Document Type

Article

Publication Date

10-2012

Source Publication

Journal of Medicinal Chemistry

Source ISSN

0022-2623

Abstract

Drugs exert desired and undesired effects based on their binding interactions with protein target(s) and off-target(s), providing evidence for drug efficacy and toxicity. Pioglitazone and rosiglitazone possess a common functional core, glitazone, which is considered a privileged scaffold upon which to build a drug selective for a given target—in this case, PPARγ. Herein, we report a retrospective analysis of two variants of the glitazone scaffold, pioglitazone and rosiglitazone, in an effort to identify off-target binding events in the rat heart to explain recently reported cardiovascular risk associated with these drugs. Our results suggest that glitazone has affinity for dehydrogenases, consistent with known binding preferences for related rhodanine cores. Both drugs bound ion channels and modulators, with implications in congestive heart failure, arrhythmia, and peripheral edema. Additional proteins involved in glucose homeostasis, synaptic transduction, and mitochondrial energy production were detected and potentially contribute to drug efficacy and cardiotoxicity.

Comments

Accepted version. Journal of Medicinal Chemistry, Vol. 55, No. 19 (October 2012): 8260-8271. DOI. © 2012 American Chemical Society Publications. Used with permission.

sem_6958acc.docx (275 kB)
ADA Accessible Version

Included in

Chemistry Commons

Share

COinS