“…Approximately 80% of CDK9 molecules form heterodimers with Cyclin T1, which is also called positive transcription elongation factor b (p-TEFb) that is required for the phosphorylation of the RNA polymerase II (RNA Pol II) C-terminal domain (CTD) and transcription elongation. While the remaining 20% form complexes with Cyclin T2A, Cyclin T2B, or Cyclin K. CDK9 expression has been found to be dysregulated in various types of cancer. − Inhibition of CDK9 results in transient transcriptional suppression and preferential depletion of apoptosis-related proteins with short half-lives, such as Mcl-1, c-Myc, and XIAP. So far, several selective CDK9 inhibitors have entered clinical research successively for the treatment of malignant hematological tumors such as acute myeloid leukemia (AML), including AZD4573, VIP152, KB-0742, et al (Figure ), and most of the design concepts of CDK9 inhibitors are focused on CDK subtype selectivity and properties suitable for achieving short target engagement. , Recent studies have shown that MYC gene mutations and abnormal Mcl-1 expression are also one of the main factors driving the onset and metastasis of CRC in addition to malignant hematological tumors. − Therefore, targeting CDK9 might work as an appealing strategy for treating CRC.…”