Selective inhibitor of erastin induced ferroptosis (EC50 = 60 nM). Specifically inhibits Ras selective lethal compound -induced death, but not cell death induced by other oxidative lethal compounds and apoptosis-inducing agents. Inhibits ferroptosis in cancer cells; also inhibits glutamate-induced cell death in organotypic rat brain slices. Prevents erastin induced accumulation of cytosolic and lipid reactive oxygen species.
|Storage||Store at +4°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 262.35. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||3.81 mL||19.06 mL||38.12 mL|
|5 mM||0.76 mL||3.81 mL||7.62 mL|
|10 mM||0.38 mL||1.91 mL||3.81 mL|
|50 mM||0.08 mL||0.38 mL||0.76 mL|
References are publications that support the products' biological activity.
Dixon et al (2012) Ferroptosis: an iron-dependent form of nonapoptotic cell death. Cell 149 1060 PMID: 22632970
Louandre et al (2013) Iron-dependent cell death of hepatocellular carcinoma cells exposed to sorafenib. Int.J.Cancer 133 1732 PMID: 23505071
Skouta et al (2014) Ferrostatins inhibit oxidative lipid damage and cell death in diverse disease models. J.Am.Chem.Soc. 136 4551 PMID: 24592866
If you know of a relevant reference for Ferrostatin 1, please let us know.
Keywords: Ferrostatin 1, supplier, Selective, inhibitors, inhibits, erastin, induced, ferroptosis, RAS, selective, lethal, compound, RSL, ROS, Other, Apoptosis, Ferroptosis, Other, Apoptosis, Tocris Bioscience
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Programmed Cell Death Poster
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.