IC50: 8.1 μM (Sulfiredoxin); ROS

J14 (0-100 μM; 0-96 hours; A549 cells) treatment inhibits the growth of A549 cells in a concentration- and a time- dependent manner, and its half inhibitory concentration for the growth of A549 cells was 15.7 μM.
J14 (20 μM; 48-72 hours; A549 cells) treatment causes not only the release of cytochrome c into the cytosol, but also the activation of caspase-3 and caspase-9. J14 induces oxidative damage to mitochondria, resulting in caspase-mediated apoptosis.
J14 treatment significantly increases the accumulation of sulfinic peroxiredoxins and intracellular ROS. Excess accumulation of intracellular ROS causes oxidative damage, leading to cell death. J14 significantly induces cell death in A549 cells in a time-dependent manner, resulting in approximately 40% cell death in 96 hours.
J14 induces oxidative mitochondrial damage and apoptosis.

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