SML2227
Emricasan
≥98% (HPLC), powder, pan-caspase inhibitor
别名:
IDN-6556, N-[2-(1,1-dimethylethyl)phenyl]-2-oxoglycyl-N-[(1S)-1-(carboxymethyl)-2-oxo-3-(2,3,5,6-tetrafluorophenoxy)propyl]-L-Alaninamide, PF-03491390
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关于此项目
经验公式（希尔记法）:
C26H27F4N3O7
化学文摘社编号:
分子量:
569.50
NACRES:
NA.77
UNSPSC Code:
12352200
MDL number:
Assay:
≥98% (HPLC)
Form:
powder
产品名称
Emricasan, ≥98% (HPLC)
InChI key
SCVHJVCATBPIHN-SJCJKPOMSA-N
SMILES string
CC(C)(C)C1=C(NC(C(N[C@@H](C)C(N[C@@H](CC(O)=O)C(COC2=C(F)C(F)=CC(F)=C2F)=O)=O)=O)=O)C=CC=C1
InChI
1S/C26H27F4N3O7/c1-12(31-24(38)25(39)32-16-8-6-5-7-13(16)26(2,3)4)23(37)33-17(10-19(35)36)18(34)11-40-22-20(29)14(27)9-15(28)21(22)30/h5-9,12,17H,10-11H2,1-4H3,(H,31,38)(H,32,39)(H,33,37)(H,35,36)/t12-,17-/m0/s1
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 2 mg/mL, clear
shipped in
wet ice
storage temp.
−20°C
Biochem/physiol Actions
Antiapoptotic caspase inhibitor; Pan-Caspase Inhibitor
Emricasan is an antiapoptotic pan-caspase inhibitor. It has been in clinical trials for the treatment of non-alcoholic steatohepatitis (NASH) with advanced fibrosis (scarring) and cirrhosis. Emricasan has also been shown to protect infected astrocytes from ZIKV-induced cell death.
Emricasan, formerly known as IDN-6556, in combination with birinapan is used to treat acute myeloid leukemia (AML). This small molecule irreversible inhibitor is under clinical investigation to reduce hepatic injury and liver fibrosis.
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
The caspase-8 inhibitor emricasan combines with the SMAC mimetic birinapant to induce necroptosis and treat acute myeloid leukemia
Brumatti G, et al.
Science Translational Medicine, 8, 339ra69-339ra69 (2016)
Carcinogenicity assessment of the pan-caspase inhibitor, emricasan, in Tg.rasH2 mice
Elbekai RH, et al.
Regulatory Toxicology and Pharmacology, 72, 169-178 (2015)
Haiyan Zhang et al.
Frontiers in cardiovascular medicine, 8, 685434-685434 (2021-08-03)
Dexrazoxane (DXZ) reduces cytotoxicity caused by Doxorubicin (DOX). However, the mechanism of DXZ in ferroptosis and cardiomyopathy remains unclear. This research, therefore, explores the role and mechanism of DXZ in DOX-induced ferroptosis and cardiomyopathy in rats. Kaplan-Meier survival analysis was
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