• SLS009 increased apoptosis more than six-fold versus daraxonrasib in a MYC-amplified, daraxonrasib-resistant patient-derived pancreatic cancer organoid model - 



     
  • Combination of SLS009 and daraxonrasib further increased apoptosis to 36.5% and necrosis to 30.6%, supporting evaluation of CDK9 inhibition as a potential strategy to enhance RAS-directed therapy -



     
  • SLS009 combined with BET inhibition demonstrated synergistic activity and sustained suppression of MYC, providing additional evidence of SLS009 activity against MYC-driven pancreatic cancer biology -



     

NEW YORK, Sept. 25, 2026 (GLOBE NEWSWIRE) -- SELLAS Life Sciences Group, Inc. (NASDAQ:SLS) ("SELLAS’’ or the "Company"), a late-stage clinical biopharmaceutical company focused on the development of novel therapies for a broad range of cancer indications, today announced preclinical data from studies evaluating SLS009 (tambiciclib), its highly selective cyclin-dependent kinases 9 (CDK9) inhibitor, in patient-derived organoid models of pancreatic ductal adenocarcinoma (PDAC). The data are being presented at the American Association for Cancer Research (AACR) Conference on Pancreatic Cancer: New Frontiers in Biology and Therapeutic Development, being held September 25–28, 2026, in San Diego. The timing of this announcement reflects AACR’s embargo policy, under which the data presented at the conference were restricted from publication until 1:00 p.m. ET today.

The studies, conducted in collaboration with researchers at the University of Wisconsin–Madison, evaluated SLS009 in MYC-amplified PDAC models, including a model resistant to the recently approved RAS inhibitor daraxonrasib (RMC-6236), as well as in combination with the BET inhibitor ZEN3694. MYC amplification is a biologically recognized mechanism of RAS targeting resistance.