Breast cancer remains the predominant malignancy in the female population and constitutes a major contributor to cancer-related mortality, supporting the urgency of discovering new therapeutic agents to improve current treatment strategies. The anti-tumor potency of Eptifibatide has been reported previously; however, the molecular mechanism responsible for its action is still unclear. The regulatory effects of Eptifibatide on cell proliferation, cell cycle, and apoptosis were investigated using MTT and flow cytometric methods. The anti-tumor activity of Eptifibatide was also examined in a mouse breast cancer model, and its regulatory effects on the activity of the PI3K/AKT and Wnt/β-catenin oncogenic signaling pathways, as well as the expression of proinflammatory cytokines, were evaluated using western blotting and real-time PCR, respectively. Eptifibatide inhibited cell cycle progression and proliferation by repressing the PI3K/AKT pathway and its downstream effector, cyclin D1. Eptifibatide inhibited tumor growth and development by inducing cell apoptosis and upregulating the expression of p53 and BAX. Treatment with Eptifibatide decreased breast cancer cell migratory and metastatic behaviors by modulating E-cadherin and MMP-2 and 9. Our study indicates that Eptifibatide may serve as an effective therapeutic option, alone or in combination with the conventional chemotherapeutic agents, for breast cancer management.

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