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hERG assays are utilized as surrogate markers to predict the risk of drug-induced delayed cardiac repolarization and Torsades de Pointes, though their predictive utility has limitations.
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Provides an overview of hERG assays and their utility in predicting drug-induced delayed cardiac repolarization and Torsades de Pointes risk.
HERG (human-ether-a-go-go-related gene) encodes for a cardiac potassium channel that plays a critical role in defining ventricular repolarization. Noncardiovascular drugs associated with a rare but potentially lethal ventricular arrhythmia (Torsades de Pointes) have been linked to delayed cardiac repolarization and block of hERG current. This brief overview will discuss the role of hERG current in cardiac electrophysiology, its involvement in drug-induced delayed repolarization, and approaches used to define drug effects on hERG current. In addition, examples of hERG blocking drugs acting differently (i.e., overt and covert hERG blockade due to multichannel block) together with the utility and limitations of hERG assays as tools to predict the risk of delayed repolarization and proarrhythmia are discussed.
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Gintant et al. (2006) conducted a review in Drug-induced delayed repolarization and Torsades de Pointes. hERG assays was evaluated. hERG assays are utilized as surrogate markers to predict the risk of drug-induced delayed cardiac repolarization and Torsades de Pointes, though their predictive utility has limitations.
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