SML2746
SRS11-92
≥98% (HPLC)
别名:
4-(Cyclohexylamino)-3-[(phenylmethyl)amino]-benzoic acid ethyl ester, Ethyl 3-(benzylamino)-4-(cyclohexylamino)benzoate
InChI key
VHQAJFNLPQULSV-UHFFFAOYSA-N
SMILES string
N(C3CCCCC3)c1c(cc(cc1)C(=O)OCC)NCc2ccccc2
assay
≥98% (HPLC)
form
powder
color
white to yellow-brown
solubility
DMSO: 2 mg/mL, clear
storage temp.
2-8°C
Quality Level
Biochem/physiol Actions
SRS11-92 is a cell penetrant and potent inhibitor of ferroptosis that attenuates the cell death associated with frataxin knockdown in healthy human fibroblasts. SRS11-92 protects against cell death in in a brain slice model of Huntington′s disease, an oligodendrocyte model of periventricular leukomalacia, and in isolated kidney proximal tubules model of kidney disfunction.
cell penetrant and potent inhibitor of ferroptosis that attenuates the cell death associated with frataxin knockdown in healthy human fibroblasts
存储类别
11 - Combustible Solids
wgk
WGK 3
法规信息
新产品
此项目有
Sam Hofmans et al.
Journal of medicinal chemistry, 59(5), 2041-2053 (2015-12-24)
Ferroptosis is a nonapoptotic, iron-catalyzed form of regulated necrosis that is critically dependent on glutathione peroxidase 4 (GPX4). It has been shown to contribute to liver and kidney ischemia reperfusion injury in mice. A chemical inhibitor discovered by high-throughput screening
Rachid Skouta et al.
Journal of the American Chemical Society, 136(12), 4551-4556 (2014-03-07)
Ferrostatin-1 (Fer-1) inhibits ferroptosis, a form of regulated, oxidative, nonapoptotic cell death. We found that Fer-1 inhibited cell death in cellular models of Huntington's disease (HD), periventricular leukomalacia (PVL), and kidney dysfunction; Fer-1 inhibited lipid peroxidation, but not mitochondrial reactive
M Grazia Cotticelli et al.
The Journal of pharmacology and experimental therapeutics, 369(1), 47-54 (2019-01-13)
Friedreich ataxia (FRDA) is a progressive neuro- and cardio-degenerative disorder characterized by ataxia, sensory loss, and hypertrophic cardiomyopathy. In most cases, the disorder is caused by GAA repeat expansions in the first introns of both alleles of the FXN gene
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