Ferroptosis
- Inhibitory Selectivity
- Solubility
| Catalog No. | Product Name | Solubility(25°C) | ||
|---|---|---|---|---|
| Water | DMSO | Alcohol | ||
| S7243 | Ferrostatin-1 (Fer-1) | <1 mg/mL | 52 mg/mL | 52 mg/mL |
| S7699 | Liproxstatin-1 | <1 mg/mL | 68 mg/mL | 21 mg/mL |
| S7242 | Erastin | <1 mg/mL | 19 mg/mL | <1 mg/mL |
| S8254 | FIN56 | <1 mg/mL | 100 mg/mL | <1 mg/mL |
| S8155 | RSL3 | <1 mg/mL | 88 mg/mL | 22 mg/mL |
- Ferroptosis Inhibitors (5)
| Catalog No. | Information | Product Use Citations | Product Validations |
|---|---|---|---|
| S7243 |
Ferrostatin-1 (Fer-1)Ferrostatin-1 (Fer-1) is a potent and selective inhibitor of ferroptosis with EC50 of 60 nM. |
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).
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| S7699 |
Liproxstatin-1Liproxstatin-1 is a potent ferroptosis inhibitor with an IC50 of 22 nM. |
(D) Indicated NRF2 knockdown HCC cells were treated with erastin (10 μM) and sorafenib (5 μM) with or without indicated inhibitors (ferrostatin-1, 1 μM; liproxstatin-1, 100 nM; ZVAD-FMK, 10 μM; necrostatin-1, 10 μM; necrosulfonamide, 0.5 μM) for 24 hours, and cell viability was assayed (n 5 3, *P < 0.05). Abbreviation: GAPDH, glyceraldehyde 3-phosphate dehydrogenase. |
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| S7242 |
ErastinErastin is a ferroptosis activator by acting on mitochondrial VDAC, exhibiting selectivity for tumor cells bearing oncogenic RAS. |
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, 100 nM; 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).
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| S8254 |
FIN56FIN56 is a specific inducer of ferroptosis . |
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| S8155 |
RSL3RSL3 is a ferroptosis activator in a VDAC-independent manner,exhibiting selectivity for tumor cells bearing oncogenic RAS. RSL3 binds, inactivates GPX4 and thus mediates GPX4-regulated ferroptosis. |
Fluvastatin treatment of HT-1080 cells decreases GPX4 protein levels in a time- and concentration-dependent manner and synergized with co-treatment with the direct GPX4 inhibitor RSL3.
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