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.

Ferroptosis:60 nM(EC50, HT-1080 cells)

METHODS: 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.
RESULTS Ferrostatin-1 attenuated the LPS-induced cell damage. [1]
METHODS: 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.
RESULTS Ferrostatin-1 inhibited the Erastin-induced accumulation of cytoplasmic and lipid ROS. [2]
METHODS: 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.
RESULTS The release of LDH was significantly increased by treatment with glutamate, and the release of LDH was inhibited by Ferrostatin-1 treatment. [3]

METHODS: 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.
RESULTS Ferrostatin-1 significantly protected mice from renal dysfunction and tubular injury in LPS-induced AKI. [4]
METHODS: 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.
RESULTS 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].