Note to Affiliates: VEN + LDAC is not approved in the EU. These are optional pages for affiliates with this combination in label. Localize use of the VENCLYXTO or VENCLEXTA brand names in accordance with your local label.
[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.
FOR NEWLY DIAGNOSED PATIENTS WITH ACUTE MYELOID LEUKAEMIA (AML) WHO ARE INELIGIBLE FOR INTENSIVE CHEMOTHERAPY1
FOR NEWLY DIAGNOSED PATIENTS WITH ACUTE MYELOID LEUKAEMIA (AML) WHO ARE INELIGIBLE FOR INTENSIVE CHEMOTHERAPY1
FOR NEWLY DIAGNOSED PATIENTS WITH ACUTE MYELOID LEUKAEMIA (AML) WHO ARE INELIGIBLE FOR INTENSIVE CHEMOTHERAPY1
[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 October 2023
Note to Affiliates: VEN + LDAC is not approved in the EU.
Use of the VENCLEXTA brand name in this piece necessitates use of the VENCLEXTA U.S. Prescribing Information (PI) in the references.