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. 

An estimated 5–15 million people worldwide have both HBV and HCV infections., 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. 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. Scarring of the liver (cirrhosis) develops nearly three times faster in co-infected patients than in those with HCV alone. Over 10 years, co-infected patients face 3.6× the liver cancer risk and 2.5× the cirrhosis risk of HBV monoinfection.

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.,,   However, fewer than 1% of co-infected patients know their status as mentioned above.

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. A systematic meta-analysis found HBV reactivation in 24% (95% CI: 19–30%) of HBsAg-positive patients undergoing DAA therapy, even with prophylactic monitoring. 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 profile as 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.