The cell cycle is a tightly regulated process that ensures accurate cell division. This review discusses the mechanisms controlling the cell cycle, including the regulation of cyclin-dependent kinases (CDKs) by cyclins, CDK inhibitors, and phosphorylation events. It also covers the quality checkpoints that ensure proper DNA replication and repair. Aberrant cell cycle regulation is a key factor in cancer development, and targeting CDKs presents opportunities for cancer therapy. CDKs are regulated by cyclins, which are expressed at specific phases of the cell cycle. CDK activity is also controlled by phosphorylation, with CDK inhibitors (CKIs) such as the INK4 and Cip/Kip families playing a crucial role in cell cycle control. Mutations in CDKs, cyclins, and CKIs are frequently observed in cancer, leading to uncontrolled cell proliferation. The review also discusses the role of checkpoint proteins, such as p53, in detecting DNA damage and preventing the progression of damaged cells. CDK inhibitors are being explored as potential cancer therapeutics, with several compounds, including flavopiridol, UCN-01, and roscovitine, entering clinical trials. These inhibitors act by competing with ATP binding to CDKs, thereby inhibiting their activity. Other CDK inhibitors include butyrolactone, flavonoids, paullones, indolinones, and non-specific inhibitors such as staurosporine. These compounds show promise in targeting CDKs and may offer new therapeutic strategies for cancer treatment.The cell cycle is a tightly regulated process that ensures accurate cell division. This review discusses the mechanisms controlling the cell cycle, including the regulation of cyclin-dependent kinases (CDKs) by cyclins, CDK inhibitors, and phosphorylation events. It also covers the quality checkpoints that ensure proper DNA replication and repair. Aberrant cell cycle regulation is a key factor in cancer development, and targeting CDKs presents opportunities for cancer therapy. CDKs are regulated by cyclins, which are expressed at specific phases of the cell cycle. CDK activity is also controlled by phosphorylation, with CDK inhibitors (CKIs) such as the INK4 and Cip/Kip families playing a crucial role in cell cycle control. Mutations in CDKs, cyclins, and CKIs are frequently observed in cancer, leading to uncontrolled cell proliferation. The review also discusses the role of checkpoint proteins, such as p53, in detecting DNA damage and preventing the progression of damaged cells. CDK inhibitors are being explored as potential cancer therapeutics, with several compounds, including flavopiridol, UCN-01, and roscovitine, entering clinical trials. These inhibitors act by competing with ATP binding to CDKs, thereby inhibiting their activity. Other CDK inhibitors include butyrolactone, flavonoids, paullones, indolinones, and non-specific inhibitors such as staurosporine. These compounds show promise in targeting CDKs and may offer new therapeutic strategies for cancer treatment.