The cyclin-dependent kinase (CDK) family of proteins perform important functions in transcription regulation or cell-cycle control.1

CDK9 plays a critical role in transcription regulation2 and does not directly affect cell-cycle control.3 CDK9-mediated transcriptional regulation of anti-apoptotic proteins, such as MCL-1, is critical for the survival of MCL-1—dependent AML* blasts.2

Inhibition of CDK9 has been shown to block MCL-1 transcription, resulting in the rapid depletion of MCL-1 protein, thus triggering apoptosis in MCL-1—dependent AML blasts.1,3,4

Watch this video to learn more about MCL-1 as an apoptosis inhibitor and what this could mean for MCL-1—dependent AML.

Learn more about our ongoing clinical trials in MCL-1—dependent AML

*The prevalence of MCL-1—dependent AML is under investigation.

1. Yin T, Lallena MJ, Kreklau EL, et al. A novel CDK9 inhibitor shows potent antitumor efficacy in preclinical hematologic tumor models. Mol Cancer Ther. 2014;13(6):1442-1456. 2. Sonawane YA, Taylor MA, Napoleon JV, Rana S, Contreras JI, Natarajan A. Cyclin dependent kinase 9 inhibitors for cancer therapy. J Med Chem. 2016;59(19):8667-8684. 3. Morales F, Giordano A. Overview of CDK9 as a target in cancer research. Cell Cycle. 2016;15(4):519-527. 4. Thomas D, Powell JA, Vergez F, et al. Targeting acute myeloid leukemia by dual inhibition of PI3K signaling and Cdk9-mediated Mcl-1 transcription. Blood. 2013;122(5):738-748.

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