Bemnifosbuvir

Additional Data Presented Demonstrate High In Vitro Antiviral Potency and In Vivo Efficacy for AT-587, Atea’s Potential First-in-Class Direct-Acting Antiviral for the Treatment of Hepatitis E Virus BOSTON, May 27, 2026 (GLOBE NEWSWIRE) -- Atea Pharmaceuticals, Inc. (Nasdaq: AVIR) (Atea or Company), a late-stage clinical biopharmaceutical company engaged in the discovery and development of oral antiviral therapeutics for serious viral diseases, today announced Phase 1 results which further demonstrate that the fixed-dose combination regimen of bemnifosbuvir and ruzasvir (BEM/RZR) for the treatment of hepatitis C virus (HCV) has a low risk of drug-drug interaction. These results support the use of BEM/RZR with commonly used medications, including the proton pump inhibitor (PPI) omeprazole and the cholesterol-lowering drug rosuvastatin. The Company is also presenting data demonstrating high in vitro antiviral potency and in vivo efficacy for AT-587, its potential first-in-class direct-acting antiviral (DAA) for the treatment of hepatitis E virus (HEV). These data are being presented at the European Association for the Study of the Liver (EASL) Congress 2026, taking place May 27-30 th in Barcelona, Spain. “These Phase 1 results reinforce the potential of the regimen of BEM/RZR to simplify treatment for patients and healthcare providers and address the evolving needs of today’s patients living with HCV,” said Jean-Pierre Sommadossi, PhD, Chief Executive Officer and Founder of Atea Pharmaceuticals. “Our market research has shown that most HCV patients in the US manage multiple medications concurrently, which can complicate care. The results being presented demonstrate that the regimen of BEM/RZR can be co-administered with PPIs and other commonly used medications without requiring dose adjustments. As we move toward topline Phase 3 results from C-BEYOND and C-FORWARD, these data give us continued confidence in the regimen's potential to deliver a best-in-class pro today’s patients living with HCV.” HCV continues to be a significant global health burden despite the availability of DAAs. According to US healthcare providers who treat patients with HCV, approximately 80 percent of patients take multiple medications to manage comorbidities and drug-drug interactions are a significant concern in HCV treatment. As a result, a new treatment option offering a low risk of drug-drug interactions together with high efficacy and short treatment duration could meaningfully address patient needs and further the goal of HCV eradication. “The data being presented for AT-587 demonstrate high in vitro antiviral potency and in vivo efficacy against HEV, underscoring its potential,” Dr. Sommadossi added. “There is a critical gap in the care of patients with chronic HEV with no approved therapies, leaving vulnerable populations including transplant recipients and other immunocompromised patients at risk for rapid disease progression to cirrhosis. Following the encouraging preclinical data, we look forward to advancing our potential first-in-class product candidate, AT-587, into a first-in-human study mid-year.” In recent years, chronic HEV genotype 3 and 4 infections have been increasingly recognized as a potentially life-threatening viral infection in immunocompromised individuals — a population that includes solid organ and hematopoietic stem-cell transplant recipients, and patients with hematologic malignancies. In these vulnerable populations, chronic HEV can result in rapid progression to cirrhosis within three to five years. There is no approved antiviral therapy for HEV, and current off-label treatments have limited efficacy and tolerability, underscoring a clear and urgent unmet medical need. Phase 1 Results for the Regimen of BEM/RZR Highlight Favorable Drug-Drug Interaction Pro Treatment of HCV Poster ID: FRI-635 Title: Proton-pump inhibitor omeprazole did not affect the plasma pharmacokinetics of bemnifosbuvir and ruzasvir fixed-dose combination in healthy participants Presenting Author: Xiao-Jian Zhou Date and Time: Friday, May 29, 8:30 a.m.