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 Products
| 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. |
(a-d) Liproxstatin-1 treatment, given immediately after reperfusion, attenuated motor function decline measured by rotarod (a), progressive neurological deficits (b), n =8, final infarct volumes (c, right) and cognitive function decline (d). Representative TTC-stained serial brain sections 24 h after MCAO/reperfusion are shown in (c, left), scale bar=1 cm.
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| S7242 |
ErastinErastin is a ferroptosis activator by acting on mitochondrial VDAC, exhibiting selectivity for tumor cells bearing oncogenic RAS. |
PANC1 and PANC2.03 cells were treated with staurosporine or erastin (D) in the absence or presence of indicated cell death inhibitors for 24 hours. Cell viability was assayed (n = 3, *P < 0.05).
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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.
|
| 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).
|
|
| S7699 |
Liproxstatin-1Liproxstatin-1 is a potent ferroptosis inhibitor with an IC50 of 22 nM. |
(a-d) Liproxstatin-1 treatment, given immediately after reperfusion, attenuated motor function decline measured by rotarod (a), progressive neurological deficits (b), n =8, final infarct volumes (c, right) and cognitive function decline (d). Representative TTC-stained serial brain sections 24 h after MCAO/reperfusion are shown in (c, left), scale bar=1 cm.
|
| Catalog No. | Information | Product Use Citations | Product Validations |
|---|---|---|---|
| S7242 |
ErastinErastin is a ferroptosis activator by acting on mitochondrial VDAC, exhibiting selectivity for tumor cells bearing oncogenic RAS. |
2017, 551(7682):639-643 2018, 154(5):1480-1493 2017, 153(5):1429-1443 |
PANC1 and PANC2.03 cells were treated with staurosporine or erastin (D) in the absence or presence of indicated cell death inhibitors for 24 hours. Cell viability was assayed (n = 3, *P < 0.05).
|
| S8254 |
FIN56FIN56 is a specific inducer of ferroptosis . |
||
| 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. |
2019, 567(7746):118-122 2017, 547(7664):453-457 2017, 171(3):628-641 |
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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