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Liproxstatin-1 is a ferroptosis inhibitor.1 It inhibits ferroptotic cell death (IC50 = 22 nM) and lipid peroxidation in mouse embryonic fibroblasts (MEFs) with an inducible knockdown of glutathione peroxidase 4 (Gpx4-/- MEFs) when used at a concentration of 50 nM. Liproxstatin-1 also inhibits ferroptosis induced by the ferroptosis-inducing agents L-buthionine sulphoximine (BSO), erastin (Item No. 17754), and (1S,3R)-RSL3 (Item No. 19288) in a concentration-dependent manner in MEFs, but does not inhibit necroptosis, apoptosis, or necrosis. It inhibits cell death and lipid peroxidation induced by (1S,3R)-RSL3 in human renal proximal tubule epithelial cells. Liproxstatin-1 (10 mg/kg) increases survival and decreases TUNEL+ kidney cells in inducible Gpx4-/- mice and reduces tissue injury in a mouse model of hepatic ischemia/reperfusion injury. It is also an antioxidant that inhibits autooxidation of lipids by trapping peroxyl radicals.2
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1. Inactivation of the ferroptosis regulator Gpx4 triggers acute renal failure in mice. Nat. Cell. Biol. 16(12), 1180-1191 (2014).
2. On the mechanism of cytoprotection by ferrostatin-
Article polyunsaturated lipid senolytics exploit a ferroptotic vulnerability in senescent cells. Cell Press Blue 1(1), 100004 (2026).
Creatine kinase B suppresses ferroptosis by phosphorylating GPX4 through a moonlighting function. Nat. Cell. Biol. 25(5), 714-725 (2023).
TMEM164 is an acyltransferase that forms ferroptotic C20:4 ether phospholipids. Nat. Chem. Biol. (2023).
PALP: A rapid imaging technique for stratifying ferroptosis sensitivity in normal and tumor tissues in situ. Cell Chem. Bio. 29, 157-170 (2022).
Defining a pharmacological inhibitor fingerprint for oxytosis/ferroptosis. Free Radic. Biol. Med. S0891-5849(21), (2021).
A novel redox modulator induces a GPX4-
CD8+ T cells regulate tumour ferroptosis during cancer immunotherapy. Nature 569(7755), 270-274 (2019).