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Epithelial ovarian cancer (EOC) is an aggressive malignancy and is most often diagnosed at an sophisticated illness stage (1). Currently, essentially the most common treatment is surgery combined with platinum-based CB1 Inhibitor list mixture chemotherapy (two). Even so, 60 of patients relapsed after first-line therapy (3), and 50 showed resistance to chemotherapy. It is generally believed that EOC chemotherapy resistance is involved inside the DNA harm response (DDR) course of action in the cell cycle (four, five), in unique single-strand DNA break repair by poly ADP-ribose polymerase (PARP) and doublestranded repair through homologous recombination repair (HRR) of the BRCA1/2 genes. Hence, it really is the essential to discovering drugs that have an effect on the mechanism of drug resistance. Presently, for the treatment of ovarian cancer, agents that target specific stages in the cell cycle, like HIV-1 Antagonist Synonyms cyclin-dependent kinase inhibitors (CDKIs), have shown superior efficacy in clinical trials. For instance, ribociclib (6), a CDK4/6 inhibitor, which acts on the G1 phase of the cell cycle has been authorized by the US Meals and Drug Administration (FDA) for the treatment of breast cancer; it has also been utilised to treat ovarian cancer in phase II clinical trials (NCT02657928). Additionally, AZD5438 (7, 8), a CDK1/2 inhibitor, enhances radiosensitivity of nonsmall cell lung cancer by impairing HRR of double-stranded breaks (DSBs) and has currently been tested in the preclinical stage. As a result, it has been recommended that targeting the cell cycle is actually a novel and effective method to treat tumors. Having said that, only a couple of CDKIs have so far been deve