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Key Documents

S9318

Sigma-Aldrich

Sandoz 58-035

>98% (HPLC), powder, acyl-CoA:cholesterol acyltransferase (ACAT) inhibitor

Synonyme(s) :

3-[Decyldimethylsilyl]-N-[2-(4-methylphenyl)-1-phenethyl]propanamide, SA 58-035

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About This Item

Formule empirique (notation de Hill):
C30H47NOSi
Numéro CAS:
Poids moléculaire :
465.79
Numéro MDL:
Code UNSPSC :
41121801
ID de substance PubChem :
Nomenclature NACRES :
NA.77

product name

Sandoz 58-035, >98% (HPLC), powder

Niveau de qualité

Pureté

>98% (HPLC)

Forme

powder

Couleur

white

Solubilité

DMSO: 16 mg/mL
H2O: insoluble

Auteur

Novartis

Température de stockage

2-8°C

Chaîne SMILES 

CCCCCCCCCC[Si](C)(C)CCC(=O)NC(Cc1ccc(C)cc1)c2ccccc2

InChI

1S/C30H47NOSi/c1-5-6-7-8-9-10-11-15-23-33(3,4)24-22-30(32)31-29(28-16-13-12-14-17-28)25-27-20-18-26(2)19-21-27/h12-14,16-21,29H,5-11,15,22-25H2,1-4H3,(H,31,32)

Clé InChI

NBYATBIMYLFITE-UHFFFAOYSA-N

Informations sur le gène

human ... SOAT1(6646)
rat ... Soat1(81782)

Application

Sandoz 58-035 was used to induce simultaneous activation of unfolded protein response (UPR) and pattern recognition receptors (PRRs) in mouse peritoneal macrophages.3

Actions biochimiques/physiologiques

Sandoz 58-035 inhibits the accumulation of cholesteryl esters and inhibits the esterification of cholesterol by 95% in arterial smooth muscle cells in culture.1 It does not affect the triglyceride metabolism by the gut.2
Acyl-CoA:cholesterol acyltransferase (ACAT) inhibitor.

Caractéristiques et avantages

This compound was developed by Novartis. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Équipement de protection individuelle

Eyeshields, Gloves, type N95 (US)


Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

Markus Trieb et al.
Journal of hepatology, 73(1), 113-120 (2020-02-18)
High-density lipoprotein cholesterol (HDL-C) levels are reduced in patients with chronic liver disease and inversely correlate with disease severity. During acute conditions such as sepsis, HDL-C levels decrease rapidly and HDL particles undergo profound changes in their composition and function.
Masato Furuhashi et al.
Scientific reports, 7(1), 217-217 (2017-03-18)
Cholesterol efflux capacity (CEC) from macrophages, the first step in the reverse cholesterol transport pathway, is inversely associated with residual risk for atherosclerotic cardiovascular disease. Fatty acid-binding protein 4 (FABP4) and FABP5 are expressed in both adipocytes and macrophages and
Julia T Stadler et al.
Biomedicines, 9(3) (2021-03-07)
Obesity increases the risk of coronary heart disease, partly due to its strong association with atherogenic dyslipidemia, characterized by high triglycerides and low high-density lipoprotein (HDL) cholesterol levels. Functional impairment of HDL may contribute to the increased cardiovascular mortality, but
Irene Schilcher et al.
Scientific reports, 7(1), 12485-12485 (2017-10-04)
Endothelial lipase (EL) is a potent modulator of the structural and functional properties of HDL. Impact of EL on cholesterol efflux capacity (CEC) of serum and isolated HDL is not well understood and apparently contradictory data were published. Here, we
Shizuya Yamashita et al.
Journal of clinical lipidology, 12(5), 1267-1279 (2018-08-06)
Cardiovascular risk is negatively correlated with cholesterol efflux capacity (CEC) from macrophages to high-density lipoproteins (HDLs) and positively correlated with fasting and nonfasting triglyceride-rich lipoproteins (TRLs). Pemafibrate, a novel selective peroxisome proliferator-activated receptor α modulator, robustly decreases the fasting TRL

Articles

Cholesterol esterification enhances transport efficiency in lipoproteins for increased blood stream transport.

Cholesterol esterification enhances transport efficiency in lipoproteins for increased blood stream transport.

Cholesterol esterification enhances transport efficiency in lipoproteins for increased blood stream transport.

Cholesterol esterification enhances transport efficiency in lipoproteins for increased blood stream transport.

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