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SML1075

Sigma-Aldrich

Atglistatin

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

Synonyme(s) :

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

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About This Item

Formule empirique (notation de Hill):
C17H21N3O
Numéro CAS:
1469924-27-3
Poids moléculaire :
283.37
Numéro MDL:
MFCD28009494
Code UNSPSC :
12352200
ID de substance PubChem :
329825457
Nomenclature NACRES :
NA.77

product name

Atglistatin, ≥98% (HPLC)

Niveau de qualité

100

Pureté

≥98% (HPLC)

Forme

powder

Couleur

white to beige

Solubilité

DMSO: 20 mg/mL, clear

Température de stockage

2-8°C

Chaîne 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)

Clé InChI

AWOPBSAJHCUSAS-UHFFFAOYSA-N

Application

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

Actions biochimiques/physiologiques

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.

Autres remarques

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

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

Certificats d'analyse (COA)

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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)
Hongyi Zhou et al.
JCI insight, 5 (2019-06-12)
Mutations in BSCL2 gene underlie human type 2 Berardinelli-Seip Congenital Lipodystrophy (BSCL2) disease. Global Bscl2-/- mice recapitulate human BSCL2 lipodystrophy and develop insulin resistance and hypertrophic cardiomyopathy. The pathological mechanisms underlying the development of lipodystrophy and cardiomyopathy in BSCL2 are
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
Lena Pernas et al.
Cell metabolism, 27(4), 886-897 (2018-04-05)
How intracellular pathogens acquire essential non-diffusible host metabolites and whether the host cell counteracts the siphoning of these nutrients by its invaders are open questions. Here we show that host mitochondria fuse during infection by the intracellular parasite Toxoplasma gondii
Kasparas Petkevicius et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 35(2), e21266-e21266 (2021-01-24)
Tissue-resident macrophages are required for homeostasis, but also contribute to tissue dysfunction in pathophysiological states. The sympathetic neurotransmitter norepinephrine (NE) induces an anti-inflammatory and tissue-reparative phenotype in macrophages. As NE has a well-established role in promoting triglyceride lipolysis in adipocytes
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