The expansion aims to assess SLS009 plus AZA/VEN in newly diagnosed AML with high-risk features starting in early 2026.

In mutation subgroups, ASXL1 mutations showed a 48% response rate (including 19% CR/CRi) and TP53 mutations showed a 57% response rate (including 29% CR/CRi).

Lead author Dr. Joshua F. Zeidner presented the ASH 2025 poster, part of session 616 on December 7 at the Orange County Convention Center in Orlando.

The regimen of SLS009 30 mg IV twice weekly added to AZA/VEN was well tolerated with no dose-limiting toxicities or treatment-related deaths.

SELLAS Life Sciences presented positive Phase 2 data at ASH 2025 in Orlando showing SLS009 combined with azacitidine and venetoclax (AZA/VEN) achieves activity in relapsed/refractory AML-MR after prior VEN exposure.

Plans are in place to expand the study into newly diagnosed high-risk AML, with a primary focus in Q1 2026 on evaluating SLS009 plus AZA/VEN in this setting.

The data release aligns with broader company activities, including GPS program development and filings, with a shelf registration noted.

The release includes forward-looking statements and investor contact information.

Across all cohorts, median overall survival exceeded historical benchmarks, with the strongest signal in the least pretreated group.

In the same data set, SLS009 plus AZA/VEN yielded a 46% overall response rate in 35 evaluable relapsed/refractory AML-MR patients previously treated with VEN-based regimens.

The least pretreated cohort showed a median overall survival of 8.9 months, substantially above a historical benchmark of about 2.5 months, while patients with one prior therapy had not yet reached median overall survival.

In patients with one prior line of therapy, the overall response rate was 58% and this group’s median overall survival was not yet reached, suggesting durable responses in less heavily pretreated patients.

SELLAS is advancing GPS (WT1-targeted) and SLS009 (tambiciclib, a CDK9 inhibitor) to counter resistance to venetoclax-based regimens, showing activity particularly in ASXL1 and TP53-mutant AML-MR.

Participant profile included a median age of 69, with 98% of patients having ELN adverse-risk AML, and common mutations in ASXL1, RUNX1, TP53, and SRSF2.