Pharmacological treatment with various anti arrhythmic agents for the termination or prevention of atrial fibrillation (AF) is not yet satisfactory. This is in part because the drugs may not be sufficiently selective for the atrium and they often cause ventricular arrhythmias. The ultra rapid delayed rectifying K⁺ current (I_Kur) is found in the atrium but not in the ventricle, and it has been recognized as a potentially promising target for anti AF drugs which would be without ventricular proarrhythmia. Several new agents that specifically block I_Kur have been developed. They block I_Kur in a voltage- and time dependent manner. Here we use mathematical models of normal and electrically remodeled human atrial action potentials (APs) to examine the effects of the blockade kinetics of I_Kur on atrial action potential duration (APD). It was found that after AF remodeling an I_Kur blocker with fast onset can effectively prolong APD at any stimulus frequency, while a blocker with slow onset prolongs APD in a frequency dependent manner only when the recovery is slow. The results suggest that the voltage- and time dependence of I_Kur blockade should be taken into account in the testing of anti AF drugs. This modeling study suggests that a simple voltage clamp protocol with a short pulse of ~ 10 ms at 1 Hz may be useful to identify the effective anti AF drugs among various I_Kur-blockers.