<p>Endothelial progenitor cells (EPCs) play a critical role in vascular repair and neovascularization by contributing to endothelial regeneration. While clopidogrel bisulfate is widely used as an antiplatelet agent, its direct cellular effects on EPC biology remain largely unexplored. This study aimed to determine whether clopidogrel bisulfate modulates human EPC proliferation, survival, and intracellular signaling in vitro. Human EPCs were isolated from peripheral blood mononuclear cells and characterized by Dil-ac-LDL uptake and CD34 immunostaining. Cells were treated with clopidogrel bisulfate (0, 5, or 10 µM) for 48&#xa0;h. Proliferation, apoptosis, and cell viability were assessed using microscopy, Annexin V/PI flow cytometry, and CCK-8 assays. Western blotting was used to evaluate apoptosis-related proteins (Bax, Bcl-2) and signaling pathways (p-ERK). Clopidogrel bisulfate-treated EPCs maintained characteristic morphology and exhibited an apparent increase in cell density compared with untreated controls, without significant induction of apoptosis. CCK-8 assay revealed increased absorbance at later reaction time points, indicating enhanced cellular metabolic activity. In addition, under basal conditions, no consistent changes in the Bax/Bcl-2 ratio or ERK phosphorylation were observed. In contrast, under H₂O₂-induced oxidative stress conditions, clopidogrel bisulfate reduced the Bax/Bcl-2 ratio and increased ERK phosphorylation, suggesting context-dependent modulation of intracellular signaling pathways. These findings suggest that clopidogrel bisulfate influences EPC behavior by modulating metabolic activity and intracellular signaling, particularly under oxidative stress conditions. Beyond its antiplatelet effects, clopidogrel bisulfate may support endothelial repair through EPC-mediated mechanisms as a therapeutic agent in vascular disease.</p>