T0070907 - CAS 313516-66-4
Catalog number: 313516-66-4
Category: Inhibitor
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T0070907 was identified as a potent and selective PPARgamma antagonist. T0070907 blocked PPARgamma function in both cell-based reporter gene and adipocyte differentiation assays. T0070907 is a novel tool for the study of PPARgamma/RXRalpha heterodimer function.
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T-0070907; T 0070907.
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1.PPARgamma antagonists exacerbate neural antigen-specific Th1 response and experimental allergic encephalomyelitis.
Raikwar HP;Muthian G;Rajasingh J;Johnson C;Bright JJ J Neuroimmunol. 2005 Oct;167(1-2):99-107.
Peroxisome proliferator-activated receptor-gamma is a nuclear receptor transcription factor that regulates cell growth, differentiation and homeostasis. PPARgamma agonists have been used in the treatment of obesity, diabetes, cancer and inflammation. We and others have shown recently that PPARgamma agonists ameliorate experimental allergic encephalomyelitis (EAE), a Th1 cell-mediated autoimmune disease model of multiple sclerosis (MS). We have further shown that PPARgamma agonists inhibit EAE through blocking IL-12 signaling leading to Th1 differentiation and the PPARgamma-deficient heterozygous mice (PPARgamma(+/-)) develop an exacerbated EAE. In this study, we show that in vivo treatment (i.p.) with 100 mug PPARgamma antagonists, Bisphenol A diglycidyl ether (BADGE) or 2-Chloro-5-nitro-N-(4-pyridyl)benzamide (T0070907), on every other day from day 0 to 30, increased the severity and duration of EAE in C57BL/6 wild-type and PPARgamma(+/-) mice. The exacerbation of EAE by PPARgamma antagonists associates with an augmented neural antigen-induced T cell proliferation, IFNgamma production or Th1 differentiation. These results further suggest that PPARgamma is a critical physiological regulator of CNS inflammation and demyelination in EAE.
2.Peroxisome proliferator-activated receptor gamma antagonists decrease Na+ transport via the epithelial Na+ channel.
Pavlov TS;Levchenko V;Karpushev AV;Vandewalle A;Staruschenko A Mol Pharmacol. 2009 Dec;76(6):1333-40. doi: 10.1124/mol.109.056911. Epub 2009 Sep 14.
The epithelial sodium channel (ENaC) is believed to represent the rate-limiting step for sodium absorption in the renal collecting duct. Consequently, ENaC is a central effector affecting systemic blood volume and pressure. Sodium and water transport are dysregulated in diabetes mellitus. Peroxisome proliferator-activated receptor gamma (PPARgamma) agonists are currently used in the treatment of type 2 diabetes, although their use remains limited by fluid retention. The effects of PPARgamma agonists on ENaC activity remain controversial. Although PPARgamma agonists were shown to stimulate ENaC-mediated renal salt absorption, probably via the serum- and glucocorticoid-regulated kinase 1, other studies reported that the PPARgamma agonist-induced fluid retention is independent of ENaC activity. Here we confirmed that four chemically distinct PPARgamma agonists [pioglitazone, rosiglitazone, troglitazone, and 15-deoxy-Delta12,14-prostaglandin J2 (PGJ2)] do not enhance Na+ transport in cultured renal collecting duct principal mpkCCDc14 cells, as assessed by short-circuit current measurements. However, the PPARgamma antagonist 2-chloro-5-nitro-N-4-pyridinyl-benzamide (T0070907), and to a lesser extent 2-chloro-5-nitrobenzanilide (GW9662), were found to decrease Na+ reabsorption across mpkCCDc14 cell layers.
3.PPARgamma regulates LIF-induced growth and self-renewal of mouse ES cells through Tyk2-Stat3 pathway.
Mo C;Chearwae W;Bright JJ Cell Signal. 2010 Mar;22(3):495-500. doi: 10.1016/j.cellsig.2009.11.003.
Embryonic stem (ES) cells are genetically normal, pluripotent cells, capable of self-renewal and multi-lineage differentiation. Leukemia inhibitory factor (LIF) is a growth factor that can maintain the pluripotency of mouse ES cells in culture. Peroxisome proliferator-activated receptors (PPARs) are nuclear receptor transcription factors that regulate growth and differentiation of many cell types. We have shown earlier that 15-Deoxy-(12,14)-Prostaglandin J2 (15d-PGJ2), a natural ligand for PPARgamma, inhibits LIF-induced proliferation of mouse ES cells in culture. In this study we demonstrate that the PPARgamma antagonist Bisphenol A diglycidyl ether (BADGE) and 2-Chloro-5-nitro-N-(4-pyridyl)benzamide (T0070907) reverse the inhibition of ES cell proliferation by PPARgamma agonists. Stable transfection of ES cells with a dominant negative PPARgamma1 mutant also reduced the inhibition of proliferation by PPARgamma agonists. While 15d-PGJ2 and ciglitazone-induced growth-arrest in ES cells by blocking LIF signaling, PPARgamma antagonists and dominant negative PPARgamma1 mutant reversed proliferation by restoring LIF-induced Tyk2-Stat3 signaling. These results suggest that PPARgamma regulates LIF-induced growth and self-renewal of mouse ES cells through Tyk2-Stat3 pathway.
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CAS 313516-66-4 T0070907

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