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Merck
CN

SML3669

Sigma-Aldrich

F-1394

≥98% (HPLC)

Synonym(s):

(1S,2S)-2-(3-neopentyl-3-nonylureido)cyclohexyl 3-((R)-2,2,5,5-tetramethyl-1,3-dioxane-4-carboxamido)propanoate, F 1394, F1394, N-[[(4R)-2,2,5,5-Tetramethyl-1,3-dioxan-4-yl]carbonyl]-β-alanine (1S,2S)-2-[[[(2,2-dimethylpropyl)nonylamino]carbonyl]amino]cyclohexyl ester

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About This Item

Empirical Formula (Hill Notation):
C33H61N3O6
CAS Number:
162490-89-3
Molecular Weight:
595.85
UNSPSC Code:
51111800
NACRES:
NA.21

Key Documents

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Quality Level

100

Assay

≥98% (HPLC)

form

(Powder or solid or semi-solid or liquid)

color

white to beige

solubility

DMSO: 2 mg/mL, clear

storage temp.

-10 to -25°C

SMILES string

CCCCCCCCCN(C(N[C@H]1CCCC[C@@H]1OC(CCNC([C@H]2C(C)(COC(C)(O2)C)C)=O)=O)=O)CC(C)(C)C

InChI key

NWLFOBZKYXKBOF-NSVAZKTRSA-N

Related Categories

Biochem/physiol Actions

F1394 is an orally available, potent and selective Acyl-CoA:cholesterol acyltransferase (ACAT) inhibitor that reduces plaque foam cell formation without inflammatory or toxic effects.
Orally available, potent and selective Acyl-CoA:cholesterol acyltransferase (ACAT) inhibitor

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

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Certificates of Analysis (COA)

Lot/Batch Number
0000242279
0000242279

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T Chiwata et al.
British journal of pharmacology, 133(7), 1005-1012 (2001-08-07)
The acyl-CoA:cholesterol acyltransferase (ACAT) enzyme is thought to be responsible for foam cell formation and the subsequent progression of atherosclerosis. The apolipoprotein E and low density lipoprotein receptor double knockout (apoE/LDLr-DKO) mouse is an animal model that develops severe hyperlipidaemia
Jaume Amengual et al.
Molecular pharmacology, 99(3), 175-183 (2021-01-02)
Acyl-CoA:cholesterol acyltransferase (ACAT) mediates cellular cholesterol esterification. In atherosclerotic plaque macrophages, ACAT promotes cholesteryl ester accumulation, resulting in foam cell formation and atherosclerosis progression. Its complete inactivation in mice, however, showed toxic effects because of an excess of free cholesterol

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