J14 |
Catalog No.GC38803 |
J14는 IC50이 8.1μM인 가역적인 설피어독신 억제제입니다. J14는 sulfiredoxin을 억제하여 산화 스트레스(세포 내 ROS 축적)를 유도하여 세포 독성과 암세포 사멸을 유발합니다.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 1043854-13-2
Sample solution is provided at 25 µL, 10mM.
J14 is a reversible sulfiredoxin inhibitor with an IC50 of 8.1 μM. J14 induces oxidative stress (intracellular ROS accumulation) by inhibiting sulfiredoxin, leading to cytotoxicity and cancer cell death[1].
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[1].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[1].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[1].J14 induces oxidative mitochondrial damage and apoptosis[1]. Cell Viability Assay[1] Cell Line: A549 cells
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[1]. Animal Model: Six-week-old BALB/c nude female mice injected with A549 cells[1]
[1]. Kim H, et al. Sulfiredoxin inhibitor induces preferential death of cancer cells through reactive oxygen species-mediated mitochondrial damage. Free Radic Biol Med. 2016 Feb;91:264-74.
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