VENCLYXTO in combination with a hypomethylating agent is indicated for the treatment of adult patients with newly diagnosed acute myeloid leukaemia (AML) who are ineligible for intensive chemotherapy.
VENCLYXTO: A FIRST-IN-CLASS, POTENT, AND SELECTIVE BCL-2 INHIBITOR THAT INDUCES APOPTOSIS IN AML CELLS1
VENCLYXTO targets a key hallmark of cancer by inducing apoptosis1
The overexpression of pro-survival BCL-2 proteins is an important driver of AML cell survival.2-4
| • | In an in vitro study, the majority of AML samples were found to have overexpressed, pro-survival BCL-2 family proteins2 |
| • | AML cells have been shown to be dependent on BCL-2 and codependent on other BCL-2 family members, such as MCL-1 and BCL-XL, for survival3,4 |
Overexpressed BCL-2 allows AML cells to evade apoptosis by sequestering pro-apoptotic proteins, preventing them from signalling the cell to die.1,5,6
VENCLYXTO selectively binds to BCL-2 to displace pro-apoptotic proteins, triggering events that lead to apoptosis.1,6
VENCLYXTO has been found in vitro to work synergistically in combination with HMAs7
AML=acute myeloid leukaemia; BCL-2=B-cell lymphoma 2; BCL-XL=B-cell lymphoma-extra large; HMA=hypomethylating agent; MCL-1=myeloid cell leukaemia 1.
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References: 1. VENCLYXTO Summary of Product Characteristics. Ludwigshafen, Germany: AbbVie Deutschland GmbH & Co. KG. December 2022. 2. Vo T-T, Ryan J, Carrasco R, et al. Relative mitochondrial priming of myeloblasts and normal HSCs determines chemotherapeutic success in AML. Cell. 2012;151(2):344-355. doi:10.1016/j.cell.2012.08.038 3. Lagadinou ED, Sach A, Callahan K, et al. BCL-2 inhibition targets oxidative phosphorylation and selectively eradicates quiescent human leukemia stem cells. Cell Stem Cell. 2013;12(3):329-341. doi:10.1016/j.stem.2012.12.013 4. Punnoose EA, Leverson JD, Peale F, et al. Expression profile of BCL-2, BCL-XL, and MCL-1 predicts pharmacological response to the BCL-2 selective antagonist venetoclax in multiple myeloma models. Mol Cancer Ther. 2016;15(5):1132-1144. doi:10.1158/1535-7163.MCT-15-0730 5. Anderson MA, Huang D, Roberts A. Targeting BCL2 for the treatment of lymphoid malignancies. Semin Hematol. 2014;51(3):219-227. doi:10.1053/j.seminhematol.2014.05.008 6. Souers AJ, Leverson JD, Boghaert ER, et al. ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets. Nat Med. 2013;19(2):202-208. doi:10.1038/nm.3048 7. Nguyen LXT, Troadec E, Kalvala A, et al. Inhibition of ROS-induced Nrf2 antioxidant pathway activation may explain synergy between venetoclax and hypomethylating agents against acute myeloid leukemia. Blood. 2017;130 (suppl 1):1367.
ALL-VNCAML-220066 March 2023