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SML1075

Sigma-Aldrich

Atglistatin

≥98% (HPLC), powder, adipose triglyceride lipase inhibitor

Sinónimos:

3-(4′-(Dimethylamino)-[1,1′-biphenyl]-3-yl)-1,1-dimethylurea

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About This Item

Fórmula empírica (notación de Hill):
C17H21N3O
Número de CAS:
1469924-27-3
Peso molecular:
283.37
Número MDL:
MFCD28009494
Código UNSPSC:
12352200
ID de la sustancia en PubChem:
329825457
NACRES:
NA.77

Nombre del producto

Atglistatin, ≥98% (HPLC)

Nivel de calidad

100

Ensayo

≥98% (HPLC)

Formulario

powder

color

white to beige

solubilidad

DMSO: 20 mg/mL, clear

temp. de almacenamiento

2-8°C

cadena SMILES

CN(C)C(NC1=CC=CC(C2=CC=C(N(C)C)C=C2)=C1)=O

InChI

1S/C17H21N3O/c1-19(2)16-10-8-13(9-11-16)14-6-5-7-15(12-14)18-17(21)20(3)4/h5-12H,1-4H3,(H,18,21)

Clave InChI

AWOPBSAJHCUSAS-UHFFFAOYSA-N

Aplicación

Atglistatin has been used as a selective inhibitor of adipose triglyceride lipase (ATGL).

Acciones bioquímicas o fisiológicas

Atglistatin is a selective inhibitor of adipose triglyceride lipase (ATGL).
Atglistatin is the first selective inhibitor of adipose triglyceride lipase (ATGL), the rate limiting enzyme involved in the mobilization of fatty acids from cellular triglyceride stores. Atglistatin has an IC50 of 0.7 μM in E.coli and no activity against monoglycerol lipase (MGL), hormone-sensitive lipase (HSL), or pancreatic lipase and lipoprotein lipase PNPLA6 and PNPLA7. ATGL generates diacylglycerol from cellular triglyceride stores, which is then degraded by hormone-sensitive lipase (HSL) and monoglyceride lipase into glycerol and fatty acids, promoting the synthesis of lipotoxic metabolites that have been associated with the development of insulin resistance. Atglistatin inhibition of ATGL has been shown to reduce fatty acid mobilization in vitro and in vivo.

Otras notas

Produced under the license of University of Graz/Graz University of Technolog

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
0000305884
0000304137
0000300944
0000219884
0000188352

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Phosphorylation of Beta-3 adrenergic receptor at serine 247 by ERK MAP kinase drives lipolysis in obese adipocytes.
Hong S, et al.
Molecular Metabolism (2018)
Junichiro Mitsui et al.
The Journal of reproduction and development, 70(2), 72-81 (2024-02-05)
After pregnancy, the corpus luteum (CL) functions as a transient endocrine gland that produces progesterone, which is necessary to maintain pregnancy. To maintain constant progesterone production, CLs are enriched in lipids as its precursors. Lipid droplets (LDs) are organelles that
Xu Xiao et al.
Nature metabolism, 5(1), 165-181 (2023-01-17)
In cell models, changes in the 'accessible' pool of plasma membrane (PM) cholesterol are linked with the regulation of endoplasmic reticulum sterol synthesis and metabolism by the Aster family of nonvesicular transporters; however, the relevance of such nonvesicular transport mechanisms
Kacey J Prentice et al.
Journal of lipid research, 64(6), 100386-100386 (2023-05-13)
Levels of circulating fatty acid binding protein 4 (FABP4) protein are strongly associated with obesity and metabolic disease in both mice and humans, and secretion is stimulated by β-adrenergic stimulation both in vivo and in vitro. Previously, lipolysis-induced FABP4 secretion was found
Xirui Liu et al.
Molecular cancer, 17(1), 90-90 (2018-05-17)
Abnormal metabolism, including abnormal lipid metabolism, is a hallmark of cancer cells. Some studies have demonstrated that the lipogenic pathway might promote the development of hepatocellular carcinoma (HCC). However, the role of the lipolytic pathway in HCC has not been
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