NCC-3902 shows therapeutic potential against atrial fibrillation by inhibiting delayed sodium channel currents and suppressing electrical activity of the pulmonary vein myocardium

Summary:
Atrial fibrillation is a type of arrhythmia in which the atria are excited in an uncontrolled manner and trigger a fatal cardiogenic stroke; thus, effective therapeutics for this disease are urgently required. Atrial fibrillation occurs when electrical excitation or spontaneous activity from the pulmonary vein myocardial layer is transmitted to the heart. However, there are no existing drugs that suppress pulmonary vein myocardial spontaneous activity. Thus, the pulmonary vein is a new therapeutic target for atrial fibrillation. A group of researchers working under Professor Hikaru Tanaka of the Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University, have previously demonstrated that delayed (sustained) sodium channel current, a new category of sodium channel current components, is involved in the spontaneous activity of the pulmonary vein myocardium. In this study, the group found that NCC-3902 inhibits that current and suppresses the electrical excitation generated in the pulmonary veins without affecting the function of the heart itself. The discovery of NCC-3902, which has a novel mechanism of action and few side effects on cardiac function, is expected to lead to new therapeutic strategies for atrial fibrillation.