CDK9 inhibitors for the treatment of solid tumors

被引:3
作者
Mo, Christiana [1 ,2 ]
Wei, Ning [1 ,2 ,3 ]
Li, Terence [1 ,2 ,3 ]
Bhat, Muzaffer Ahmed [1 ,2 ,3 ]
Mohammadi, Mahshid [1 ,2 ,3 ]
Kuang, Chaoyuan [1 ,2 ,3 ]
机构
[1] Montefiore Einstein, Dept Oncol, Bronx, NY 10461 USA
[2] Montefiore Einstein Comprehens Canc Ctr, Bronx, NY USA
[3] Montefiore Einstein, Dept Mol Pharmacol, Bronx, NY USA
关键词
CDK9; Cancer therapeutics; Targeted therapy; Solid tumors; CYCLIN-DEPENDENT KINASE; CANCER STEM-CELLS; GENE COPY NUMBER; TRANSCRIPTION ELONGATION; TARGETING CDK9; PANCREATIC-CANCER; PHASE-I; P-TEFB; EXPRESSION; RECEPTOR;
D O I
10.1016/j.bcp.2024.116470
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Cyclin-dependent kinase 9 (CDK9) regulates mRNA transcription by promoting RNA Pol II elongation. CDK9 is now emerging as a potential therapeutic target for cancer, since its overexpression has been found to correlate with cancer development and worse clinical outcomes. While much work on CDK9 inhibition has focused on hematologic malignancies, the role of this cancer driver in solid tumors is starting to come into focus. Many solid cancers also overexpress CDK9 and depend on its activity to promote downstream oncogenic signaling pathways. In this review, we summarize the latest knowledge of CDK9 biology in solid tumors and the studies of small molecule CDK9 inhibitors. We discuss the results of the latest clinical trials of CDK9 inhibitors in solid tumors, with a focus on key issues to consider for improving the therapeutic impact of this drug class.
引用
收藏
页数:17
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