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SML1075

Sigma-Aldrich

Atglistatin

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

Synonym(s):

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

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About This Item

Empirical Formula (Hill Notation):
C17H21N3O
CAS Number:
1469924-27-3
Molecular Weight:
283.37
MDL number:
MFCD28009494
UNSPSC Code:
12352200
PubChem Substance ID:
329825457
NACRES:
NA.77

product name

Atglistatin, ≥98% (HPLC)

Quality Level

100

Assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 20 mg/mL, clear

storage temp.

2-8°C

SMILES string

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)

InChI key

AWOPBSAJHCUSAS-UHFFFAOYSA-N

Application

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

Biochem/physiol Actions

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.

Other Notes

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

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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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
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
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
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