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SELLAS Life Sciences Announces Preclinical Data for SLS009

SELLAS Life Sciences Group announced preclinical data from studies evaluating SLS009, its highly selective cyclin-dependent kinases 9 inhibitor, in patient-derived organoid models of pancreatic ductal adenocarcinoma. The data are being presented at the American Association for Cancer Research Conference on Pancreatic Cancer: New Frontiers in Biology and Therapeutic Development, being held September 25-28, 2026, in San Diego. 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, as well as in combination with the BET inhibitor ZEN3694. MYC amplification is a biologically recognized mechanism of RAS targeting resistance. In a MYC-amplified, daraxonrasib-resistant patient-derived PDAC organoid model, SLS009 at 200 nM, daraxonrasib at 100 nM, and the combination of both agents were evaluated. Daraxonrasib was administered continuously, while SLS009 was removed after 24 hours to approximate its in vivo pharmacokinetic profile, with apoptosis and necrosis assessed at 72 hours. A separate MYC-amplified patient-derived PDAC organoid model evaluated SLS009 in combination with the BET inhibitor ZEN3694. The combination demonstrated synergistic activity, including increased cancer cell death and sustained suppression of MYC transcription. Notably, these effects were observed at a ZEN3694 concentration substantially below reported physiologically achievable exposure levels. Key findings: SLS009 demonstrated substantially greater single-agent activity than daraxonrasib in the daraxonrasib-resistant model, inducing 17.9% apoptosis versus 2.8% with daraxonrasib and 14.5% necrosis versus 2.7%. The combination of SLS009 and daraxonrasib further increased cancer cell death, inducing 36.5% apoptosis and 30.6% necrosis, compared with 17.9% and 14.5%, respectively, with SLS009 alone and 2.8% and 2.7%, respectively, with daraxonrasib monotherapy. SLS009 combined with ZEN3694 demonstrated synergistic activity, producing greater apoptosis and necrosis than either agent alone. The SLS009/ZEN3694 combination produced sustained suppression of MYC RNA and reduced expression of MYC and MCL-1 proteins, consistent with disruption of transcriptional pathways supporting tumor cell survival. Together, the findings support further investigation of CDK9 inhibition as a strategy to enhance RAS-directed therapy and potentially address MYC-associated resistance in pancreatic cancer. The BET combination data provide additional mechanistic support for SLS009-based approaches designed to disrupt MYC-dependent transcriptional programs and suggest the potential to enhance BET inhibition at lower drug exposures.