Objective To explore the anti-tumor activity of lobaplatin in colon cancer cells, to elucidate the underlying molecular mechanisms, and to provide theoretical evidence for clinical application. Methods Colon cancer cell line SW480 was cultured in vitro. MTT colorimetric assay and colony formation assay were used to detect the inhibitory effect of different concentrations of lobaplatin on colon cancer SW480 cells at 24, 48 and 72 h. The apoptosis rate of the cells was detected by flow cytometry. Western blot was used to detect the expression of the apoptosis-related proteins caspase-3, BAD and BCL-2 in SW480 cells after lobaplatin treatment. The mechanism of lobaplatin-induced apoptosis was investigated by adding AKT inhibitors and agonists and detecting the expression levels of caspase-3, AKT, pAKT, BAD, p-BAD and BCL-2. Results Lobaplatin significantly inhibited the growth of cultured SW480 cells in a dose- and time- dependent manner. Lobaplatin induced apoptosis of colon cancer SW480 cells. Lobaplatin induced downregulation of anti- apoptotic BCL-2 protein expression and upregulated pro-apoptotic BAD and caspase-3 protein expression in the cells. Addition of AKT inhibitor MK - 2206 significantly decreased pAKT, p-BAD, and BCL-2 expression, and significantly increased caspase-3 expression. Addition of AKT agonist SC97 significantly increased pAKT, p-BAD, and BCL-2 protein expression, and significantly decreased caspase-3 protein expression. Conclusions Lobaplatin significantly inhibited proliferation and induced apoptosis of human colon cancer SW480 cells. Lobaplatin may play a role in promoting apoptosis through the AKT/ BCL-2/ BAD signaling pathway, and it is an effective anti-colon cancer drug.