RESUMO
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.
Assuntos
Antiarrítmicos/síntese química , Fibrilação Atrial/tratamento farmacológico , Imidazolidinas/síntese química , Canal de Potássio Kv1.5/antagonistas & inibidores , Sulfonamidas/síntese química , Animais , Antiarrítmicos/farmacocinética , Antiarrítmicos/farmacologia , Linhagem Celular , Cricetinae , Cricetulus , Cães , Humanos , Imidazolidinas/farmacocinética , Imidazolidinas/farmacologia , Técnicas In Vitro , Microssomos Hepáticos/metabolismo , Técnicas de Patch-Clamp , Solubilidade , Estereoisomerismo , Relação Estrutura-Atividade , Sulfonamidas/farmacocinética , Sulfonamidas/farmacologiaRESUMO
Blockade of the Kv1.5 ion channel is a potentially atrial-selective avenue for the treatment of atrial fibrillation and atrial flutter. The development and biological evaluation of a series of thiazolidine-based blockers of Kv1.5 is described.
