Pibrentasvir

WATERTOWN, Mass.--(BUSINESS WIRE)--Mar. 30, 2026-- Enanta Pharmaceuticals, Inc. (NASDAQ:ENTA), a clinical-stage biotechnology company dedicated to creating small molecule drugs for viral infections and immunological diseases today announced that preclinical data from the Company’s STAT6 inhibitor program will be presented in four posters at IMMUNOLOGY2026™, the annual meeting of the American Association of Immunologists (AAI), being held April 15-19, 2026 in Boston, MA. Details of the presentations are as follows: Poster Number: 573 Abstract Number: 2257506 Title: Oral STAT6 Inhibitor EPS-3903 Demonstrates Good Preclinical In Vivo Tolerability without Reactive Metabolites or Metabolic/Safety Liabilities Date: Thursday, April 16, 2026 Time: 11:30 AM – 12:30 PM ET Session Type: Therapeutic Approaches to Autoimmunity (THER) Session Title: Therapeutics for Autoimmune Diseases I Location: Exhibit Hall Presenter: Jonathan Kibel and Meng Huang, Ph.D. Poster Number: 193 Abstract Number: 2253997 Title: EPS-3903 Is a Potent and Selective Oral STAT6 Inhibitor that Blocks Th2 Inflammation in an Ovalbumin Asthma Mouse Model Date: Friday, April 17, 2026 Time: 11:30 AM – 12:30 PM ET Session Type: Immediate Hypersensitivity, Asthma, and Allergic Responses (HYP) Session Title: Airway Hypersensitivity and Asthma Location: Exhibit Hall Presenter: Yaohui Nie, Ph.D. Poster Number: 194 Abstract Number: 2257118 Title: Discovery and Characterization of a Potent and Selective Oral Inhibitor of STAT6 for the Treatment of Allergic Diseases Date: Friday, April 17, 2026 Time: 2:30 – 3:30 PM ET Session Type: Immediate Hypersensitivity, Asthma, and Allergic Responses (HYP) Session Title: Airway Hypersensitivity and Asthma Location: Exhibit Hall Presenter: Joyce Sweeney Gibbons, Ph.D. Poster Number: 723 Abstract Number: 2257175 Title: Potent STAT6 Inhibitor EPS-3903 Demonstrates Excellent Preclinical Pharmacokinetics Enabling Sustained STAT6 Inhibition following Once-Daily Oral Dosing in Humans Date Saturday, April 18, 2026 Time: 11:30 AM – 12:30 PM ET Session Type: Therapeutic Approaches to Autoimmunity (THER) Session Title: Therapeutics for Autoimmune Diseases I Location: Exhibit Hall Presenter: Daniel Leonard and Tianzhu Zang, Ph.D. Further information about IMMUNOLOGY2026TM can be found here. Posters will be available on the Company’s website here following each presentation. About Enanta Pharmaceuticals, Inc. Enanta is using its robust, chemistry-driven approach and drug discovery capabilities to become a leader in the discovery and development of small molecule drugs for viral infections and immunological diseases. Enanta’s clinical programs are currently focused on respiratory syncytial virus (RSV) and its earlier-stage immunology pipeline aims to develop treatments for inflammatory diseases by targeting key drivers of the type 2 immune response, with KIT, STAT6 and MRGPRX2 inhibition. Glecaprevir, a protease inhibitor discovered by Enanta, is part of one of the leading treatment regimens for curing hepatitis C virus (HCV) infection and is sold by AbbVie in numerous countries under the tradenames MAVYRET® (U.S.) and MAVIRET® (ex-U.S.) (glecaprevir/pibrentasvir). A portion of Enanta’s royalties from HCV products developed under its collaboration with AbbVie contribute ongoing funding to Enanta’s operations. Please visit www.enanta.com for more information. View source version on businesswire.com: https://www.businesswire.com/news/home/20260316632112/en/ Media and Investors Contact: Jennifer Viera 617-744-3848 jviera@enanta.com Source: Enanta Pharmaceuticals, Inc.

