Influence of Molecular Abnormalities on Response of VAH vs. VEN+HMA in RR-AML

Venetoclax-based regimens have heen used in the salvage therapy of relapsed/resfractory (RR) acute myeloid leukemia (AML). More and more studies have shown that molecular abnormalities and venetoclax combined regimens significantly impact the response of venetoclax-based therapy. Our exploratory study revealed that venetoclax plus azacytidine combined with homoharringtonine (VAH) had remarkably higher response than venetoclax plus hypomethylating agents (HMA) in RR-AML. Yet the influence of molecular abnormalities on the response of VAH regimen remains unknown.

Inclusion criteria

• RR-AML
• Patients must have been treated for at least one cycle of VEN-based regimen and finished outcome assessment.

Exclusion criteria

• Acute promyelocytic leukemia (AML subtype M3)
• Previous exposure to the treatment of VEN-based regimen
• Cardiac dysfunction (particularly congestive heart failure, unstable coronary artery disease and serious cardiac ventricular arrhythmias requiring antiarrhythmic therapy)
• Respiratory failure (PaO2 ≤60mmHg)
• Hepatic abnormalities (total bilirubin ≥2 times the upper limit of normal [ULN], alanine aminotransferase (ALT) or aspartate aminotransferase (AST) ≥2 times the ULN)
• Renal dysfunction (creatinine ≥2 times the ULN or creatinine clearance rate < 30 mL/min)
• ECOG performance status 3, 4 or 5
• Substantial history of neurological, psychiatric, endocrine, metabolic, immunological, or any other medical condition not suitable for the trial (investigators' decision)
• Active acute or chronic graft-versus-host disease (GVHD). Active acute GVHD or chronic GVHD is defined as GVHD requiring either at least 1 mg/kg per day of prednisone (or equivalent) or treatment beyond systemic corticosteroids.
• Patients with pregnancy
• Uncontrolled active infection
• Clinically significant coagulation abnormalities