J14 treatment (50 mg/kg; intraperitoneal injection; daily; for 16 days; BALB/c nude female mice) significantly reduces the average tumor volume. The masses and weights of the primary tumors from J14-treated mice are considerably lower compared to those from control mice^[1].

J14 treatment (0-100 µM; 0-96 hours; A549 cells) inhibits A549 cell growth in both a concentration- and time-dependent manner, with IC50 of 15.7 µM^[1].

J14 treatment (20 µM; 48-72 hours; A549 cells) triggers the release of cytochrome c into the cytosol and activates caspase-3 and caspase-9. This leads to oxidative damage to mitochondria, culminating in caspase-mediated apoptosis^[1].

J14 treatment significantly boosts the accumulation of sulfinic peroxiredoxins and intracellular ROS. The excessive buildup of intracellular ROS leads to oxidative damage and subsequent cell death. J14 markedly induces cell death in A549 cells in a time-dependent manner, achieving about 40% cell death within 96 hours^[1].

J14 triggers oxidative damage in mitochondria and induces apoptosis^[1].