Abstract
Atrial fibrillation is the most prevalent form of cardiac arrhythmia. Current treatments extend the atrial effective refractory period by nonselective blockade of cardiac ion channels. An alternative approach selectively targeting the Kv1.5 ion channel offers the opportunity for therapeutic benefit with decreased risk of adverse cardiovascular events. KVI-020 (4g) successfully demonstrated antiarrhythmic efficacy in a canine arrhythmia model, and these findings support its utility as an antiarrhythmic agent.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Anti-Arrhythmia Agents / chemical synthesis*
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Anti-Arrhythmia Agents / pharmacokinetics
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Anti-Arrhythmia Agents / pharmacology
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Atrial Fibrillation / drug therapy*
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Cell Line
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Cricetinae
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Cricetulus
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Dogs
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Humans
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Imidazolidines / chemical synthesis*
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Imidazolidines / pharmacokinetics
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Imidazolidines / pharmacology
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In Vitro Techniques
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Kv1.5 Potassium Channel / antagonists & inhibitors*
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Microsomes, Liver / metabolism
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Patch-Clamp Techniques
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Solubility
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Stereoisomerism
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Structure-Activity Relationship
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Sulfonamides / chemical synthesis*
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Sulfonamides / pharmacokinetics
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Sulfonamides / pharmacology
Substances
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1-(methylsulfonylamino)-3-(2-(4-methoxyphenyl)ethyl)-4-(4-methoxyphenyl)-2-imidazolidinone
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Anti-Arrhythmia Agents
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Imidazolidines
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KCNA5 protein, human
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Kv1.5 Potassium Channel
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Sulfonamides