Ferrostatin-1 (Fer-1) is a potent and selective inhibitor of iron death. Ferrostatin-1 potently inhibits Erastin-induced iron death in HT-1080 cells with an EC₅₀ of 60 nM. Ferrostatin-1 also exhibits antioxidant and antifungal activities.

NIH3T3 cells:0.22 μM, LLC-MK2 cells:> 240 μM, IMR-32 cells:18 nM, Lymphocyte:48 nM (EC₅₀), Ferroptosis:60 nM (EC₅₀), HT1080 cells:95 nM, RAW 264.7 cells:0.04 μM (EC₅₀), Fibroblast:33 nM (EC₅₀), HT22 cells:81.2 nM (EC₅₀)

Method: Human bronchial epithelial cells BEAS-2B were co-treated with LPS (10 mg/L) and Ferrostatin-1 (2 μM) for 16 h. The growth inhibition of the cells was detected by CCK-8 method.
Result: Ferrostatin-1 attenuated the LPS-induced cell damage. ^[1]
Method: Human fibrosarcoma cells HT-1080 were treated with Ferrostatin-1 (0.5 μM) and Erastin (10 μM) for 4 h, and ROS levels produced by the cells were measured by Flow Cytometry.
Result: Ferrostatin-1 inhibited the Erastin-induced accumulation of cytoplasmic and lipid ROS. ^[2]
Method: Mouse hippocampal neuronal cells HT-22 were treated with Ferrostatin-1 (3-12 μM) for 16 h, then treated with 5 mM glutamate for 24 h, and then LDH release was measured.
Result: The release of LDH was significantly increased by treatment with glutamate, and the release of LDH was inhibited by Ferrostatin-1 treatment. ^[3]

Method: To investigate whether iron death is associated with LPS-induced acute kidney injury (AKI), Ferrostatin-1 (5 mg/kg) was administered intraperitoneally in a single dose to C57BL/6 mice, and infectious AKI was induced by intraperitoneal injection of LPS (10 mg/kg) 30 min later.
Result: Ferrostatin-1 significantly protected mice from renal dysfunction and tubular injury in LPS-induced AKI. ^[4]
Method: To investigate whether iron disorders are associated with acute liver disease and its molecular mechanism, Ferrostatin-1 (2.5 μM/kg) was intraperitoneally injected into ICR mice once a day for three days, followed by intraperitoneal injection of TAA (250 mg/kg/day) for three consecutive days, to establish an acute liver injury (ALI) model in mice.
Result: Ferrostatin-1 pretreatment significantly reduced TAA-induced changes in plasma ALT, AST and LDH levels, inhibited the expression of TfR1, Fpn and Ft-L proteins, and decreased iron accumulation without affecting the expression of xCT or GPX4 in the liver. Ferrostatin-1 prevents hepatic iron by decreasing death. ^[5]

Cell viability was typically assessed in 384-well format by Alamar Blue fluorescence (ex/em 530/590) measured on a Victor3 plate reader. In some experiments, Trypan Blue dye exclusion counting was performed using an automated cell counter. Cell viability under test conditions is reported as a percentage relative to the negative control treatment [1].

Ethanol: 26.20 mg/mL (99.87 mM), Sonication is recommended.

DMSO: 237.50 mg/mL (905.29 mM), Sonication is recommended.

10% DMSO+90% Saline: 4.29 mg/mL (16.35 mM), Solution.

10% DMSO+40% PEG300+5% Tween 80+45% Saline: 20 mg/mL (76.23 mM), Suspension.