The present study evaluated the effect of anagliptin on intimal hyperplasia following carotid artery injury in Sprague‑Dawley rats. Sprague‑Dawley rats weighing 280‑300 g were injured using a 2F Fogarty balloon embolectomy catheter. The rats were divided into injury‑(saline) and anagliptin‑(10 mg/kg/day) treated groups. vascular injuries were induced in the left carotid artery, followed by evaluation of neointima formation at 28 days. The right and left carotid arteries were harvested and evaluated with histological evaluation, and the plasma activity of glucagon‑like peptide 1 receptor (GLP‑1), stromal cell‑derived factor (SDF)‑1α, interleukin (IL)‑6, IL‑1β and tumor necrosis factor (TNF)‑α were detected by ELISA analysis. Treatment with anagliptin decreased balloon injury‑induced neointima formation, compared with the injury group (P<0.01). Body weight and food consumption did not alter following treatment with anagliptin. Anagliptin caused an increase in the serum active GLP‑1 concentration, compared with the injury group. In addition, serum SDF‑1α was significantly decreased by treatment with anagliptin (P<0.001). Anagliptin altered the serum activity of IL‑6, IL‑1β and TNF‑α (P<0.01). The results of the present study demonstrated that anagliptin appeared to attenuate neointimal formation by inhibiting inflammatory cytokines and chemokines following balloon injury, and that treatment with a dipeptidyl peptidase 4 inhibitor may be useful for future preclinical studies and potentially for the inhibition of thrombosis formation following percutaneous coronary intervention.