Preclinical data for MDL-001 establish proof-of-concept for an oral therapy targeting HCV/HBV co-infection, a population with an over 100x elevated liver cancer risk. San Diego, CA — 2/18/26 — Model Medicines , an AI-native biotechnology company, today announced preclinical data demonstrating that MDL-001 has potent antiviral activity against both hepatitis C virus (HCV) and hepatitis B virus (HBV). These results establish preclinical proof of concept for a single non-nucleoside agent targeting HCV/HBV co-infection, one of the most dangerous and underserved populations in hepatology. Follow this link to view the full preclinical readout for MDL-001 . Additional data on MDL-001 is also available on modelmedicines.com . “These data represent an important inflection point for the MDL-001 program,” said Daniel Haders II, PhD, Founder and CEO of Model Medicines. “For the first time, we demonstrate that a single, oral, direct-acting antiviral can potently suppress both HCV and HBV in preclinical models. This creates a credible path toward a unified therapeutic strategy for co-infected persons, something the field has lacked despite decades of antiviral innovation.” A Hidden Epidemic With Dire Consequences Chronic viral hepatitis is a global crisis of staggering scale. The World Health Organization (WHO) estimates that 254 million people live with chronic hepatitis B and approximately 58 million with chronic hepatitis C. Chronic viral hepatitis is responsible for roughly 1.3 million deaths annually, making it the second deadliest communicable disease worldwide. [1] An estimated 5–15 million people worldwide have both HBV and HCV infections. [2] , [3] Most will never be diagnosed. Only 13% of HBV infections and 36% of HCV infections are diagnosed globally. Fewer than 1% of co-infected patients know their status. [4] The substantial population of undiagnosed and untreated individuals strongly suggests that the true patient population is considerably larger than current estimates reflect. The clinical consequences of this diagnostic failure are severe. Coinfection with these viruses causes a multiplicative acceleration of liver disease. Patients carrying both viruses are over 100 times more likely to develop liver cancer than uninfected individuals, far exceeding the risk of either infection alone. [5] Scarring of the liver (cirrhosis) develops nearly three times faster in co-infected patients than in those with HCV alone. [6] Over 10 years, co-infected patients face 3.6× the liver cancer risk and 2.5× the cirrhosis risk of HBV monoinfection. [7] Current Standards of Care Leave Co-Infected Patients Vulnerable Current treatment guidelines from the AASLD (2025), WHO (2024), and EASL (2025) recommend a two-drug approach for co-infected patients: direct-acting antivirals (DAAs) such as sofosbuvir/velpatasvir to cure HCV, combined with nucleos(t)ide analogue suppressive therapy such as tenofovir disoproxil fumarate (TDF) or tenofovir alafenamide (TAF), for HBV. [8] , [9] , [10] However, fewer than 1% of co-infected patients know their status as mentioned above. [11] The current standard-of-care paradigm introduces a dangerous paradox for both patients with diagnosed and undiagnosed co-infection. HCV approved Direct-Acting Antivirals (DAAs) can trigger HBV reactivation upon HCV viral clearance due to the loss of HCV-mediated suppression of HBV. The FDA issued a black box warning on all approved DAAs in October 2016 after reports of severe HBV reactivation, including fatal cases. [12] A systematic meta-analysis found HBV reactivation in 24% (95% CI: 19–30%) of HBsAg-positive patients undergoing DAA therapy, even with prophylactic monitoring. [13] Reactivation events can produce severe hepatic flare-ups, fulminant hepatitis, and liver failure. No approved single-agent therapy directly addresses both HCV and HBV. No major clinical trial in the HBV functional cure pipeline specifically enrolls co-infected patients. This population remains systematically understudied and underserved. The Unmet Need: A Single Agent for Dual Infection The ideal