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 enhancing the expression of p53 and BAX. Treatment with Eptifibatide inhibited migratory and metastatic behaviors in breast cancer cells by downregulating matrix remodeling proteins, including MMP-2 and MMP-9, and upregulating the cell adhesion protein, Ecadherin. Our study indicates that Eptifibatide may serve as an effective therapeutic option, either as a standalone treatment or in combination with standard chemotherapy drugs, for breast cancer management

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