Pyruvate kinase M2 (PKM2), a key regulator of glycolysis, is frequently overexpressed in endometrial cancer and contributes to tumor progression through metabolic reprogramming. This study investigated the effects of Compound 7d, a PKM2 inhibitor, on glycolytic metabolism, cell-cycle progression, and apoptosis in Ishikawa endometrial cancer cells. Compound 7d reduced cell viability in a concentration-dependent manner and suppressed glycolytic activity, as demonstrated by decreases in the glycolytic proton efflux rate (PER) and extracellular acidification rate (ECAR) at subcytotoxic concentrations. It also reduced PKM2 mRNA expression and immunocytochemical staining, indicating the disruption of PKM2-associated glycolytic regulation. Cell cycle analysis showed an accumulation of the G₂/M phase population. This effect was accompanied by increased expression of cyclin B1 and histone H3 phosphorylation on Ser10, as well as decreased inhibitory phosphorylation of CDK1 on Tyr15, consistent with mitotic arrest. Furthermore, Compound 7d increased the Bax/Bcl-2 ratio and activated the caspase cascade, resulting in caspase-dependent apoptosis. Collectively, these findings demonstrate that Compound 7d suppresses the growth of Ishikawa endometrial cancer cells by inhibiting PKM2-associated glycolytic metabolism and inducing G₂/M phase arrest and apoptosis. Thus, targeting PKM2 with Compound 7d may represent a potential metabolic therapeutic strategy for endometrial cancer.