NEW YORK — September 25, 2026
SELLAS Life Sciences Group presented new preclinical data for SLS009 (tambiciclib) in patient-derived pancreatic ductal adenocarcinoma (PDAC) models at the 2026 American Association for Cancer Research (AACR) Conference on Pancreatic Cancer. The studies, conducted with researchers at the University of Wisconsin–Madison, evaluated the selective CDK9 inhibitor SLS009 in MYC-amplified PDAC models, including a model resistant to the RAS inhibitor daraxonrasib (RMC-6236), as well as in combination with the BET inhibitor ZEN3694. The findings showed increased cancer-cell death with SLS009 treatment and provided preclinical evidence supporting further investigation of CDK9 inhibition as a strategy for addressing MYC-associated resistance to RAS-directed therapies.
SLS009 Shows Activity in Daraxonrasib-Resistant PDAC Model
SLS009 demonstrated greater single-agent activity than daraxonrasib in a MYC-amplified, daraxonrasib-resistant patient-derived PDAC organoid model. At the concentrations evaluated, SLS009 induced 17.9% apoptosis and 14.5% necrosis, compared with 2.8% apoptosis and 2.7% necrosis with daraxonrasib alone. When SLS009 was combined with daraxonrasib, apoptosis increased to 36.5% and necrosis to 30.6%, exceeding the effects observed with either agent individually. In the study design, daraxonrasib was administered continuously while SLS009 was removed after 24 hours to approximate its reported in vivo pharmacokinetic profile, with apoptosis and necrosis assessed after 72 hours. These findings are preclinical and do not establish clinical efficacy in pancreatic cancer patients.
BET Combination Demonstrates Synergistic MYC Suppression
The SLS009 and ZEN3694 combination demonstrated synergistic activity in a separate MYC-amplified patient-derived PDAC organoid model. The combination produced greater apoptosis and necrosis than either treatment alone and resulted in sustained suppression of MYC RNA and reduced MYC and MCL-1 protein expression. The effects were observed at a ZEN3694 concentration below reported physiologically achievable exposure levels, according to SELLAS. The findings provide mechanistic support for combining CDK9 and BET inhibition to disrupt transcriptional programs associated with MYC-driven tumor-cell survival. SELLAS said the results may support additional investigation of SLS009-based combinations in molecularly defined pancreatic cancer populations.
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SELLAS Advances SLS009 Combination Development
The AACR findings add to SELLAS’ broader development program for SLS009, an investigational CDK9 inhibitor designed to disrupt transcriptional processes involved in cancer-cell survival. The company is evaluating whether CDK9 inhibition can complement RAS-directed therapy and potentially address resistance associated with MYC amplification in pancreatic cancer. Three studies were presented at the AACR conference covering MYC allelic imbalance and therapeutic response, BET/CDK9 inhibition and CDK9/KRASG12D inhibition in PDAC models. While the organoid findings provide a rationale for further research, clinical studies will be required to determine whether the observed activity and combination effects translate into meaningful therapeutic benefit in patients. SELLAS plans to continue evaluating SLS009 as part of its broader oncology development strategy.
Source :SELLAS Life Sciences press release
