Novel CDK-7 Inhibitor Suppresses Transcription of Oncogenes and Enhances Venetoclax-Mediated Apoptosis in Acute Myeloid Leukemia

Background: Acute myeloid leukemia (AML) remains a highly fatal disease. Based on the available evidence of deregulated pathways of proliferation and apoptosis in AML, we hypothesize that pharmacological modulation of AML blasts by inhibitors of BCL-2 (Venetoclax) and novel CDK7 inhibitor (CRI-256) will be potently synergistic for the treatment of AML.