The hERG channel: Tuned in? Chemical strategies for dialing out an off-target source of candidate failure

TOXI 44

Brian Springhthorpe, Brian.Springthorpe@astrazeneca.com, Department of Chemistry, AstraZeneca R&D Charnwood, Bakewell Road, Loughborough, LE11 5RH, England
The rapid component of the delayed rectifier potassium current (IKr ) is carried by channels encoded by the human ether-a-go-go-related gene (hERG) and plays a key role in cardiac repolaristion. Pharmacological inhibition of this channel can lead to prolongation of the QT interval which is associated with a potentially fatal arrhythmia called Torsades de Pointes (TdP). Drug-induced TdP has led to the withdrawal of a number of drugs and has resulted in regulatory guidelines aimed at ensuring that the clinical risk of a compound causing QT interval prolongation is assessed. This presentation will briefly introduce the terms hERG, QT and TdP and describe chemical approaches which have been shown to reduce activity at the hERG channel, including correlations with physicochemical parameters. The presentation will also briefly discuss the overall risk assessment of pre-clinical compounds and recommend a safety margin which may de-risk the possibility of QT interval prolongation in man.