Next, to confirm the induction of mitochondrial-related apoptosis caused by compound-6d, we evaluated the levels of activated caspase 3 and PARP, and found that the cleaved forms of caspase 3 and PARP were notably increased in CRC and other cancer cells (such as A549, U87, and PANC-1) after treatment with compound 6d, but not in MCF7 cells due to a deletion mutation in exon 3 of the caspase 3 gene [28] (Figure 2B and Figure S2). Here, CASP3 is linked to cancer.