Ferrostatin-1 (Fer-1)

Catalog No.S7243 Batch:S724302

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Technical Data

Formula

C15H22N2O2
Molecular Weight 262.35 CAS No. 347174-05-4
Solubility (25°C)* In vitro DMSO 55 mg/mL (209.64 mM)
Ethanol 55 mg/mL (209.64 mM)
Water Insoluble
In vivo (Add solvents to the product individually and in order)
Homogeneous suspension
CMC-NA
≥5mg/ml Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
Clear solution
5% DMSO 40% PEG 300 5%tween 80 50%ddH2O

Validated by Selleck labs. Should you need adjustments to this formulation, contact our sales team for custom testing.

 1.000mg/ml (3.81mM) Taking the 1 mL working solution as an example, add 50 μL of 20 mg/ml clarified DMSO stock solution to 400 μL of PEG300, mix evenly to clarify it; add 50 μL of Tween80 to the above system, mix evenly to clarify it; then continue to add 500 μL ddH2O Dilute to 1 mL. The mixed solution should be used immediately for optimal results. 
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description Ferrostatin-1 (Fer-1) is a potent and selective inhibitor of ferroptosis with EC50 of 60 nM.
Targets
Ferroptosis [1]
(HT-1080 cells)
60 nM(EC50)
In vitro

Ferrostatin-1 (Fer-1) (2 μM) prevents erastin-induced ferroptosis in cancer cells, as well as glutamate-induced cell death in postnatal rat brain slices. It is a lipid ROS scavenger, with the N-cyclohexyl moiety serving as a lipo-philic anchor within biological membranes. This compound 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. It 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 vivo

Ferrostatin-1 (Fer-1), a synthetic antioxidant, is a potent and selective inhibitor of ferroptosis. It acts via a reductive mechanism to prevent damage to membrane lipids and thereby inhibits cell death.

Protocol (from reference)

Cell Assay:

[1]
  • Cell lines

    HT-1080 cells

  • Concentrations

    60 nM (EC50)

  • Incubation Time

    24 h

  • Method

    After treatment with erastin, cells were incubated with ferrostatin-1 (Fer-1) at 37˚C for 24 hr, and viability was assessed using Alamar Blue assay.
Animal Study:

[2]
  • Animal Models

    C57BL/6 mice

  • Dosages

    10 mg/kg

  • Administration

    i.n.

References

  • https://pubmed.ncbi.nlm.nih.gov/22632970/
  • https://pubmed.ncbi.nlm.nih.gov/35197442/

Customer Product Validation

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).

Data from [ , , Hepatology, 2016, 64(2):488-500 ]

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).

Data from [ , , Cancer Res, 2017, 77(8):2064-2077 ]

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).

Data from [ , , Oncogene, 2015, 10.1038/onc.2015.32 ]

(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.

Data from [ , , Mol Carcinog, 2018, 57(11):1566-1576 ]

Selleck's Ferrostatin-1 (Fer-1) Has Been Cited by 681 Publications

Ferroptosis-Mediated Hippocampal Neuronal Loss Post-mTBI: Chromatin Accessibility Profiling and Single-Nucleus Transcriptomics [ Adv Sci (Weinh), 2026, 13(12):e12362] PubMed: 41397940
Homoisoflavanone Delays Colorectal Cancer Progression via DNA Damage-Induced Mitochondrial Apoptosis and Parthanatos-Like Cell Death [ Adv Sci (Weinh), 2026, 13(19):e11406] PubMed: 41603109
FAAH initiates a positive feedback loop to promote lung adenocarcinoma progression through inhibition of ferroptosis [ Cell Death Differ, 2026, 10.1038/s41418-026-01742-5 10.1038/s41571-023-00798-3 10.1158/0008-5472.CAN-24-1607 10.1126/scitranslmed.abk2756 10.1038/s41580-024-00703-5 10.1038/s4] PubMed: 41998116
H3K18 lactylation-mediated SPHK1-SIRT1 feedback loop accelerates pyroptosis of tubular epithelial cells in sepsis-associated acute kidney injury [ Theranostics, 2026, 16(9):4768-4786] PubMed: 41799201
Slc7a11-Mediated Cystine/Glutamate Antiport Reprograms Macrophage Polarization and Ameliorates Atherosclerosis [ MedComm (2020), 2026, 7(3):e70646] PubMed: 41777250
Ipriflavone From Aquilaria malaccensis Lam. Exosome-Like Nanoparticles Targets Prolyl Hydroxylase Domain Protein 2 (PHD2) to Enhance Hypoxia-Inducible Factor-α (HIF-α) Hydroxylation Thereby Alleviating Hypoxia-Induced Gastrointestinal Mucosal Ferroptosis [ MedComm (2020), 2026, 7(4):e70722] PubMed: 41969632
Ferroptosis modulates invasion and migration in prostate cancer PC-3M subclones [ Exp Cell Res, 2026, 454(2):114847] PubMed: 41325788
Epstein-Barr Virus Latent Membrane Protein 1 Suppresses Ferroptosis via Pentose Phosphate Pathway and Glutathione Metabolism [ bioRxiv, 2026, 2026.03.09.710628] PubMed: 41959453
Inhibition of heme biosynthesis triggers cuproptosis in acute myeloid leukemia [ Cell, 2025, S0092-8674(25)01233-4] PubMed: 41265435
Lymphoma accelerates T cell and tissue aging [ Cancer Cell, 2025, S1535-6108(25)00329-0] PubMed: 40845845

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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.