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PZ0190

Sigma-Aldrich

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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About This Item

Fórmula empírica (notación de Hill):
C29H43NO4S
Número de CAS:
166518-60-1
Peso molecular:
501.72
Número MDL:
MFCD00934956
Código UNSPSC:
12352200
ID de la sustancia en PubChem:
329823764

Ensayo

≥98% (HPLC)

Formulario

powder

color

white to tan

solubilidad

DMSO: ≥40 mg/mL

enfermedades relevantes

Alzheimer′s disease; cardiovascular diseases

temp. de almacenamiento

room temp

cadena SMILES

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

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)

Clave InChI

PTQXTEKSNBVPQJ-UHFFFAOYSA-N

Categorías relacionadas

Aplicación

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.

Acciones bioquímicas o fisiológicas

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

Información legal

Sold for research purposes under agreement from Pfizer Inc.

Código de clase de almacenamiento

11 - Combustible Solids

Clase de riesgo para el agua (WGK)

WGK 3

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable

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Certificados de análisis (COA)

Lot/Batch Number
0000351974
0000351974
0000237848
061M4740V
0000184190

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Colin Berry et al.
Circulation, 115(14), 1851-1857 (2007-03-29)
The relative merits of quantitative coronary analysis (QCA) and intravascular ultrasound (IVUS) for the assessment of progression/regression in coronary artery disease are uncertain. To explore this subject further, we analyzed the angiographic and IVUS data derived from a contemporary clinical
Stephen G Worthley et al.
Pathophysiology of haemostasis and thrombosis, 36(1), 9-17 (2008-03-12)
The ability to modify the enzymatic processes involved in promoting atherosclerotic plaque disruption and to serially monitor atherosclerotic evolution could provide novel information in the management of patients with atherosclerosis. We studied the effects of a statin (atorvastatin) and its
Marcelo F Di Carli et al.
Journal of nuclear medicine : official publication, Society of Nuclear Medicine, 52(9), 1369-1377 (2011-08-19)
The metabolic syndrome affects 25% of the U.S. population and greatly increases the risk of diabetes and coronary artery disease (CAD). We tested the hypothesis that the metabolic syndrome is associated with impaired coronary vasodilator function, a marker of atherosclerotic
Jasminder Sahi et al.
The Journal of pharmacology and experimental therapeutics, 306(3), 1027-1034 (2003-05-27)
In vitro and clinical studies were conducted to characterize the potential of avasimibe, an acyl-CoA/cholesterol acyltransferase inhibitor to cause drug-drug interactions. Clinically, 3- and 6-fold increases in midazolam (CYP3A4 substrate) oral clearance were observed after 50 and 750 mg of
Akira Miyazaki et al.
Current drug targets. Cardiovascular & haematological disorders, 5(6), 463-469 (2006-03-01)
Acyl-coenzyme A: cholesterol acyltransferase (ACAT) is an intracellular enzyme that catalyzes the formation of cholesterol esters from cholesterol and fatty acyl-coenzyme A. Animal experiments showed that ACAT inhibitors reduce plasma cholesterol levels by suppressing absorption of dietary cholesterol and by
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