J14 is an ATP- competitive Srx inhibitor with IC50 value of 8.1μM. J14 leads to intracellular ROS accumulation and can selectively kill cancer cells through a ROS-mediated cell death mechanism.
J14 is a reversible inhibitor of sulfiredoxin, exhibiting an IC50 of 8.1 μM. By inhibiting sulfiredoxin, J14 induces oxidative stress (intracellular ROS accumulation), resulting in cytotoxicity and cancer cell death[1].
体内研究
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].
体外研究
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].
作用机制
J14 binds to the ATP binding site, acting as a competitive inhibitor of ATP.
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