196808-24-9

Peroxisome proliferator-activated receptor (PPAR) γ is a nuclear receptor that, when activated, regulates fatty acid storage and glucose metabolism. The best known class of PPARγ ligands are the thiazolidinediones, including troglitazone (Item No. 71750) and rosiglitazone (Item No. 71740). GW 1929 is a non-thiazolidinedione activator of PPARγ that binds with a K_i value of 1.4 nM, with greater than 1,000-fold selectivity over other PPAR subtypes. It has anti-hyperglycemic and anti-hyperlipidemic activity when given orally in mouse and rat models of type 2 diabetes. Both in vitro and in vivo effects of GW 1929 on PPARγ greatly exceed those produced by troglitazone. In addition, GW 1929 has neuroprotective effects in global cerebral ischemic-reperfusion injury that are related to reduced inflammation and apoptotic DNA fragmentation.

GW1929 has been used as a peroxisome proliferator-activated receptor γ (PPARγ) ligand:
Investigating its impact on the expression of plant homeodomain finger protein 16 (Phf16) and patatin-like phospholipase domain containing 3 (Pnpla3) in relation to adipogenesis.
Examining its influence on complement component 3 (C3) gene expression in human hepatoma cells.
Activating PPARγ in human breast cancer cells.

ChEBI:GW 1929 is a member of benzophenones.

Highly selective orally active peroxisome proliferator-activated receptor (PPAR) γ agonist (pEC 50 values are 8.05, < 4 and < 4 for human PPAR γ , PPAR α and PPAR δ receptors respectively). Decreases glucose, fatty acid and triglyceride levels following oral administration in vivo .

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 was tested on currents through l-type voltage-dependent calcium channels (vdcc) in freshly isolated smooth muscle cells. using ba2+ as the charge carrier through vdcc, the ic50s for gw1929 and pioglitazone were determined to be 5.0 +/- 0.7 and 10.0 +/- 0.8 μm, respectively. gw1929 and pioglitazone were both effective on inhibiting vdcc and relaxing pressurized arteries, indicating the vasodilation of resistance arteries might be explained by the inhibition of calcium entry through vdcc [1].

gw1929 treatment attenuated the neurological damage in focal cerebral ir injury significantly. in addition, the neuroprotective effects of gw1929 were found to be associated with significant reduction in the levels of mmp-9, cox-2, inos, tnfα and il-6. neuroprotective effects of gw1929 related with significant reduction in tunel positive cells in ir challenged brain [2].

5.0 μm

Store at -20°C

[1] heppner tj,bonev ad,eckman dm,gomez mf,petkov gv,nelson mt. novel ppargamma agonists gi 262570, gw 7845, gw 1929, and pioglitazone decrease calcium channel function and myogenic tone in rat mesenteric arteries. pharmacology.2005 jan;73(1):15-22.
[2] kaundal rk,sharma ss. ameliorative effects of gw1929, a nonthiazolidinedione pparγ agonist, on inflammation and apoptosis in focal cerebral ischemic-reperfusion injury. curr neurovasc res.2011 aug 1;8(3):236-45.