Sellas Life Sciences announces preclinical data of SLS009 in AML

SELLAS Life Sciences (SLS) announced that preclinical efficacy of SLS009 in TP53 mutated Acute Myeloid Leukemia cells are being presented in a poster session at the American Association for Cancer Research taking place from April 25th – 30th at McCormick Place Convention Center, Chicago, IL. Patients with TP53-mutated AML continue to face extremely poor outcomes, even with intensive chemotherapy or the addition of stem cell transplantation. Preclinical data suggest that SLS009, a highly selective CDK9 inhibitor, can induce apoptosis downstream of p53 by targeting critical proteins such as MCL-1 and survivin, regardless of p53 status. Immunoblot analysis reveals near-complete removal of these proteins in treated cells within 8 hours of exposure to SLS009. Furthermore, the treatment reduced TP53-mutated leukemia cell populations by up to 97% in combination with azacitidine-venetoclax, and by up to 80% as monotherapy. “These findings are an exciting step forward in addressing one of the most challenging subsets of AML,” said Angelos Stergiou, CEO. “The ability of SLS009 to overcome TP-53 driven resistance in preclinical models, combined with the positive data we have seen in our ongoing Phase 2 AML program, including a response in a patient with a TP53 mutation, gives us hope that we may one day offer an effective therapeutic option to patients with AML who have long been underserved.” SLS009 is currently in Phase 2 clinical trials in patients with relapsed or refractory (AML following venetoclax-based regimens, including patients with TP53-mutated leukemia. Recently announced data revealed that r/r AML patients receiving 30 mg of SLS009 BIW achieved a mOS of 8.8 months for all patients, while the mOS in AML myelodysplasia-related-changes patients reached 8.9 months – far surpassing the historical benchmark of 2.5 months. Among patients with mutation ASXL1, 4/6 responded; among those with RUNX1 3/5 responded, and among those with TP53 1/3 responded. In addition, there were 3 patients with adverse karyotypes, and 1 responded.