IM-54 is a cell-permeable oxidative stress-induced necrosis inhibitor. IM-54 inhibits H2O2- and TBHP-induced mitochondrial-associated necrosis signals to reduce oxidative stress-induced cell death. IM-54 can be used for research on oxidative damage, ischemia-reperfusion injury, myocardial infarction, and stroke-related cell necrosis[1-4].
3µM IM-54 was used to treat nitidine chloride-induced H1688 and A549 cells for 48h, and did not protect against cell death[5]. 210nM IM-54 was used to treat H2O2-induced HL-60 cells for 0.5h, inhibited necrotic cell death and reduced lactate dehydrogenase release[6]. 3µM IM-54 was used to treat 4-hydroxychalcone-induced SK-N-BE(2) and IMR-32 cells for 1h, prevented cell death and decreased reactive oxygen species[7].
References:[1] Uemichi Y, Yasuda S, Mabuchi M, et al. Effects of Azelastine on Glioblastoma Cells. Anticancer Res. 2025 Jul;45(7):2763-2771.
[2] Sodeoka M, Dodo K. Development of selective inhibitors of necrosis. Chem Rec. 2010 Oct;10(5):308-14.
[3] Tomasek T, Ware LB, Bastarache JA, et al. Cell-free hemoglobin-mediated human lung microvascular endothelial barrier dysfunction is not mediated by cell death. Biochem Biophys Res Commun. 2021 Jun 4;556:199-206.
[4] Zeng F, Sherry J P, Bols N C. Evaluating the toxic potential of benzothiazoles with the rainbow trout cell lines, RTgill-W1 and RTL-W1. Chemosphere. 2016 Aug;155:308-318.
[5] Yu F, Tan W, Chen Z, et al. Nitidine chloride induces caspase 3/GSDME-dependent pyroptosis by inhibting PI3K/Akt pathway in lung cancer. Chin Med. 2022 Sep 29;17(1):115.
[6] Dodo K, Katoh M, Shimizu T, et al. Structure-Activity Relationship Study of 3-Amino-2-indolyllactam Derivatives: Development of Inhibitors of Oxidative Stress-Induced Necrosis. Chem Pharm Bull. 2016 Jul;64(7):886-898.
[7] Alshangiti A, Tuboly E, Hegarty S, et al. 4-Hydroxychalcone Induces Cell Death via Oxidative Stress in MYCN-Amplified Human Neuroblastoma Cells. Oxidative Medicine and Cellular Longevity. 2019 Dec 5;2019:1670759.