Basic information Safety Supplier Related

AA9

Basic information Safety Supplier Related

AA9 Basic information

Product Name:
AA9
Synonyms:
  • SRS11-92
  • Benzoic acid, 4-(cyclohexylamino)-3-[(phenylmethyl)amino]-, ethyl ester
  • HT-1080,FRDA,Friedreich,Inhibitor,cell death,ataxia,SRS-11-92,SRS1192,Ferroptosis,inhibit,SRS11 92,SRS11-92
  • Ethyl 3-(benzylamino)-4-(cyclohexylamino)benzoate
  • SRS11-92, 10 mM in DMSO
CAS:
1467047-25-1
MF:
C22H28N2O2
MW:
352.47
Mol File:
1467047-25-1.mol
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AA9 Chemical Properties

Boiling point:
523.7±45.0 °C(Predicted)
Density 
1.152±0.06 g/cm3(Predicted)
storage temp. 
4°C, protect from light
solubility 
DMF: 30 mg/ml; DMF:PBS (pH 7.2) (1:4): 0.2 mg/ml; DMSO: 10 mg/ml; Ethanol: 10 mg/ml
form 
A crystalline solid
pka
5.48±0.20(Predicted)
color 
White to off-white
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AA9 Usage And Synthesis

Uses

SRS11-92, a Ferrostatin-1 (Fer-1) analogue, is a potent ferroptosis inhibitor. SRS11-92 inhibits ferroptotic cell death induced by Erastin in HT-1080 human fibrosarcoma cells (EC50=6 nM)[1].

Definition

ChEBI: SRS11-92 is an ethyl ester resulting from the formal condensation of the carboxy group of 3-(benzylamino)-4-(cyclohexylamino)benzoic acid with ethanol. It is a potent inhibitor of ferroptosis induced by erastin in HT-1080 human fibrosarcoma cells (EC50 = 6 nM). It has a role as a ferroptosis inhibitor. It is a substituted aniline, an ethyl ester, a secondary amino compound and a diamine. It is functionally related to a ferrostatin-1.

Biological Activity

SRS11-92 is a cell penetrant and potent inhibitor of ferroptosis th at 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.

in vivo

SRS11-92, used at 500 nM, is efficacious in protecting human and mouse cellular models of Friedreich ataxia (FRDA) treated with ferric ammonium citrate (FAC) and an inhibitor of glutathione synthesis (BSO), whereas caspase-3 inhibitors fail to show significant biological activity[2].

References

[1] Skouta R, et al. Ferrostatins inhibit oxidative lipid damage and cell death in diverse disease models. J Am Chem Soc. 2014;136(12):4551-4556. DOI:10.1021/ja411006a
[2] Cotticelli MG, et al. Ferroptosis as a Novel Therapeutic Target for Friedreich's Ataxia. J Pharmacol Exp Ther. 2019;369(1):47-54. DOI:10.1124/jpet.118.252759

AA9Supplier

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