posted on 2005-10-20, 00:00authored byGary M. Coppola, Paivi J. Kukkola, James L. Stanton, Alan D. Neubert, Nicholas Marcopulos, Natalie A. Bilci, Hua Wang, Hollis C. Tomaselli, Jenny Tan, Thomas D. Aicher, Douglas C. Knorr, Arco Y. Jeng, Beatriz Dardik, Ricardo E. Chatelain
High-throughput screening identified 5 as a weak inhibitor of 11β-HSD1. Optimization of the
structure led to a series of perhydroquinolylbenzamides, some with low nanomolar inhibitory
potency. A tertiary benzamide is required for biological activity and substitution of the terminal
benzamide with either electron-donating or -withdrawing groups is tolerated. The majority of
the compounds show selectivity of >20 to >700-fold over 11β-HSD2. Analogues which showed
>50% inhibition of 11β-HSD1 at 1 μM in an cellular assay were screened in an ADX mouse
model. A maximal response of >70% reduction of liver corticosterone levels was observed for
three compounds; 9m, 25 and 49.