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Submit ReviewSR 1664 is an antidiabetic agent; binds to PPARγ and potently inhibits Cdk5-mediated PPARγ phosphorylation (IC50 = 80 nM; Ki = 28.67 nM) without exhibiting PPARγ agonist activity. Does not inhibit Cdk5-dependent phosphorylation of Rb. Reduces fasting insulin levels and improves insulin sensitivity in a mouse model of diabetes.
M. Wt | 547.6 |
Formula | C33H29N3O5 |
Storage | Store at -20°C |
Purity | ≥97% (HPLC) |
CAS Number | 1338259-05-4 |
PubChem ID | 53239854 |
InChI Key | IIJDFXNUWZTHIM-NRFANRHFSA-N |
Smiles | CC2=C(C)N(CC3=CC=C(C4=CC=CC=C4C(O)=O)C=C3)C1=CC=C(C(N[C@H](C5=CC=C([N+]([O-])=O)C=C5)C)=O)C=C12 |
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
References are publications that support the biological activity of the product.
Norris and Sigmund (2012) A second chance for a PPARγ targeted therapy? Circ.Res. 110 8 PMID: 22223206
Choi et al (2011) Antidiabetic actions of a non-agonist PPARγ ligand blocking Cdk5-mediated phosphorylation. Nature 477 477 PMID: 21892191
Keywords: SR 1664, SR 1664 supplier, SR1664, antidiabetics, diabetes, PPARgamma, PPARg, peroxisome, proliferator, activated, receptor, ligand, Cdk5, phosphorylation, LBD, Receptors, 4409, Tocris Bioscience
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Epilepsy is a brain disease that affects 60 million people globally. More than 20 anti-seizure drugs are currently available, but these do not address the underlying causes of the condition. This poster summarizes current knowledge about the development of the condition and highlights some approaches that have disease-modifying effects in proof-of-concept studies.