Pharmacogenetic issues in thorough QT trials

Richard S. Judson, Benjamin A. Salisbury, Carol R. Reed, Michael J. Ackerman

Research output: Contribution to journalReview articlepeer-review

10 Scopus citations


Drug-induced QT prolongation (DI-LQT), through its associated arrhythmias, is a leading cause of drugs being withdrawn from the market. As a consequence, the US FDA and other regulatory agencies are mandating that all new drugs go through a so-called 'Thorough QT' (TQT) study to evaluate the potential for 'QT liability', specifically the potential for a drug to cause a discernible increase in the QT interval. Several genetic factors that modulate the risk of DI-LQT have been discovered. These are genes responsible for the congenital long QT syndrome, drug metabolism genes (mainly CYP2D6 and CYP3A4), and genes in other regulatory pathways. Here, we briefly review the links between genetic variants and drug-induced QT risk, and propose approaches to consider for using pharmacogenetics in planning and analyzing TQT studies.

Original languageEnglish (US)
Pages (from-to)153-162
Number of pages10
JournalMolecular Diagnosis and Therapy
Issue number3
StatePublished - 2006

ASJC Scopus subject areas

  • Molecular Medicine
  • Genetics
  • Pharmacology


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