Journal
BRITISH JOURNAL OF PHARMACOLOGY
Volume 167, Issue 5, Pages 932-945Publisher
WILEY
DOI: 10.1111/j.1476-5381.2012.02020.x
Keywords
arrhythmia; Torsade de Pointes; computer model; hERG; QT prolongation
Categories
Funding
- European Commission's Virtual Physiological Human Initiative
- British Heart Foundation
- GlaxoSmithKline
- Affiliates scheme
- GlaxoSmithKline Plc
- BBSRC [BB/I012117/1] Funding Source: UKRI
- EPSRC [EP/I017909/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/I012117/1] Funding Source: researchfish
- British Heart Foundation [PG/09/031/27221, FS/12/17/29532] Funding Source: researchfish
- Engineering and Physical Sciences Research Council [EP/I017909/1] Funding Source: researchfish
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Concerns over cardiac side effects are the largest single cause of compound attrition during pharmaceutical drug development. For a number of years, biophysically detailed mathematical models of cardiac electrical activity have been used to explore how a compound, interfering with specific ion-channel function, may explain effects at the cell-, tissue- and organ-scales. With the advent of high-throughput screening of multiple ion channels in the wet-lab, and improvements in computational modelling of their effects on cardiac cell activity, more reliable prediction of pro-arrhythmic risk is becoming possible at the earliest stages of drug development. In this paper, we review the current use of biophysically detailed mathematical models of cardiac myocyte electrical activity in drug safety testing, and suggest future directions to employ the full potential of this approach. LINKED ARTICLE This article is commented on by Gintant, pp. 929931 of this issue. To view this commentary visit http://dx.doi.org/10.1111/j.1476-5381.2012.02096.x
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