Abstract

Venetoclax, an oral selective BCL-2 inhibitor, is well known to induce apoptosis in B cells and measurable residual disease (MRD)-negative complete response in patients with chronic lymphocytic leukaemia.1 As monotherapy, venetoclax had little effect in acute myeloid leukaemia,2 but when combined with either low-dose cytarabine or a hypomethylating agent, such as azacytidine or decitabine, it provided a marked improvement in response rate compared with either drug alone.3 A subsequent prospective randomised, double-blind study (VIALE-A)4 convincingly showed improved response rate and overall survival with venetoclax plus azacytidine compared with azacytidine alone as primary treatment for patients with acute myeloid leukaemia judged to be ineligible for intensive combined chemotherapy, most of whom were aged 75 years or older.

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