SML1075
Atglistatin
≥98% (HPLC), powder, adipose triglyceride lipase inhibitor
Synonym(s):
3-(4′-(Dimethylamino)-[1,1′-biphenyl]-3-yl)-1,1-dimethylurea
Sign In to View Organizational & Contract Pricing.
Select a Size
Change View
About This Item
Empirical Formula (Hill Notation):
C17H21N3O
CAS Number:
Molecular Weight:
283.37
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
MDL number:
Product Name
Atglistatin, ≥98% (HPLC)
Quality Level
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 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.
Other Notes
Produced under the license of University of Graz/Graz University of Technolog
Still not finding the right product?
Explore all of our products under Atglistatin
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Choose from one of the most recent versions:
Already Own This Product?
Find documentation for the products that you have recently purchased in the Document Library.
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