| Literature DB >> 23098566 |
Pengcheng P Shao1, Feng Ye, Prasun K Chakravarty, Deepu J Varughese, James B Herrington, Ge Dai, Randal M Bugianesi, Rodolfo J Haedo, Andrew M Swensen, Vivien A Warren, McHardy M Smith, Maria L Garcia, Owen B McManus, Kathryn A Lyons, Xiaohua Li, Mitchell Green, Nina Jochnowitz, Erin McGowan, Shruti Mistry, Shu-Yu Sun, Catherine Abbadie, Gregory J Kaczorowski, Joseph L Duffy.
Abstract
The voltage-gated calcium channel Ca(v)2.2 (N-type calcium channel) is a critical regulator of synaptic transmission and has emerged as an attractive target for the treatment of chronic pain. We report here the discovery of sulfonamide-derived, state-dependent inhibitors of Ca(v)2.2. In particular, 19 is an inhibitor of Ca(v)2.2 that is selective over cardiac ion channels, with a good preclinical PK and biodistribution profile. This compound exhibits dose-dependent efficacy in preclinical models of inflammatory hyperalgesia and neuropathic allodynia and is devoid of ancillary cardiovascular or CNS pharmacology at the doses tested. Importantly, 19 exhibited no efficacy in Ca(v)2.2 gene-deleted mice. The discovery of metabolite 26 confounds further development of members of this aminopiperidine sulfonamide series. This discovery also suggests specific structural liabilities of this class of compounds that must be addressed.Entities:
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Year: 2012 PMID: 23098566 DOI: 10.1021/jm301056k
Source DB: PubMed Journal: J Med Chem ISSN: 0022-2623 Impact factor: 7.446