J14 是一种可逆 sulfiredoxin 抑制剂，IC₅₀ 为 8.1 μM。J14 通过抑制 sulfiredoxin 诱导氧化应激 (导致细胞内 ROS 积累)，从而导致细胞毒性和癌细胞死亡。

J14 is a reversible sulfiredoxin inhibitor with an IC 50 of 8.1 μM. J14 induces oxidative stress (intracellular ROS accumulation) by inhibiting sulfiredoxin, leading to cytotoxicity and cancer cell death.

Solid

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. has not independently confirmed the accuracy of these methods. They are for reference only.

Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years；4°C 2 years

[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.

In Vitro: DMSO : ≥ 125 mg/mL (241.76 mM)配制储备液