BADGE
PPARγ antagonist / PPARγ antagonist with μM affinity in 3T3-L1 and 3T3-F442A preadipocyte cells. Selective over PPARδ and PPARα. Antagonizes the ability of rosiglitazone to stimulate transcriptional activity of PPARγ and abolishes its anti-inflammatory effects in a mouse model1. Induces apoptosis via PPARγ-independent mechanisms2. Induces adipogenesis in human and mouse mesenchymal stromal stem cells and in mouse 3T3-L1 preadipocytes at low nM concentrations via a PPARγ independent mechanism3. Increases osteoblastogenesis and bone mass in a mouse model4. Active in vivo.
Biochemicals & reagents
1675-54-3
Bisphenol A diglycidyl ether
1) Cuzzocrea et al. (2004), Rosiglitazone , a ligand of the peroxisome proliferator-activated receptor-gamma, reduces acute inflammation; Eur. J. Pharmacol., 483 79 2) Fehlberg et al. (2003), Bisphenol A diglycidyl ether-induced apoptosis involves Bax/Bid-dependent mitochondrial release of apoptosis-inducing factor (AIF), cytochrome c and Smac/DIABLO; Br. J. Pharmacol., 139 495 3) Chamorro-Garcia et al. (2012), Bisphenol A diglycidyl ether induces adipogenic differentiation of multipotent stromal stem cells through a peroxisome proliferator-activatedf receptor gamma-independent mechanism; Environ. Health Perspect., 120 984 4) Duque et al. (2013), Pharmacological inhibition of PPARgamma increases osteoblastogenesis and bone mass in male C57BL/6 mice; J. Bone Miner. Res., 28 639
-20°C
TARGET: Transcription factor -- PATHWAY: Fatty acid metabolism; Apoptosis inducer; PPAR; Transcription -- RESEARCH AREA: Stem cells; Cell death -- DISEASE AREA: Inflammation; Diabetes