Nearly three months after winning a contentious bid to buy obesity drugmaker Metsera Inc. for $10 billion, Pfizer Inc. reported its first statistically significant top-line data of the acquired lead, ultra-long-acting glucagon-like peptide-1 (GLP-1) receptor agonist, showing a mean placebo-adjusted weight loss of up to 12.3% at 28 weeks, as well as competitive tolerability.

Genentech Inc. is paying $200 million up front and up to $1.5 billion in milestone payments to license one of Suzhou Sanegene Bio Inc.’s RNAi programs. Metabolic and autoimmune-focused Sanegene did not disclose specifics around the licensed candidate, except that it was derived from its LEAD (Ligand and Enhancer Assisted Delivery) platform.

Metabolic dysfunction-associated steatohepatitis (MASH) involves hepatic steatosis, inflammation, and fibrosis driven in part by hepatic stellate cell (HSC) activation. Dual inhibition of ACLY and ACSS2 restricts complementary hepatic sources of acetyl-CoA, a key driver of lipogenesis and MASH pathology.

As the march toward a new therapy continues in metabolic dysfunction-associated steatohepatitis (MASH), new approaches are drawing Wall Street’s attention. Among them is Inventiva SA’s pan-PPAR approach.

More than four years after a phase II/III trial with Sanofi SA’s oral glucosylceramide synthase inhibitor venglustat was stopped for lack of benefit in autosomal dominant polycystic kidney disease, the company rolled out mixed phase III data from two more efforts.

Liver fibrosis in the course of metabolic dysfunction-associated steatohepatitis could be significantly reduced using CAR T-cells generated in vivo. Scientists at the Icahn School of Medicine at Mount Sinai have developed an experimental cell therapy that eliminates only one type of liver cell, the stellate cells that express fibroblast activation protein alpha. This strategy not only reduced fibrosis but also reversed liver damage.