Could you elaborate on the significance of the 33% overall response rate (ORR) observed in the 60 mg QW cohort and the 50% ORR in the 30 mg BIW cohort of the SLS009 Phase 2a trial? How do these rates compare to standard treatments for r/r AML?

The trial data indicates that SLS009 was well-tolerated across all doses with no dose-limiting toxicities. How does the safety profile of SLS009 compare to other treatments currently available for r/r AML patients?

The 100% overall response rate in patients with ASXL1 mutations in the 30 mg BIW cohort is remarkable. What could be the underlying reasons for such a high response rate in this specific genetic subgroup?

The trial has expanded to include two additional cohorts focusing on patients with ASXL1 and other myelodysplasia-related molecular mutations. What are the expected outcomes from these focused cohorts, and how might this data influence future treatment protocols?

Patients in the 45 mg QW cohort had a median overall survival (OS) of 5.4 months compared to 2.5 months with standard care. What does this improvement suggest about the potential of SLS009 as a new treatment option for r/r AML?

The study aims to identify biomarkers for the target patient population. How important is biomarker identification in developing targeted therapies for AML, and what progress has been made so far in this area?

With median overall survival not yet reached in the higher dose cohorts (60 mg QW and 30 mg BIW), what are the prospects for long-term efficacy of SLS009? What follow-up studies or data might be necessary to confirm these initial findings?

Considering the promising initial data, what steps are necessary to transition SLS009 from clinical trials to a widely accepted treatment option for r/r AML? What challenges do you foresee in this process?