hERG Inhibitors with Similar Potency But Different Binding Kinetics Do Not Pose the Same Proarrhythmic Risk: Implications for Drug Safety Assessment.

Drug Mode of Action and hERG-Related Safety Introduction Since the discovery of the link that exists between drug-induced hERG inhibition and Torsade de Pointes (TdP), extreme attention has been given to avoid new drugs inhibiting this channel. hERG inhibition is routinely screened for in new drugs...

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Publicado en:Journal of Cardiovascular Electrophysiology Vol. 25; no. 2; pp. 197 - 208
Autores principales: Veroli, Giovanni Y., Davies, Mark R., Zhang, Henggui, Abi-Gerges, Najah, Boyett, Mark R.
Formato: equations & formulas research tables/charts Journal Article
Publicado: Wiley-Blackwell Feb2014
Acceso en línea:Ver este registro en EBSCOhost
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      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        atl: hERG Inhibitors with Similar Potency But Different Binding Kinetics Do Not Pose the Same Proarrhythmic Risk: Implications for Drug Safety Assessment.
      aug:
        au:
          Veroli, Giovanni Y.
          Davies, Mark R.
          Zhang, Henggui
          Abi-Gerges, Najah
          Boyett, Mark R.
        affil: Institute of Cardiovascular Sciences, University of Manchester; Translational Safety, Drug Safety & Metabolism
      sug:
        subj:
          Potassium
          Membrane Proteins Antagonists and Inhibitors
          Membrane Proteins Drug Effects
          Kinetics
          Arrhythmia Risk Factors
          Drugs, Investigational Administration and Dosage
          Drugs, Investigational Adverse Effects
          Animal Studies
          Dogs
          Models, Statistical
          Descriptive Statistics
          Action Potentials
          Simulations
          Data Analysis Software
          Electrophysiology
          Funding Source
      ab: Drug Mode of Action and hERG-Related Safety Introduction Since the discovery of the link that exists between drug-induced hERG inhibition and Torsade de Pointes (TdP), extreme attention has been given to avoid new drugs inhibiting this channel. hERG inhibition is routinely screened for in new drugs and, typically, IC50 values are compared to projected plasma concentrations to define a safety margin. Methods and Results We aimed to show that drugs with similar hERG potency are not uniformly pro-arrhythmic-this depends on the drug binding kinetics and mode of action (trapped or not) rather than the IC50 value only. We used a mathematical model of hERG and its related encoded current IKr to simulate drug binding in different configurations. Expression systems mimicking the screening process were first investigated. hERG model was then incorporated into a canine action potential (AP) and tissue model to study the impact of drug binding configurations on AP and pseudo-ECG (QT interval prolongation). Our data show that: (1) trapped and not trapped configurations and different binding kinetics could be identified during hERG screening; (2) slow binding, not trapped drugs, induced less AP prolongation and minimal QT interval prolongation (4.7%) at a concentration equal to the IC50 whereas maximal pro-arrhythmic risk was observed for trapped drugs at the same concentration (QT interval prolongation, 23.1%). Conclusion Our study demonstrates the need for screening for hERG binding configurations rather than potency alone. It also demonstrates the potential link between hERG, drug mode of action and TdP, and the need to question the current regulatory guidance.
      pubtype: Academic Journal
      doctype:
        equations & formulas
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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