PZ0190
Avasimibe
≥98% (HPLC)
Sinónimos:
CI-1011; PD 148515; [[2,4,6-tris(1-methylethyl)phenyl]acetyl]-, 2,6-bis(1-methylethyl)phenyl ester] sulfamic acid
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Acerca de este artículo
Fórmula empírica (notación de Hill):
C29H43NO4S
Número CAS:
Peso molecular:
501.72
UNSPSC Code:
12352200
PubChem Substance ID:
MDL number:
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Permítanos ayudarleNombre del producto
Avasimibe, ≥98% (HPLC)
InChI
1S/C29H43NO4S/c1-17(2)22-14-25(20(7)8)27(26(15-22)21(9)10)16-28(31)30-35(32,33)34-29-23(18(3)4)12-11-13-24(29)19(5)6/h11-15,17-21H,16H2,1-10H3,(H,30,31)
SMILES string
CC(C)c1cc(C(C)C)c(CC(=O)NS(=O)(=O)Oc2c(cccc2C(C)C)C(C)C)c(c1)C(C)C
InChI key
PTQXTEKSNBVPQJ-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
powder
color
white to tan
solubility
DMSO: ≥40 mg/mL
relevant disease(s)
Alzheimer′s disease; cardiovascular diseases
storage temp.
room temp
Quality Level
Categorías relacionadas
Application
Avasimibe has been used as an inhibitor of acyl-coenzyme A: cholesterol acyltransferase (ACAT) in Huh7.5.1 cells for testing its combination with direct-acting antivirals (DAAs) and to test its effect on lipid droplet accumulation in acidosis-adapted cancer cells. It may be used as an inhibitor of ACAT to assess cholesterol esterification in Trypanosoma cruzi.
Biochem/physiol Actions
Avasimibe (CI-1011) is an orally bioavailable Acyl-CoA:Cholesterol O-Acyltransferase (ACAT) inhibitor. It was originally developed as an antilepic drug, and was shown to significantly reduce plasma total triglyceride and VLDL-cholesterol, but later clinical trials were disappointing. ACAT has also been investigated as a potential therapeutic target for Alzheimer′s disease. Recent studies have looked at the effects of avasimibe in reducing amyloid pathology by limiting generation and increasing clearance of diffusible amyloid-beta (Abeta).
Avasimibe is an orally bioavailable Acyl-CoA:Cholesterol O-Acyltransferase (ACAT) inhibitor
Clase de almacenamiento
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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Yves Rival et al.
DNA and cell biology, 23(5), 283-292 (2004-06-01)
It is now recognized that atherosclerosis complications are related to the unstable character of the plaque rather than its volume. Vulnerable plaques often contain a large lipid core, a reduced content of smooth muscle cells, and accumulation of inflammatory cells.
John R Burnett et al.
Biochimica et biophysica acta, 1738(1-3), 10-18 (2006-01-24)
Previously, we have shown, in vivo, that the acyl coenzyme A: cholesterol acyltransferase (ACAT) inhibitor avasimibe decreases hepatic apolipoprotein (apo) B secretion into plasma. To test the hypothesis that avasimibe modulates postprandial triglyceride-rich lipoprotein (TRL) metabolism in vivo, an oral
John R Burnett et al.
Current opinion in investigational drugs (London, England : 2000), 3(9), 1328-1333 (2002-12-25)
Avasimibe (also known as CI-1011 or PD-148515) is a selective acyl-coenzyme A:cholesterol O-acyltransferase (ACAT) inhibitory lipid-regulating agent under development by Pfizer (formerly Parke-Davis) for the potential treatment of hyperlipidemia and atherosclerosis. The compound is currently undergoing phase III clinical trials
Jean-Claude Tardif et al.
Circulation, 110(21), 3372-3377 (2004-11-10)
Inhibition of the acyl coenzyme A:cholesterol acyltransferase (ACAT) enzyme may prevent excess accumulation of cholesteryl esters in macrophages. The ACAT inhibitor avasimibe was shown to reduce experimental atherosclerosis. This study was designed to investigate the effects of avasimibe on human
Jean-Claude Tardif et al.
The American journal of cardiology, 98(1), 23-27 (2006-06-21)
We assessed vascular changes during atherosclerosis regression. Compensatory enlargement of coronary arteries accommodates plaque burden during atherosclerosis development. Lipid-lowering therapy has altered the natural history of coronary atherosclerosis, but the arterial changes that occur during disease regression need to be
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