Metabolic Dysfunction-Associated Steatohepatitis (MASH)-Cirrhosis Clinical Trials: Lessons Learned and Future Directions.
Metabolic dysfunction-associated steatohepatitis (MASH)-cirrhosis represents a critical and growing global health burden due to its progression to hepatic decompensation, hepatocellular carcinoma (HCC
APA
Patil R, Dunn W, et al. (2026). Metabolic Dysfunction-Associated Steatohepatitis (MASH)-Cirrhosis Clinical Trials: Lessons Learned and Future Directions.. Drugs, 86(5), 627-643. https://doi.org/10.1007/s40265-026-02301-5
MLA
Patil R, et al.. "Metabolic Dysfunction-Associated Steatohepatitis (MASH)-Cirrhosis Clinical Trials: Lessons Learned and Future Directions.." Drugs, vol. 86, no. 5, 2026, pp. 627-643.
PMID
41831171
Abstract
Metabolic dysfunction-associated steatohepatitis (MASH)-cirrhosis represents a critical and growing global health burden due to its progression to hepatic decompensation, hepatocellular carcinoma (HCC), and liver-related mortality. A growing number of MASH-related HCCs contribute to the increasing need for liver transplantation. Under current regulatory guidance, Phase 3 trials in compensated MASH cirrhosis compare drug versus placebo on time to a composite endpoint for outcomes. Composite endpoints are major adverse liver outcomes (MALO)-hepatic decompensation (ascites requiring treatment, variceal hemorrhage, hepatic encephalopathy, MELD ≥ 15), liver transplantation-and all‑cause mortality. Future trial sample size hinges on the annual event rate and expected effect size. From prior studies, event rates are ~ 3-20% higher with risk features. Progression to large gastroesophageal varices is now an accepted endpoint and will typically add a 3-5% yearly event rate to the baseline MALO event rate. Effect sizes on hard outcomes in metabolic chronic diseases often range from 0.70-0.85. Trials should enroll high‑risk patients (defined as those with clinically significant portal hypertension [CSPH], Child Turcotte Pugh A cirrhosis, and magnetic resonance elastography measurements > 6.5 kPa), plan 3-5 years of follow‑up and enroll using noninvasive criteria. Accelerated approval based on histologic reversal of cirrhosis is potentially possible; the SYMMETRY Phase 2b trial achieved F4 regression within 96 weeks with efruxifermin. Levers to increase regression include an upper limit for liver stiffness measurement(LSM), a platelet threshold (> 110,000/µL), limiting CSPH, and prespecified proportions with FIB‑4 > 3.5 or enhanced liver fibrosis (ELF) > 11.3. Ongoing studies include but are not limited to survodutide, a glucagon/GLP-1 receptor dual agonist targeting metabolic drivers, efruxifermin, an FGF21 analog, and a conditionally approved drug resmetirom, which is a selective thyroid hormone receptor β agonist.
MeSH Terms
Humans; Liver Cirrhosis; Fatty Liver; Carcinoma, Hepatocellular; Liver Neoplasms; Clinical Trials, Phase III as Topic