–5:00 p.m. CEST A Phase 1 study in healthy adults (n=20) showed the regimen of BEM/RZR was generally safe and well-tolerated when administered alone or concomitantly with omeprazole, a commonly used medication among HCV-infected patients to treat stomach acid conditions. These results support co-administration of BEM/RZR with PPIs, which often reduce the solubility of DAAs, decreasing their absorption/bioavailability and negatively impacting DAA efficacy. Omeprazole dosed at 20 mg, a common dose for gastroesophageal reflux disease, did not affect plasma exposure to BEM/RZR. Omeprazole dosed at 40 mg administered two hours before BEM/RZR to allow maximal acid-suppressive effect only slightly reduced plasma exposure to BEM/RZR. Co-administered BEM/RZR did not meaningfully affect the pharmacokinetic (PK) pro omeprazole. Poster ID: FRI-636 Title: Bemnifosbuvir and ruzasvir administered as a fixed-dose combination have low potential to inhibit P-gp, BCRP or OATP1B1/3 mediated transport Presenting Author: Xiao-Jian Zhou Date and Time: Friday, May 29, 8:30 a.m.–5:00 p.m. CEST A Phase 1 study in healthy adults evaluated interactions between the regimen of BEM/RZR and digoxin (n=18) or rosuvastatin (n=18), sensitive substrates of the drug transporters P-gp and BCRP/OATP1B1/1B3, respectively. These transporters are important for how drugs are absorbed, enter the liver and are cleared from the body. Results demonstrated that BEM/RZR administered with digoxin and rosuvastatin was well tolerated with all treatment-emergent adverse events mild in severity. A single dose of BEM/RZR slightly increased the plasma exposure of digoxin and rosuvastatin. With a geometric mean ratio of less than 2, BEM/RZR has low potential to exhibit clinically meaningful inhibition of these transporters. These results demonstrate that no dose adjustments are needed for drugs that are substrates of these transporters when co-administered with BEM/RZR. AT-587 Results Demonstrate High In Vitro Antiviral Potency and In Vivo Efficacy Against HEV Poster ID: TOP-631 Title: Discovery and preclinical pro a first-in-class potent hepatitis E virus inhibitor AT-587 Presenting Author: Qi Huang Date and Time: Thursday, May 28, 8:30 a.m.–5:00 p.m. CEST Results presented support AT-587 as an oral nucleotide analog exhibiting promising preclinical antiviral potency against HEV. In vitro studies demonstrated that AT-587 is a potent inhibitor of HEV replication. Specifically, AT-587 was 30 to 150-fold more potent in vitro against HEV than sofosbuvir (SOF) and ribavirin, which is currently used off-label. AT-587 showed no toxicity in in vitro studies. AT-587 also demonstrated activity against flaviviruses, rubella and chikungunya. In addition, new results showed that AT-587 inhibited HEV-3 activity in vivo . Using HEV-3-infected gerbil models, fecal samples from the treated groups had significantly lower HEV RNA levels than the control group. In addition, the viral loads in the liver and intestinal samples were significantly lower in the treated groups compared to control. Notably, AT-587 also retained high potency against ribavirin (G1634R) and SOF (A1343V) clinical resistance strains in vitro , further differentiating its pro existing off-label treatment options. About Bemnifosbuvir and Ruzasvir for HCV Bemnifosbuvir has been shown in in vitro studies to be approximately 10-fold more active than SOF against a panel of laboratory strains and clinical isolates of HCV GT 1–5. In vitro studies have also demonstrated bemnifosbuvir remained fully active against SOF resistance-associated substitutions (S282T), with up to 58-fold more potency than SOF. The PK pro bemnifosbuvir supports once-daily dosing for the treatment of HCV. Bemnifosbuvir has been shown to have a low risk for drug-drug interactions. Bemnifosbuvir has been administered to over 3,000 subjects and has been well-tolerated at doses up to 550 mg for durations up to 12 weeks in healthy subjects and patients. Ruzasvir has demonstrated highly potent and pan-genotypic antiviral activity in preclinical (picomolar range) and clinical studies. Ruzasvir has been administered to over 2,800 HCV-infected patients at daily doses of up to 180 mg for 12 weeks and has demonstrated a favorable safety profile. The PK pro ruzasvir supports once-daily dosing. About HCV HCV is a blood-borne, single-stranded (ss) RNA virus that primarily infects liver cells. HCV is a leading cause of chronic liver