X.-Y. Ye et al. / Bioorg. Med. Chem. Lett. 20 (2010) 2933–2937
2937
A.; Bolton, S. A.; Ryono, D. E.; Zhang, H.; Lim, N.-K.; Chen, B.-C.; Locke, K. T.;
O’Malley, K. M.; Zhang, L.; Srivastava, R. A.; Miao, B.; Meyers, D. S.;
Monshizadegan, H.; Search, D.; Grimm, D.; Zhang, R.; Harrity, T.; Kunselman,
L. K.; Cap, M.; Kadiyala, P.; Hosagrahara, P.; Zhang, L.; Xu, C.; Li, Y.-X.;
Muckelbauer, J. K.; Chang, C.; An, Y.; Krystek, S. R.; Blanar, M. A.; Zahler, R.;
Mukherjee, R.; Cheng, P. T. W.; Tino, J. A. J. Med. Chem., accepted for publication.
References and notes
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a
EC50 was decreased about 15- to 20-fold, presumably due to the increased
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l
}
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substrate. EC50 values (
as the concentration of the test ligand (
induction of HEK293 cells. The ‘intrinsic activity’ of a test ligand is defined as
its activity at 1 M (expressed as a percentage) relative to the activity of the
primary standards at 1 M. The maximal efficacy was measured in percentage
related to the standards (fenofibrate at 100 is 100% for PPAR
rosiglitazone at 1 M is 100% for PPAR ). See: (a) Lehmann, J. M.; Moore, L.
l
M) for PPAR
a
l
or
c agonist activity were calculated
M) required for the half-maximal fold
l
l
lM
a;
l
c
B.; Smith-Oliver, T. A.; Wilkison, W. O.; Willson, T. M.; Kliewer, S. A. J. Biol.
Chem. 1995, 270, 12953; (b) see Ref. 6 and the references cited therein.
16. Compounds 2i and 2j have the (S)-configuration, as indicated in Scheme 1. We
have found that their corresponding (R)-enantiomers are less active.
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dehydrogenase complex and modulates oxidative metabolism of glucose. It is
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a agonists, and serves as a
PD marker for PPAR activity. See: (a) Liu, P. C. C.; Huber, R.; Stow, M. D.;
a
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well documented in the literature and are consistent with our observations.
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