In Vitro: UCL 1684 (dibromide) (0.5 μM; HEK cells) produces direct atrial-selective inhibition of sodium channel current (INa) and shifts SS inactivation of the cardiac sodium channels. UCL 1684 (dibromide) (0.5 μM) induces PRR, decreases V max, increases DTE, and extends the shortest S1-S1 interval.
In Vivo: UCL 1684 (dibromide) (3 mg/kg; i.v.) increases wenckebach cycle length to 115.0±5.1 % of baseline value.