disease and liver transplants, spreading via blood transfusion, hemodialysis and needle sticks, with approximately 240,000 deaths occurring each year. Despite the availability of DAAs, HCV continues to be a significant global healthcare issue. An estimated 50 million people worldwide are chronically infected with HCV and there are approximately one million new infections each year. In the US, approximately four million people are estimated to have HCV with annual new infections outpacing treatment rates. HCV infections in the US predominate in patients in the age group between 20 and 49 years old, and it is estimated that less than 10% of HCV-infected patients in the US have cirrhosis. Chronic HCV infection is a leading cause of liver cancer in the US, Europe and Japan. About HEV HEV is a ssRNA virus which infects the liver and remains an under-recognized global health challenge with an estimated 20 million acute infections annually. Waterborne transmission of HEV genotypes 1 and 2 causes mostly acute self-limiting hepatitis in developing regions, whereas foodborne transmission of HEV genotype 3 predominates in the US and Europe and may cause chronic hepatitis in immunocompromised patients, which can lead to cirrhosis in three to five years. There is a growing number of immunocompromised patients, a population that includes solid organ transplant and hematopoietic stem cell transplant recipients and patients with hematologic malignancies such as multiple myeloma. Each year, in the US and Europe, 3% of the approximately 450,000 patients who have these underlying medical conditions are at risk of developing chronic HEV. There is currently no approved antiviral therapy for HEV, and current off-label treatments have limited efficacy and tolerability, underscoring a clear and urgent unmet medical need. Atea’s initial HEV clinical efforts will focus on developing AT-587 for the treatment of immunocompromised patients with chronic HEV. About Atea Pharmaceuticals Atea is a late-stage clinical biopharmaceutical company focused on discovering, developing and commercializing oral antiviral therapies to address the unmet medical needs of patients with serious viral infections. Leveraging Atea’s deep understanding of antiviral drug development, nucleos(t)ide chemistry, biology, biochemistry and virology, Atea has built a proprietary nucleos(t)ide prodrug platform to develop novel product candidates to treat single-stranded ribonucleic acid, or ssRNA, viruses, which are a prevalent cause of serious viral diseases. Atea plans to continue to build its pipeline of antiviral product candidates by augmenting its nucleos(t)ide platform with other classes of antivirals that may be used in combination with its nucleos(t)ide product candidates. Atea’s Phase 3 program is evaluating the FDC regimen of bemnifosbuvir, a nucleotide analog polymerase inhibitor, and ruzasvir, an NS5A inhibitor, to treat HCV. Atea anticipates initiating clinical development of AT-587, a nucleotide analog, for the treatment of HEV in mid-2026. For more information, please visit Forward-Looking Statements This press release includes “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements in this press release include but are not limited to statements regarding the potential best-in-class pro the BEM/RZR regimen for the treatment of HCV, the potential to develop a product for the treatment of HEV, anticipated milestone events and timelines for clinical trials including the timeline for readout of the HCV Phase 3 clinical trials results and initiation of the HEV clinical development, future results of operations and business strategy. When used herein, words including “expected,” “should,” “anticipated,” “believe,” “will,” “plans”, and similar expressions are intended to identify forward-looking statements. In addition, any statements or information that refer to expectations, beliefs, plans, projections, objectives, performance or other characterizations of future events or circumstances, including any underlying assumptions, are forward-looking. All forward-looking statements are based upon Atea’s current expectations and various assumptions. Atea believes there is a reasonable basis for its expectations and beliefs, but they are inherently uncertain. Atea