Objective: Cyclin dependent kinases (CDKs) are involved in temporal regulation of the cell cycle and transcription and play central roles in cancer development and metastasis. CDK7 activates cell cycle CDKs and is a member of the general transcription factor TFIIH. In this study, we evaluate the therapeutic effects of CDK7 inhibition in ovarian cancer using in vitro and in vivo models. Methods: We analyzed the clinical significance of CDK7 expression using TCGA data. Using CDK7 siRNA or covalent CDK7 inhibitor (THZ1), we performed the cell proliferation, apoptosis and the effects of cell cycle analysis in ovarian cancer cell lines including A2780, HeyA8, A2780-CP20 and RMG1. Based on in vitro results, we also performed in vivo experiments including cell line xenograft (A2780) and patient-derived xenografts (PDXs). Results: Higher CDK7 expression is significantly associated with poor progression-free survival of ovarian cancer patients in the analysis of TCGA data. CDK7 suppression with its siRNA or THZ1 significantly decreased cell proliferation and increased apoptosis with cell line experiments. Moreover, combination treatment with CDK7 inhibition and cisplatin decreased cell proliferation in drug-resistant A2780-CP20 cells. In the flow cytometric analysis to check the influence in cell cycle of CDK7 inhibition, we found that THZ1 triggered G0/G1 cell cycle arrest in a dose-dependent manner. In in vivo therapeutic experiment with cell line xenograft, CDK7 suppression with its siRNA or THZ1 could significantly decrease the tumor weight in A2780 and HeyA8 models. Moreover, we also found similar effect of this treatment in a PDX model with clear cell carcinoma. Conclusion: These results showed that CDK7 suppression with its siRNA or THZ1 could significantly suppress ovarian cancer growth in in vitro and in vivo by triggering G0/G1 cell cycle arrest. Therefore, CDK7 might be a novel promising therapeutic target for ovarian cancer and will be explored in the near future for therapy of ovarian cancer.