. There were no discontinuations, serious AEs, clinically significant changes in vital signs, or ECGs observed. 膚鬱網願壓壓獵廠鹽觸 (範遞獵選醖襯糧鬱製觸 )	积极	2021-03-06
				Placebo
EASL2020	临床2期	丙型肝炎	10	AT-527 550 mg + Daclatasvir 60 mg	製窪壓簾獵顧選築糧構(餘鬱遞窪壓鏇鏇簾鏇蓋) = 鏇鑰築獵鹽鑰構膚鏇窪壓鏇憲築簾壓窪簾襯簾 (醖衊醖鬱範膚鹹構鑰憲 ) 更多	积极	2020-08-27
NCT03219957 (Pubmed \| Antimicrob Agents Chemother)	临床1期	丙型肝炎	88	AT-527	簾憲壓糧襯鑰窪獵艱餘(範鏇願夢築願獵簾鏇襯) = 齋觸築鏇顧製簾顧網膚夢夢餘遞鹽夢製衊壓積 (蓋繭選築製餘網繭衊鬱 )	-	2019-09-30