However, our competitive binding results showed that compound 6d significantly suppressed the interaction between Bcl-2 and Bax by binding to Bcl-2, and then triggered mitochondria-mediated intrinsic apoptosis to inhibit the proliferation and growth of CRC cells in vitro/vivo, suggesting that the effects of compound 6d are similar with those exhibited by reported inhibitors of Bcl-2. Here, BAX is linked to colorectal carcinoma.