
- Ferrostatin-1 (Fer-1)
Liproxstatin-1A potent ferroptosis inhibitor |
Sample solution is provided at 25 µL, 10mM.
































Quality Control & MSDS
- View current batch:
- Purity = 99.71%
- COA (Certificate Of Analysis)
- HPLC
- NMR (Nuclear Magnetic Resonance)
- MSDS (Material Safety Data Sheet)
- Datasheet
Chemical structure

Cell experiment [1]: | |
Cell lines | Gpx4-/- cells |
Preparation method | The solubility of this compound in DMSO is > 10.5 mg/mL. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below - 20 °C for several months. |
Reacting condition | 72 hrs |
Applications | Liproxstatin-1 inhibited the growth of Gpx4-/- cells with an IC50 value of 22 nM. At the dose of 50 nM, Liproxstatin-1 completely prevented lipid peroxidation. Liproxstatin-1 (200 nM) dose-dependently protected Gpx4-/- cells against ferroptosis-inducing agents, such as L-buthionine sulphoximine (10 μM), erastin (1 μM) and RSL3 (0.5 μM), whereas it failed to rescue cell death caused by staurosporine (0.2 μM) and H2O2 (200 μM). |
Animal experiment [1]: | |
Animal models | GreERT2; Gpx4fl/fl mice |
Dosage form | 10 mg/kg; i.p. |
Applications | In GreERT2; Gpx4fl/fl mice, Liproxstatin-1 significantly extended the survival period. The TUNEL staining results after 9-day treatment showed a markedly reduced number of TUNEL+ cells in the Liproxstatin-1 treatment group than in the vehicle control group, indicating that Liproxstatin-1 delayed ferroptosis in tubular cells. |
Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
References: [1]. Friedmann Angeli JP, Schneider M, Proneth B, et al. Inactivation of the ferroptosis regulator Gpx4 triggers acute renal failure in mice. Nat Cell Biol, 2014, 16(12): 1180-1191. |

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Cas No. | 950455-15-9 | SDF | Download SDF |
Synonyms | N/A | ||
Chemical Name | N-(3-chlorobenzyl)-4"H-spiro[piperidine-4,3"-quinoxalin]-2"-amine | ||
Canonical SMILES | ClC1=CC(CNC(C2(CCNCC2)N3)=NC4=C3C=CC=C4)=CC=C1 | ||
Formula | C19H21ClN4 | M.Wt | 340.85 |
Solubility | ≥10.5mg/mL in DMSO | Storage | Store at -20°C |
Physical Appearance | A solid | Shipping Condition | Evaluation sample solution : ship with blue ice.All other available size:ship with RT , or blue ice upon request |
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. |
Liproxstatin-1 is a potent inhibitor of ferroptosis with IC50 value of 22 nM [1].
Ferroptosis is an iron-dependent non-apoptotic form of cell death induced by small molecules in engineered cells overexpressing oncogenic RAS and specific tumour types [1].
Liproxstatin-1 is a potent ferroptosis inhibitor. Liproxstatin-1 showed inhibition against ferroptosis-inducing agent (FIN) -triggered cell death. In Gpx4-/- cells, liproxstatin-1 inhibited RSL3-induced BODIPY 581/591 C11 oxidation. In primary human renal proximal tubule epithelial cells (HRPTEpiCs), liproxstatin-1 inhibited RSL3-induced cell death. Knock down Gpx4 in the immortalized human renal proximal tubule epithelial cell line (HK-2) cells made cells more sensitive to FIN [1].
On TAM treatment of CreERT2; Gpx4fl/fl mice, liproxstatin-1 significantly extended survival time and reduced number of TUNELC cells, which suggested that liproxstatin-1 delayed ferroptosis in tubular cells. In a hepatic ischaemia/reperfusion injury model, liproxstatin-1 mitigated tissue injury induced by ischaemia/reperfusion [1].
Reference:[1]. Friedmann Angeli JP, Schneider M, Proneth B, et al. Inactivation of the ferroptosis regulator Gpx4 triggers acute renal failure in mice. Nat Cell Biol, 2014, 16(12): 1180-1191.
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