This confirmed that compound 1 induced breast cancer cells apoptosis via the intrinsic and extrinsic pathways through the expression of Bim, Bad, and tBid proapoptotic proteins and then accelerated the pore formation at the outer mitochondrial membrane and activated initiator caspase-9 and executioner caspase-3 as the sequelae for apoptosis induction. Here, CASP3 is linked to breast carcinoma.