AZD-1305

AZD-1305 is an antiarrhythmic agent and atrial selective sodium channel/potassium channel blocker, which can significantly prolongs action potential duration and reduces excitability, cause atrial selective ERP prolongation and acute termination of atrial fibrillation. AZD1305 can be used for atrial fibrillation research^[1][2]. In Vitro:AZD-1305 (1,3 μM) induces atrial selective PRR in isolated coronary-perfused preparations ^[1].
AZD-1305 (1,3 μM) produces a greater use-dependent reduction of maximum rate of rise of the action potential upstroke (V_max) in atrial versus ventricular preparations^[1].
AZD-1305 (1,3 μM) causes a greater increase in sodium channel–mediated parameters conduction velocity and diastolic threshold of excitation in atrial versus ventricular coronaryperfused preparations^[1].
AZD-1305 (5 μM) induces greater tonic and steadystate inhibitions of atrial sodium channels than ventricular sodium channels in isolated coronary-perfused preparations^[1].
AZD-1305 (1-10 μM) causes a significant decrease in V_max, action potential amplitude, and takeoff potential in canine pulmonary vein sleeve preparations, and significantly increases action potential duration at 90% repolarization^[2].
AZD-1305 (1-10 μM) significantly increases the basic cycle length at which 1:1 activation is maintained in canine pulmonary vein sleeve preparations, and pretreatment with amiodarone significantly potentiates the effect of AZD1305^[2].
In Vivo:AZD-1305 (steady state plasma concentrations of 1.2 and 4.5 μM, i.v.drip) produces a greater prolongation of repolarization and ERP in canine atrium of Beagle dogs than in ventricle^[1].
AZD-1305 (steady state plasma concentrations of 1.2 and 4.5 μM, i.v.drip) increases conduction time and depress excitability in atria versus ventricles of Beagle dogs ^[1].
AZD-1305 (steady state plasma concentrations of 1-3 μM, i.v.drip) terminates persistent AF and prevents induction of AF in an ACh-mediated model of AF in Beagle dogs ^[1].