G5668
GW1929 hydrate
>98% (HPLC), solid
Synonym(s):
N-(2-Benzoylphenyl)-O-[2-(methyl-2-pyridinylamino)ethyl]-L-tyrosine hydrate
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About This Item
Empirical Formula (Hill Notation):
C30H29N3O4 · xH2O
CAS Number:
Molecular Weight:
495.57 (anhydrous basis)
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
Recommended Products
Quality Level
Assay
>98% (HPLC)
form
solid
solubility
DMSO: 20 mg/mL
originator
GlaxoSmithKline
SMILES string
[H]O[H].CN(CCOc1ccc(C[C@H](Nc2ccccc2C(=O)c3ccccc3)C(O)=O)cc1)c4ccccn4
InChI
1S/C30H29N3O4.H2O/c1-33(28-13-7-8-18-31-28)19-20-37-24-16-14-22(15-17-24)21-27(30(35)36)32-26-12-6-5-11-25(26)29(34)23-9-3-2-4-10-23;/h2-18,27,32H,19-21H2,1H3,(H,35,36);1H2/t27-;/m0./s1
InChI key
XSITZVFUXCLFMK-YCBFMBTMSA-N
Gene Information
human ... PPARG(5468)
Application
GW1929 has been used as a peroxisome proliferator-activated receptor γ (PPARγ) ligand:
- to study its effects on plant homeodomain finger protein 16 (Phf16) and patatin-like phospholipase domain containing 3 (Pnpla3) expression involved in adipogenesis
- to study its effects on complement component 3 (C3) gene expression in human hepatoma cells
- to activate PPARγ in human breast cancer cells
Biochem/physiol Actions
GW1929 is a non-thiazolidinedione and is involved in cell growth inhibition and regulating gene expression. It exhibits neuroprotective effects against global cerebral ischemic-reperfusion injury by DNA fragmentation and minimizing the inflammation. GW1929 participates in the inhibition of α7 N-acetylcholine receptor expression and promoter activity. It also influences the early growth response-1 (Egr-1) protein expression.
GW1929 is a high affinity agonist of PPAR-γ.
Features and Benefits
This compound is featured on the Nuclear Receptors (PPARs) page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.
This compound was developed by GlaxoSmithKline. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.
Legal Information
Sold for research purposes only, pursuant to an agreement with GlaxoSmithKline
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
Certificates of Analysis (COA)
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Seo-Hyuk Chang et al.
Journal of cellular biochemistry, 120(3), 3599-3610 (2018-10-03)
Adipocyte differentiation is controlled by multiple signaling pathways. To identify new adipogenic factors, C3H10T1/2 adipocytes were treated with previously known antiadipogenic phytochemicals (resveratrol, butein, sulfuretin, and fisetin) for 24 hours. Commonly regulated genes were then identified by transcriptional profiling analysis. Three
Ravinder K Kaundal et al.
Behavioural brain research, 216(2), 606-612 (2010-09-14)
Transient global cerebral ischemia results in acute neurodegeneration in selective brain areas. Global cerebral ischemic-reperfusion (IR) injury induced selective hippocampal damage results into various neurobehavioral deficits including spatial memory and learning deficiencies. In this study, we have investigated the protective
Miaozhen Pan et al.
Experimental eye research, 202, 108332-108332 (2020-11-06)
Form deprivation myopia (FDM) is characterized by loss of choroidal thickness (ChT), reduced choroidal blood perfusion (ChBP), and consequently scleral hypoxia. In some tissues, changes in levels of peroxisome proliferator-activated receptor γ (PPARγ) expression modulate hypoxia-induced pathological responses. We determined
Vladimir S Shavva et al.
European journal of cell biology, 97(3), 204-215 (2018-03-20)
C3 is an acute phase protein, and thus its plasma concentration increases quickly and drastically during the onset of inflammation. Insulin plays a complex role in inflammation. Elevated level of plasma C3 was shown to correlate with heightened fasting insulin
Swei Sunny Hahn et al.
Cellular signalling, 26(4), 730-739 (2014-01-15)
Studies demonstrated that peroxisome proliferator-activated receptor gamma (PPARγ) ligands reduce nicotine-induced non small cell lung carcinoma (NSCLC) cell growth through inhibition of nicotinic acetylcholine receptor (nAChR) mediated signaling pathways. However, the mechanisms by which PPARγ ligands inhibited nAChR expression remain
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