Structural basis of drug binding to hERG K+ channels

TOXI 42

Michael C Sanguinetti, sanguinetti@cvrti.utah.edu, Department of Physiology and Nora Eccles Harrison Cardiovascular Research & Training Institute, University of Utah, Salt Lake City, UT 84112
Block of hERG K+ channels by a surprisingly large number of drugs prolongs the QT interval of the body surface electrocardiogram and increases the risk of cardiac arrhythmia. This side effect is a major hurdle to the development of new drugs. The molecular determinants of hERG channel block have been defined using a site-directed mutagenesis approach. hERG channels are formed by coassembly of 4 subunits, each containing 6 alpha-helical transmembrane domains. Two aromatic residues, Tyr652 and Phe656 located in the S6 domain of hERG, and 2 polar residues, Thr623 and Ser624, are critical for interaction with structurally diverse drugs. By contrast, hERG channel agonists bind to specific residues located between the S5 and S6 domains. Blocker potency is well correlated with hydrophobicity of Phe656 and an aromatic side group at position 652, suggesting the importance of a cation-pi interaction between Tyr652 and a basic N of the drug.