therapeutic for HCV/HBV co-infection would be an oral, well-tolerated, direct-acting antiviral with simultaneous activity against both viruses through a single mechanism of action. Such an agent would eliminate the need for fragmented drug regimens, reduce the risk of HBV reactivation during HCV clearance, and simplify treatment delivery. MDL-001: Preclinical Proof-of-Concept for Dual-Virus Targeting MDL-001 targets the Thumb-1 domain of viral RNA-dependent RNA polymerases (RdRp), a conserved allosteric site. Preclinical data demonstrate that oral MDL-001: ● Achieves clinically meaningful viral load reductions in both HCV and HBV models. ● Maintains activity across viral replication mechanisms (DNA/RNA) using a single, direct-acting, non-nucleoside mechanism. ● Establishes preclinical proof-of-concept for dual-targeting chronic viral liver disease, including co-infection settings. In the HCV setting, MDL-001 has previously demonstrated equivalency to sofosbuvir in preclinical models. In HBV, MDL-001 achieved statistically significant multi-log viral suppression. “Co-infection is where antiviral regimens tend to fail patients the most,” said David “Davey” Smith, MD, MAS, FACP, FIDSA, Assistant Vice Chancellor of Clinical and Translational Research University of California San Diego. “A well-tolerated, oral agent with direct activity against both viruses would be a meaningful clinical advance.” Market and Patient Impact The combined global hepatitis therapeutics market exceeds $16 billion annually, dominated by Gilead Sciences and AbbVie. The co-infection-addressable market is estimated at $500 million to $2 billion per year, constrained primarily by diagnostic gaps rather than treatment demand. WHO 2030 elimination targets call for 90% diagnosis and 80% treatment, expanding screening mandates across the US and globally. The addressable patient population is expected to grow substantially with these initiatives. The HCV/HBV co-infection results reported here further expand MDL-001’s pro a pan-hepatic (HCV, HBV, and HDV) antiviral, complementing previously reported activity across respiratory viruses, including RSV, SARS-CoV-2, and influenza. Together, the ability of MDL-001 to effectively target diverse human pathogens strongly suggests its likely utility in outbreaks of novel viral pathogens. MDL-001 has demonstrated a favorable safety profile, with over 400 animals evaluated in vivo. IND-enabling studies are ongoing, with regulatory submission targeted in late 2026 and clinical trials expected early 2027. About HCV/HBV Co-Infection An estimated 5–15 million people worldwide are co-infected with HCV and HBV. This population experiences dramatically accelerated progression to cirrhosis and hepatocellular carcinoma, with HCC risk over 100-fold higher than the uninfected population. Current treatment requires separate antiviral regimens for each virus: DAAs (sofosbuvir/velpatasvir or glecaprevir/pibrentasvir) for HCV and nucleos(t)ide analogues (entecavir, TDF, or TAF) for HBV. No approved single-agent therapy addresses both infections simultaneously. About UN Sustainable Development Goal 3.3: Eliminating Viral Hepatitis by 2030 The United Nations Sustainable Development Goal 3.3 calls for ending the epidemics of viral hepatitis by 2030. The World Health Organization’s Global Health Sector Strategy on Viral Hepatitis (2022–2030) targets a 90% reduction in new hepatitis B and C infections and a 65% reduction in hepatitis-related mortality by 2030, compared to 2015 baselines. Despite the availability of effective vaccines and curative therapies, gaps in diagnosis, treatment access, and prevention continue to hinder elimination efforts. Viral hepatitis causes more than one million deaths annually, largely from chronic hepatitis B and C. Achieving these targets will require innovation capable of addressing both mono- and co-infections. Next-generation antivirals such as MDL-001, with broad-spectrum activity and an oral, outpatient-ready profile, represent the type of therapeutic advance needed to simplify treatment, expand access in