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Metabolic dysfunction-associated steatohepatitis (MASH) with significant fibrosis (F2-F3) is a critical stage of metabolic dysfunction-associated steatotic liver disease (MASLD), during which intervention may avert transition to cirrhosis, hepatocellular carcinoma, and liver-related death

Constitutive hGPR17L activity inhibited GLP-1 secretion, and MDL29,951 treatment further inhibited this secretion, which was attenuated by treatment with the GPR17 antagonist HAMI3379

The rise of biologics, including recombinant proteins, gene therapies, and cell therapies, is reshaping the landscape of modern therapeutics, offering new strategies to address previously undruggable targets

A summary of products characteristics for Rybelsus (semaglutide

This review examines the biological mechanisms underlying GLP-1 RA therapy in MASLD/MASH, analyzes the mechanistic distinctions between mono-, dual-, and triple agonists, and synthesizes current clinical evidence supporting their utilization in individuals with this condition.