may not realize its expectations, and its beliefs may not prove correct. Actual results could differ materially from those described or implied by such forward-looking statements as a result of various important factors, including, without limitation, uncertainties inherent in the drug discovery and development process and the regulatory submission or approval process, unexpected or unfavorable safety or efficacy data or results observed during clinical trials or in data readouts; delays in or disruptions to clinical trials or our business; our reliance on third parties over which we may not always have full control; our ability to manufacture sufficient commercial product; competition from approved treatments for HCV; dependence on the success of Atea’s most advanced product candidates, in particular the BEM/RZR regimen for the treatment of HCV; as well as the other important factors discussed under the caption “Risk Factors” in Atea’s Quarterly Report on Form 10-Q for the quarter ended March 31, 2026 as such factors may be updated from time to time in its other filings with the SEC, which are accessible on the SEC’s website at These and other important factors could cause actual results to differ materially from those indicated by the forward-looking statements made in this press release. Any such forward-looking statements represent management’s estimates as of the date of this press release. While Atea may elect to update such forward-looking statements at some point in the future, except as required by law, it disclaims any obligation to do so, even if subsequent events cause our views to change. These forward-looking statements should not be relied upon as representing Atea’s views as of any date subsequent to the date of this press release. Contacts Jonae Barnes SVP, Investor Relations and Corporate Communications 617-818-2985 barnes.jonae@ateapharma.com Joyce Allaire LifeSci Advisors jallaire@lifesciadvisors.com

Bemnifosbuvir（BEM）是一种靶向丙型肝炎病毒（Hepatitis C Virus, HCV）NS5B聚合酶的高效泛基因型抑制剂。研究人员在一项纳入30例患者的Ⅰ期剂量递增临床试验中评估了其抗病毒活性，受试者每日一次给药，持续7天。治疗开始后，血浆HCV RNA呈双相下降，最高剂量组在治疗24小时后平均降低2.3 log10IU/mL，至第7天平均降低4.4 log10IU/mL；大多数患者丙氨酸氨基转移酶（Alanine Aminotransferase, ALT）恢复至正常范围。研究人员采用拟合HCV RNA与ALT动力学的多尺度数学模型，量化BEM的抗病毒活性并解析其作用模式。结果显示，仅将BEM视为典型HCV RNA聚合酶抑制剂、仅抑制细胞内HCV RNA产生的模型，拟合效果不如包含多重作用模式的模型——后者同时涵盖抑制病毒组装与分泌、增强细胞内HCV RNA降解的机制。BEM对细胞内HCV RNA产生的抑制效率随剂量升高而增强（150 mg/天：88.2%，300 mg/天：98.8%，600 mg/天：99.5%），而病毒组装与释放的抑制效率在各剂量下均维持在约95%。细胞内HCV RNA降解速率呈剂量依赖性增强：与150 mg/天组相比，300 mg/天组降解速率提高1.5倍，600 mg/天组提高2.7倍。HCV基因型1b与3之间、代偿期肝硬化与非肝硬化患者之间，未检测到抗病毒活性的显著差异。本研究针对丙型肝炎病毒（HCV）感染这一全球重大公共卫生问题展开。尽管直接抗病毒药物（Direct-Acting Antivirals, DAAs）已将HCV感染转变为可治愈疾病，但基因型3感染、代偿期肝硬化、既往治疗失败等亚组仍存在疗效不足、治疗选择有限的问题，且泛基因型药物的全球可及性不均衡，治疗中断或失败仍可能导致病毒耐药与疾病进展。在此背景下，新型NS5B聚合酶抑制剂Bemnifosbuvir（BEM）因无线粒体毒性、支持每日一次给药等优势成为潜在治疗方案，但其体内完整作用模式尚未明确。研究人员通过开展Ⅰ期临床试验结合多尺度数学建模，旨在解析BEM是否仅通过抑制HCV RNA复制发挥抗病毒作用，还是同时存在抑制病毒组装分泌、增强细胞内病毒RNA降解等多重机制，为优化剂量选择、联合用药方案及精准治疗提供依据。该研究发表于《Clinical Pharmacology & Therapeutics》。 研究采用的关键技术方法包括：基于一项Ⅰ期多剂量递增临床试验的样本队列（30例慢性HCV感染者，按150 mg/天、300 mg/天、600 mg/天接受BEM单药治疗7天，覆盖基因型1b、2、3及代偿期肝硬化人群），采集纵向血浆HCV RNA与ALT数据；应用已验证的多尺度宿主-病毒动力学模型，该模型在经典靶细胞受限模型基础上整合细胞内HCV RNA（Intracellular HCV RNA, R）复制、病毒颗粒组装分泌及ALT动态过程；采用混合效应建模方法（Monolix软件），同步拟合所有剂量组、所有个体的HCV RNA与ALT时间序列数据，通过负对数似然（-LL）与校正贝叶斯信息准则（BICc）比较80种不同作用模式模型的拟合优度，量化药物各作用模式的效力与剂量依赖性。 研究结果如下： BEM具有多重作用模式：通过比较不同作用模式的模型，单一作用模式（仅抑制RNA复制或仅抑制组装分泌）的拟合优度显著低于多重作用模式模型。最优模型为三重作用模式：剂量依赖性的细胞内HCV RNA产生抑制（εα）、剂量依赖性的细胞内HCV RNA降解增强（κ），以及剂量非依赖性的病毒组装与分泌抑制（εs）。其中，εs在各剂量下均维持在约95%的高效水平，而εα与κ随剂量升高显著增强：150 mg/天组εα为88.2%、κ较基线升高1.05倍；300 mg/天组εα为98.8%、κ升高1.5倍；600 mg/天组εα为99.5%、κ升高2.7倍。模型对个体HCV RNA下降轨迹与ALT动态均实现良好拟合，且未检测到药物对HCV负链RNA复制模板降解的显著作用。 BEM在不同基因型与肝硬化阶段均保持高效：300 mg/天与600 mg/天剂量下，BEM的三重作用模式均达到高效水平。600 mg/天组中，基因型1b与3感染者的病毒下降动力学无显著差异；代偿期肝硬化患者的病毒下降速度略快于非肝硬化患者，但第7天病毒载量无统计学差异；性别也未显著影响病毒下降反应。该剂量下，患者治疗24小时平均病毒载量下降2.3 log10IU/mL，第7天下降4.4 log10IU/mL，且绝大多数患者ALT恢复正常。 讨论部分指出，传统NS5B抑制剂主要被认为通过抑制RNA复制发挥作用，但本研究通过多剂量动力学建模首次证实，BEM作为NS5B抑制剂存在三重作用模式：除剂量依赖性的RNA复制抑制外，还包括高效的病毒组装分泌抑制（非剂量依赖性）与剂量依赖性的细胞内RNA降解增强。这种多重机制协同加速了病毒清除与ALT复常，且不受基因型或肝硬化状态影响，支持其作为泛基因型、全病程适用药物的潜力。研究的局限性包括样本量较小（尤其代偿期肝硬化仅6例）、未解析组装分泌抑制与RNA降解增强的具体生化机制、未整合药代动力学/药效学（PK/PD）数据与免疫应答过程。后续更大规模的Ⅱ期临床试验（BEM联合NS5A抑制剂Ruzasvir）已验证了BEM的高效与泛基因型活性，进一步支持本研究的结论。总体而言，本研究展示了定量系统药理学在早期临床试验中解析复杂抗病毒机制的价值，可为后续药物研发、剂量优化与精准治疗策略制定提供关键依据。