abstract
- Cyclin-dependent kinases (CDKs) drive cell cycle progression and control transcriptional processes. The sustained cell proliferation resulting from dysregulation of the cell cycle and activation of CDKs is a hallmark of cancer. Inhibiting CDKs is a very interesting and promising approach for creating anticancer medications. The dysregulation or overexpression of the CDK4/6 complex results in aberrant cell proliferation and the emergence of cancer. It serves as a checkpoint during the cell cycle transition from the cell growth (G1) to the DNA synthesis (S) phase. As a result, CDK4/6 targeting has been suggested as a paradigm change in the anticancer strategy. With medications like palbociclib, ribociclib, and abemaciclib, the design and development of efficient CDK4/6 inhibitors is progressively emerging as a viable cancer therapy. Third-generation CDK inhibitors, in particular, offer an ideal compromise between anticancer activity and general toxicity by specifically inhibiting CDK4/6 and controlling the cell cycle by blocking the G1 to S phase transition. The purpose of this chapter was to describe how CDK4/6 inhibitors affect cancer cells and how they affect cell regulation. We investigated potential future uses for drug-like compounds that target particular CDK4/6 therapies in more detail. © 2024 Elsevier Inc. All rights reserved.