Fer-1 (Ferrostatin-1)

Catalog No.S7243 Batch:S724304

Print

Technical Data

Formula

C15H22N2O2
Molecular Weight 262.35 CAS No. 347174-05-4
Solubility (25°C)* In vitro DMSO 52 mg/mL (198.2 mM)
Ethanol 52 mg/mL (198.2 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.
* <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 Fer-1 (Ferrostatin-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 (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. [1]
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.[2]

Protocol (from reference)

Cell Assay:

[1]
  • Cell lines

    HT-1080 cells

  • Concentrations

    60 nM (EC50)

  • Incubation Time

    24 h

  • Method

    Erastin treated cells were incubated with ferrostatin-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 Fer-1 (Ferrostatin-1) has been cited by 667 publications

Lymphoma accelerates T cell and tissue aging [ Cancer Cell, 2025, S1535-6108(25)00329-0] PubMed: 40845845
Radiotherapy promotes cuproptosis and synergizes with cuproptosis inducers to overcome tumor radioresistance [ Cancer Cell, 2025, S1535-6108(25)00132-1] PubMed: 40215978
Cytosolic cytochrome c represses ferroptosis [ Cell Metab, 2025, S1550-4131(25)00149-4] PubMed: 40233758
RIPK1 senses S-adenosylmethionine scarcity to drive cell death and inflammation [ Cell Metab, 2025, S1550-4131(25)00294-3] PubMed: 40570842
Harnessing the FGFR2/NF2/YAP signaling-dependent necroptosis to develop an FGFR2/IL-8 dual blockade therapeutic strategy [ Nat Commun, 2025, 16(1):4128] PubMed: 40319089
Senescence-associated lysosomal dysfunction impairs cystine deprivation-induced lipid peroxidation and ferroptosis [ Nat Commun, 2025, 16(1):6617] PubMed: 40731111
Obesity-associated macrophages dictate adipose stem cell ferroptosis and visceral fat dysfunction by propagating mitochondrial fragmentation [ Nat Commun, 2025, 16(1):7564] PubMed: 40813577
S100P is a ferroptosis suppressor to facilitate hepatocellular carcinoma development by rewiring lipid metabolism [ Nat Commun, 2025, 16(1):509] PubMed: 39779666
Iron supplementation alleviates pathologies in a mouse model of facioscapulohumeral muscular dystrophy [ J Clin Invest, 2025, e181881] PubMed: 40591405
PIP5K1A Suppresses Ferroptosis and Induces Sorafenib Resistance by Stabilizing NRF2 in Hepatocellular Carcinoma [ Adv Sci (Weinh), 2025, 12(30):e04372] PubMed: 40405713

RETURN POLICY
Selleck Chemical’s Unconditional Return Policy ensures a smooth online shopping experience for our customers. If you are in any way unsatisfied with your purchase, you may return any item(s) within 7 days of receiving it. In the event of product quality issues, either protocol related or product related problems, you may return any item(s) within 365 days from the original purchase date. Please follow the instructions below when returning products.

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.