Double pharmacological challenge on repolarization opens new avenues for drug safety research

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Standard

Double pharmacological challenge on repolarization opens new avenues for drug safety research. / Thomsen, Morten Bækgaard.

I: British Journal of Pharmacology, Bind 151, Nr. 7, 08.2007, s. 909-11.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Thomsen, MB 2007, 'Double pharmacological challenge on repolarization opens new avenues for drug safety research', British Journal of Pharmacology, bind 151, nr. 7, s. 909-11. https://doi.org/10.1038/sj.bjp.0707299

APA

Thomsen, M. B. (2007). Double pharmacological challenge on repolarization opens new avenues for drug safety research. British Journal of Pharmacology, 151(7), 909-11. https://doi.org/10.1038/sj.bjp.0707299

Vancouver

Thomsen MB. Double pharmacological challenge on repolarization opens new avenues for drug safety research. British Journal of Pharmacology. 2007 aug.;151(7):909-11. https://doi.org/10.1038/sj.bjp.0707299

Author

Thomsen, Morten Bækgaard. / Double pharmacological challenge on repolarization opens new avenues for drug safety research. I: British Journal of Pharmacology. 2007 ; Bind 151, Nr. 7. s. 909-11.

Bibtex

@article{10ac0868e12244b1ae68dd7cf151f1ce,
title = "Double pharmacological challenge on repolarization opens new avenues for drug safety research",
abstract = "The pharmaceutical industry is testing new potential drugs for their propensity to prolong human cardiac repolarization, and regards this as a sign of proarrhythmic risk. Many studies have dethroned the common perception that prolonged repolarization is a reliable surrogate marker for torsades de pointes (TdP) arrhythmia. Both the pharmaceutical industry and the regulatory bodies are neglecting the available proarrhythmia models. In vitro studies have suggested that combined pharmacological hits on repolarization will produce a superior substrate for in vivo proarrhythmia, compared to the single-drug assessment. By using consecutive pharmacological challenges, a simple model is proposed, in which combinatorial pharmacology is employed to provoke TdP in the conscious dog. The pharmaceutical industry interested in evaluating the proarrhythmic potential of their present and future drugs now has a simple means of doing so.",
keywords = "Animals, Chromans, Delayed Rectifier Potassium Channels, Dogs, Drug Synergism, Drug Toxicity, Electrocardiography, Humans, Long QT Syndrome, Phenethylamines, Potassium Channel Blockers, Potassium Channels, Voltage-Gated, Rabbits, Risk Factors, Sulfonamides, Torsades de Pointes",
author = "Thomsen, {Morten B{\ae}kgaard}",
year = "2007",
month = aug,
doi = "10.1038/sj.bjp.0707299",
language = "English",
volume = "151",
pages = "909--11",
journal = "British Journal of Pharmacology",
issn = "0007-1188",
publisher = "Wiley",
number = "7",

}

RIS

TY - JOUR

T1 - Double pharmacological challenge on repolarization opens new avenues for drug safety research

AU - Thomsen, Morten Bækgaard

PY - 2007/8

Y1 - 2007/8

N2 - The pharmaceutical industry is testing new potential drugs for their propensity to prolong human cardiac repolarization, and regards this as a sign of proarrhythmic risk. Many studies have dethroned the common perception that prolonged repolarization is a reliable surrogate marker for torsades de pointes (TdP) arrhythmia. Both the pharmaceutical industry and the regulatory bodies are neglecting the available proarrhythmia models. In vitro studies have suggested that combined pharmacological hits on repolarization will produce a superior substrate for in vivo proarrhythmia, compared to the single-drug assessment. By using consecutive pharmacological challenges, a simple model is proposed, in which combinatorial pharmacology is employed to provoke TdP in the conscious dog. The pharmaceutical industry interested in evaluating the proarrhythmic potential of their present and future drugs now has a simple means of doing so.

AB - The pharmaceutical industry is testing new potential drugs for their propensity to prolong human cardiac repolarization, and regards this as a sign of proarrhythmic risk. Many studies have dethroned the common perception that prolonged repolarization is a reliable surrogate marker for torsades de pointes (TdP) arrhythmia. Both the pharmaceutical industry and the regulatory bodies are neglecting the available proarrhythmia models. In vitro studies have suggested that combined pharmacological hits on repolarization will produce a superior substrate for in vivo proarrhythmia, compared to the single-drug assessment. By using consecutive pharmacological challenges, a simple model is proposed, in which combinatorial pharmacology is employed to provoke TdP in the conscious dog. The pharmaceutical industry interested in evaluating the proarrhythmic potential of their present and future drugs now has a simple means of doing so.

KW - Animals

KW - Chromans

KW - Delayed Rectifier Potassium Channels

KW - Dogs

KW - Drug Synergism

KW - Drug Toxicity

KW - Electrocardiography

KW - Humans

KW - Long QT Syndrome

KW - Phenethylamines

KW - Potassium Channel Blockers

KW - Potassium Channels, Voltage-Gated

KW - Rabbits

KW - Risk Factors

KW - Sulfonamides

KW - Torsades de Pointes

U2 - 10.1038/sj.bjp.0707299

DO - 10.1038/sj.bjp.0707299

M3 - Journal article

C2 - 17549050

VL - 151

SP - 909

EP - 911

JO - British Journal of Pharmacology

JF - British Journal of Pharmacology

SN - 0007-1188

IS - 7

ER -

ID: 45965505