SUPPRESSION OF THE APOPTOTIC PATHWAY IS A KEY MECHANISM FOR THE SURVIVAL AND PROLIFERATION OF HEMATOLOGIC CANCER CELLS 3

  • Overexpressed BCL-2 allows hematologic cancer cells to evade apoptosis by sequestering pro-apoptotic proteins
  • VENCLEXTA selectively binds to BCL-2, displacing pro-apoptotic proteins, and triggering events that lead to apoptosis

BCL-2 is expressed in the majority of patients with AML 4-6

  • Approximately 80% of AML patients overexpress a BCL-2 pro-survival protein 7
  • In non-clinical studies, VENCLEXTA has demonstrated cytotoxic activity in tumor cells that overexpress BCL-2

Initiation of VENCLEXTA in patients with AML does not require biomarker or cytogenetic testing results 1

AML=acute myeloid leukemia; BCL-2=B cell lymphoma 2.