resource-limited settings, and accelerate progress toward global elimination. About MDL-001 MDL-001 is an oral, direct-acting, broad-spectrum antiviral targeting the Thumb-1 allosteric domain of viral RNA-dependent RNA polymerases. Its novel mechanism enables activity across multiple viral families, including hepatitis viruses and respiratory pathogens, with a pharmacokinetic and safety pro for outpatient use. About Model Medicines Model Medicines is an AI-first biotechnology company engineering first-in-class small molecules that target the biological linchpins underlying disease. The company’s research spans infectious disease, oncology, and inflammation, with programs designed around conserved biological choke points that drive multiple pathologies. Model Medicines has discovered a direct-acting, non-nucleoside, broad-spectrum antiviral (MDL-001) and a BRD4 inhibitor with no measurable activity against BRD2/3 (MDL-4102). Its work demonstrates how large-scale computation can uncover entirely new classes of drugs once thought unreachable. Model Medicines is advancing a new generation of therapeutics that redefine what is possible in modern drug discovery. Learn more at Media Contact: Patrick O’Neill Head of Partnerships & Investor Relations media@modelmedicines.com [1] World Health Organization. Global hepatitis report 2024: action for access in low- and middle-income countries. Geneva: World Health Organization; 2024. Available from: [2] Mavilia MG, Wu GY. HBV-HCV Coinfection: Viral Interactions, Management, and Viral Reactivation. J Clin Transl Hepatol. 2018 Sep 28;6(3):296-305. doi: 10.14218/JCTH.2018.00016. Epub 2018 Jul 6. PMID: 30271742; PMCID: PMC6160312. [3] Maqsood Q, Sumrin A, Iqbal M, Younas S, Hussain N, Mahnoor M, Wajid A. Hepatitis C virus/Hepatitis B virus coinfection: Current prospectives. Antivir Ther. 2023 Aug;28(4):13596535231189643. doi: 10.1177/13596535231189643. PMID: 37489502. [4] World Health Organization. Global hepatitis report 2024: action for access in low- and middle-income countries. Geneva: World Health Organization; 2024 Apr 9. 242 p [5] Awadh AA, Alharthi AA, Alghamdi BA, Alghamdi ST, Baqays MK, Binrabaa IS, Malli IA. Coinfection of Hepatitis B and C Viruses and Risk of Hepatocellular Carcinoma: Systematic Review and Meta-analysis. J Glob Infect Dis. 2024 Dec 21;16(4):127-134. doi: 10.4103/jgid.jgid_211_23. PMID: 39886088; PMCID: PMC11775402. [6] Butt AA, Yan P, Aslam S, Shaikh OS, Abou-Samra AB. Hepatitis C Virus (HCV) Treatment With Directly Acting Agents Reduces the Risk of Incident Diabetes: Results From Electronically Retrieved Cohort of HCV Infected Veterans (ERCHIVES). Clin Infect Dis. 2020 Mar 3;70(6):1153-1160. doi: 10.1093/cid/ciz304. PMID: 30977808. [7] Maqsood Q, Sumrin A, Iqbal M, Younas S, Hussain N, Mahnoor M, Wajid A. Hepatitis C virus/Hepatitis B virus coinfection: Current prospectives. Antivir Ther. 2023 Aug;28(4):13596535231189643. doi: 10.1177/13596535231189643. PMID: 37489502. [8] Ghany MG, Feld JJ, Chang KM, Janssen HLA, Nguyen MH, Perrillo R, Reddy KR, Saberi B, Schwarz KB, Tana MM, Wong GL, Terrault NA. AASLD/IDSA practice guideline on treatment of chronic hepatitis B. Hepatology. 2025 Nov 4. doi: 10.1097/HEP.0000000000001549. Epub ahead of print. PMID: 41186418. [9] World Health Organization. Guidelines for the prevention, diagnosis, care and treatment for people with chronic hepatitis B infection. Geneva: World Health Organization; 2024 Mar 29. 272 p. [10] European Association for the Study of the Liver. EASL Clinical Practice Guidelines on the management of hepatitis B virus infection. J Hepatol. 2025 Aug;83(2):502-583. doi: 10.1016/j.jhep.2025.03.018. Epub 2025 May 10. PMID: 40348683. [11] World Health Organization. Global hepatitis report 2024: action for access in low- and middle-income countries. Geneva: World Health Organization; 2024 Apr 9. 242 p [12] Food and Drug Administration (US). FDA warns about the risk of hepatitis B reactivating in some patients treated with direct-acting antivirals for hepatitis C. Silver Spring (MD): FDA; 2016 Oct 4 [cited 2026 Feb 11]. [13]