Molecular Weight(MW): 262.35
Ferrostatin-1 (Fer-1) is a potent and selective inhibitor of ferroptosis with EC50 of 60 nM.
Cited by 15 Publications
5 Customer Reviews
Indicated HCC cells were treated with sorafenib (5 µM) and erastin (10 µM) with or without cell death inhibitors (ferrostatin-1, 1 µM; liprostatin-1, 100nM; ZVAD-FMK,10 µM; necrosulfonamide, 0.5 µM) for 24 hours and cell viability was assayed (n=3, *p < 0.05 versus sorafenib or erastin treatment group).
Hepatology, 2016, 64(2):488-500. Ferrostatin-1 (Fer-1) purchased from Selleck.
A, Indicated human PDAC cells were treated with erastin (2.5-40 μmol/L) with or without a cell death inhibitor (ferrostatin-1, 1 μmol/L; liprostatin-1, 1 μmol/L; ZVAD-FMK, 10 μmol/L; necrosulfonamide, 0.5 μmol/L) for 24 hours. Cell death was assayed using a CCK8 kit (n = 3;* , P < 0.05).
Cancer Res, 2017, 77(8):2064-2077. Ferrostatin-1 (Fer-1) purchased from Selleck.
Inhibition of HSF1-dependent HSPB1 expression increased erastin-induced ferroptosis. Effects of deferoxamine (100 μM), ferrostain-1 (1 μM), Z-VAD-FMK (10 μM), necrostain 1 s (Nec-1 s, 10 μM) and cyclosporin A (CsA, 5 μM) on erastin-induced growth inhibition at 24 h in indicated HeLa (j) and U2OS (k) cells (n =3, *P<0.05 versus erastin group).
Oncogene, 2015, 10.1038/onc.2015.32. Ferrostatin-1 (Fer-1) purchased from Selleck.
(B,C) Pharmacological inhibition of multiple components in the glutaminolysis pathway abrogated anti-miR-9 mediated ferroptosis cell death and lipid accumulation. A375 Cells transfected with control or miR-9 antagomirs were treated with erastin (5 μM, B)/RSL3 (0.1 μM, C) and GPNA (5 mM)/Compound 968 (20 μM)/Fer-1 (1 μM) for 24 hr. The cell viability was assayed using a CCK8 kit and the lipid accumulation was measured by MDA assay. Data shown represent mean ± SD from three independent experiments. Statistical significance was calculated using one-way ANOVA. n.s., non-significant; *, p < 0.05. (D,E) Pharmacological inhibition of multiple components in the glutaminolysis pathway abrogated anti-miR-9 mediated ferroptosis cell death and lipid accumulation. G-361 Cells transfected with control or miR-9 antagomirs were treated with erastin (10 μM, D)/RSL3 (0.5 μM, E) and GPNA (5 mM)/Compound 968 (20 μM)/Fer-1 (1 μM) for 24 hr. The cell viability was assayed using a CCK8 kit and the lipid accumulation was measured by MDA assay.
Mol Carcinog, 2018, 57(11):1566-1576. Ferrostatin-1 (Fer-1) purchased from Selleck.
FANCD2+/+ and FANCD2-/- BMSCs were treated with erastin (1.25 μM) in the absence or presence of ferroptosis inhibitor (ferrostatin-1, 500 nM; liprostatin-1, 200 nM; b-mercaptoethanol, 50 μM; N-acetylcysteine, 100 mM) or autophagy inhibitor (chloroquine, 10 μM; 3-methyladenine, 5 mM) for 24 h. Cell viability was assayed (n = 3, *P < 0.05 versus erastin treatment group)
Biochem Biophys Res Commun, 2016, 480(3):443-449. Ferrostatin-1 (Fer-1) purchased from Selleck.
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Choose Selective Ferroptosis Inhibitors
|Description||Ferrostatin-1 (Fer-1) is a potent and selective inhibitor of ferroptosis with EC50 of 60 nM.|
Ferrostatin-1 (2 μM) prevents erastin-induced ferroptosis in cancer cells, as well as glutamate-induced cell death in postnatal rat brain slices. Ferrostatin-1 is a lipid ROS scavenger, with the N-cyclohexyl moiety serving as a lipo-philic anchor within biological membranes. Ferrostatin-1 does not inhibit extracellular signal -regulated kinase (ERK) phos-phorylation or arrest the proliferation of HT-1080 cells, suggesting that it does not inhibit the MEK/ERK pathway, chelate iron, or inhibit protein synthesis. Ferrostatin-1 does, however, prevent erastin-induced accumulation of cytosolic and lipid ROS. Ferrostatin-1 readily oxidizes the stable radical 2,2-diphenyl-1-picrylhydrazyl (DPPH) under cell-free conditions. 
|In vitro||DMSO||52 mg/mL (198.2 mM)|
|Ethanol||52 mg/mL (198.2 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+50% PEG 300+5% Tween 80+ddH2O
For best results, use promptly after mixing.
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