Objective  To investigate the formation and mechanism of dipeptidylpeptidase-4 inhibitor anagliptin inhibiting lung metastasis of colorectal cancer.  Methods   Twenty-four male BALB/c mice were randomly divided into normal group, model group, anagliptin group. The control group did not undergo any treatment. The model group was injected with 0.1 ml CT-26 cells of 109 cells/L. once through the tail vein of the mouse to construct a lung metastasis model, while the anagliptin group was injected intraperitoneally 20mg/(kg·d) 0 day after  constructing a lung metastasis model. The mice were sacrificed after 14 days. HE staining was used to detect the morphological alteration. Determination of CT-26 cell viability through MTT assay and CT-26 cell apoptosis was detected by flow cytometry and live/dead cell staining. Reactive oxygen species(ROS) production was measured by ROS kit. Western blotting was conducted to measure the expression level of Bcl-2, Bax, cleaved-caspase-3, superoxide dismutase(SOD-1) and SOD-2.  Results   HE staining showed that the administration of anagliptin could significantly inhibit the abnormal changes in the model group. Anagliptin inhibited the viability of CT-26 cells above 2 mmol/L. Anagliptin promoted the apoptosis of CT-26 cells. Incubation of anagliptin in CT-26 cells significant promoted the production of ROS. Incubation of anagliptin stimulated the expressions of Bax and cleaved-Caspase-3, while down-regulated the expression of Bcl-2 in CT-26 cells. Administration of anagliptin decreased the expression of SOD-1, but not SOD-2.  Conclusion   Anagliptin promotes apoptosis of colorectal cancer cells and inhibits the formation of lung metastatic tumors through the SOD-1/ROS pathway.