Objective：To explore the potential mechanisms of Chouchunpi San（CCPS）on colorectal cancer based on cell experiments and network pharmacology. Methods：The targets of CCPS active compounds and colorectal cancer were screened by network pharmacology. The protein-protein interaction（PPI）network were constructed，and the potential targets of CCPS were predicted. Enrichment analysis was conducted to predict pathways through which CCPS may exert its anti-colorectal cancer effects. The effect of CCPS on the viability of colorectal cancer cells was detected by CCK-8 assay，and the effects of different concentrations of CCPS on apoptosis of colorectal cancer cells were detected by flow cytometry. Wounding-healing assay was employed to investigate the impact of CCPS on the migration capacity of colorectal cancer cells. The expression of STAT3 protein in colorectal cancer cells after CCPS induction was determined by Western blot. Results：There are 117 active components，920 potential targets，and 787 drug and disease intersection targets of CCPS were retrieved through the database. Protein-protein interaction（PPI）network analysis identified core targets such as STAT3，MAPK1，AKT1，and MYC.The results of GO enrichment and KEGG pathway analysis indicated that CCPS in mainly involved in biological processes relalted to cell apoptosis and oxidative stress response，and the pathways involved included cancer pathway，AGE-RAGE signaling pathway，and PI3K-Akt signaling pathway.Molecular docking results showed that STAT3 had a highly binding affinity with its core compound licochalcone A. Cell experiments demonstrated that CCPS inhibited the proliferation and migration capacity of colorectal cancer cells and significantly promoted cell apoptosis. Western blot results showed that the expression of STAT3 protein in cells significantly decreased after treatment with different concentrations of CCPS，and the decrease was concentration-dependent. Conclusion：This study revealed the multi-component，multi-target，and multi-pathway mechanisms of CCPS in the treatment of colorectal cancer. CCPS significantly inhibited the proliferation and migration capacity of colorectal cancer cells and its mechanism may be related to the targeted reduction of STAT3 protein levels.