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S9318

Sigma-Aldrich

Sandoz 58-035

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

Sinonimo/i:

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

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About This Item

Formula empirica (notazione di Hill):
C30H47NOSi
Numero CAS:
78934-83-5
Peso molecolare:
465.79
Numero MDL:
MFCD00161339
Codice UNSPSC:
41121801
ID PubChem:
24278227
NACRES:
NA.77

Nome del prodotto

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

Livello qualitativo

100

Saggio

>98% (HPLC)

Stato

powder

Colore

white

Solubilità

DMSO: 16 mg/mL
H2O: insoluble

Ideatore

Novartis

Temperatura di conservazione

2-8°C

Stringa SMILE

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)
NBYATBIMYLFITE-UHFFFAOYSA-N

Informazioni sul gene

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

Applicazioni

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

Azioni biochim/fisiol

Acyl-CoA:cholesterol acyltransferase (ACAT) inhibitor.
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

Caratteristiche e vantaggi

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

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable

Dispositivi di protezione individuale

Eyeshields, Gloves, type N95 (US)

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Certificati d'analisi (COA)

Lot/Batch Number
065M4602V
122M4604V
022M4605V
103K4708

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Makiko Fukunaga et al.
Experimental cell research, 316(19), 3272-3281 (2010-09-22)
Mast cell is one of the central effectors in inflammatory responses. Recent studies suggest that a promising therapeutic approach for various inflammatory immune diseases, including rheumatoid arthritis, multiple sclerosis, and type I allergies, is to inhibit mast cell growth and/or
C Mazière et al.
Biochimica et biophysica acta, 1300(1), 30-34 (1996-03-29)
The effects of interleukin 1beta (IL1) in the range of concentration of 10-30 ng/ml on cholesterol metabolism were investigated in the monocyte-macrophage cell line J774. IL1 enhanced cholesterol esterification by [14C]oleic acid and acyl-coenzyme A cholesterol acyl transferase activity in
K Cianflone et al.
Atherosclerosis, 107(2), 125-135 (1994-06-01)
This study examines the effects of extracellular albumin on hepatic apo B-100 metabolism. To do so, a transformed human liver cell line, HepG2, was used as a hepatocyte model and the concentration of albumin in the medium was varied between
H Hakamata et al.
Arteriosclerosis and thrombosis : a journal of vascular biology, 14(11), 1860-1865 (1994-11-01)
The species difference in the turnover rates of the cholesteryl ester (CE) cycle in macrophage foam cells (MFC) was examined in mice and rats. MFC were induced by acetyl-LDL and pulsed with [3H]oleate, followed by a chase with [14C]oleate. The
Charlotte P J Talbot et al.
Atherosclerosis, 274, 23-28 (2018-05-11)
Obesity is associated with a lower HDL-mediated cholesterol efflux from macrophages and a higher CETP (cholesteryl ester transfer protein) activity, but effects of weight loss are not clear. In addition, associations with visceral and subcutaneous adipose tissue are not known.
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Articoli

Cholesterol Esterification

Cholesterol undergoes esterification to improve transport. Cholesterol esters are more easily packaged into the interior of lipoproteins - increasing the quantity that can be readily transported in the blood stream.

Antilipemic Agents

Randomized controlled clinical studies have suggested 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are effective in both primary and secondary prevention of cardiovascular disease (CVD) events.

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