Peptide News Digest

#Nejm

2 stories

Clinical Trials · View digest

Boehringer Ingelheim Survodutide Full 48-Week Phase 2 MASH Data in NEJM (EASL 2026): GLP-1/Glucagon Dual Agonist Drives MASH Improvement Without Fibrosis Worsening in 47-62% vs 14% Placebo

Boehringer Ingelheim's survodutide full 48-week Phase 2 MASH dataset published in the New England Journal of Medicine alongside the EASL 2026 presentation. MASH improvement without worsening of fibrosis occurred in 47% of the 2.4 mg group, 62% of the 4.8 mg group, and 43% of the 6.0 mg group, versus 14% on placebo. Up to 52% of survodutide-treated adults achieved significant improvement across fibrosis stages F1, F2, and F3 versus around 26% on placebo. Survodutide is an investigational long-acting glucagon/GLP-1 receptor dual agonist (BI 456906, partnered with Zealand Pharma) for once-weekly subcutaneous administration. The Phase 3 program is advancing through LIVERAGE (~1,800 adults with MASH F2-F3) and LIVERAGE-Cirrhosis (~1,590 adults with compensated MASH cirrhosis F4). Survodutide also posted 16.6% weight loss in the SYNCHRONIZE-1 obesity Phase 3 (April 2026). The NEJM publication is the strongest peer-reviewed validation of the GLP-1/glucagon dual mechanism in MASH to date.

Clinical Trials · View digest

Daraxonrasib NEJM Publication (May 2026): Revolution Medicines' RAS(ON) Inhibitor Hit 35% ORR + 13.1-Month OS in RAS G12-Mutated Pancreatic Cancer Phase 1/2

The New England Journal of Medicine published Revolution Medicines' daraxonrasib (RMC-6236) Phase 1/2 data in previously treated advanced RAS-mutated pancreatic adenocarcinoma in May 2026. In the subgroup of 26 patients with G12 mutations treated at the 300 mg dose, objective response rate hit 35% with median progression-free survival 8.5 months and median overall survival 13.1 months — outcomes meaningfully better than the historical 5-month median OS in second-line PDAC. The mechanism is unusual: daraxonrasib is an oral small molecule that acts as a molecular glue, recruiting the peptidyl-prolyl isomerase cyclophilin A to form a tri-complex with active GTP-bound mutant RAS, blocking effector binding and downstream signaling. The drug targets KRAS, HRAS, and NRAS in the on-state — a mechanistically distinct approach from Chugai's LUNA18 cyclic peptide RAS inhibitor. FDA granted Expanded Access. The cyclophilin A-mediated mechanism puts peptidyl-prolyl chemistry at the center of a major oncology readout.