Cisplatin has been a cornerstone of Ovarian cancer (OC) treatment since its clinical introduction in the 1970s, with platinum-based regimens forming the core of first-line therapy. However, approximately 70% of patients eventually experience disease recurrence and develop resistance to platinum. To date, few clinically viable alternatives to cisplatin have emerged for the effective management of OC. Therefore, this study aims to identify a novel agent capable of enhancing cisplatin sensitivity and overcoming chemoresistance in ovarian cancer. This study evaluates the anti-tumor effects of GL-V9 in ovarian cancer, elucidates its underlying mechanisms, and evaluates its potential for clinical translation. The mechanisms underlying the effects of GL-V9 were investigated using streptavidin pull-down assays, functional analyses (cell viability, clonogenic survival, and apoptosis), and Western blotting. The antitumor efficacy of GL-V9 alone and in combination with cisplatin was further evaluated in an A2780 ovarian cancer xenograft model. We found that GL-V9, a flavonoid derived from Scutellaria, exerted potent antitumor effects in OC by inducing apoptosis and inhibiting proliferation. Furthermore, GL-V9 enhanced cisplatin sensitivity and reversed cisplatin resistance. Mechanistically, GL-V9 directly bound to and inhibited acetyl-CoA carboxylase 1 (ACC1), leading to elevated intracellular reactive oxygen species (ROS) levels. Both in vitro and in vivo experiments confirmed that GL-V9, alone or in combination with cisplatin, significantly suppressed tumor growth without observable toxicity. GL-V9 overcomes cisplatin resistance in ovarian cancer by targeting ACC1 and elevating ROS levels, highlighting its potential as a clinically translatable therapeutic strategy.