Pharmacological study of the safety, efficacy, and potential of M201-A on paroxysmal and persistent atrial fibrillation.

ABSTRACT: Conversion and prevention of atrial fibrillation (AF) are essential requirements for its treatment. Abnormal leakage of calcium from the sarcoplasmic reticulum via the ryanodine receptor 2 (RyR2) during diastole is considered a major cause of AF. Although catheter ablation has made it possible to stop persistent AF, it does not address recurrence. In this context, we describe the additional pharmacological and antiarrhythmic effects of the RyR2 inhibitor M201-A, including the results of a phase I study. M201-A inhibited G-protein-gated atrial K⁺ channel at an IC₅₀ value of 0.35 μM, which was associated with a 38% increase in the atrial effective refractory period (ERP) and high atrial selectivity with an atrial ERP/ventricular ERP of 5.7. M201-A inhibited rapid compon

SUBMITTER: Kaneko N 

PROVIDER: S-EPMC12489371 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature