Some drugs that block the human ether-a-go-go-related gene (hERG) channel, the delayed rectifier potassium current (I_Kr), exert antiarrhythmic action by prolonging action potential (AP). However, the excessive AP prolongation increases the risk of lethal arrhythmias. We recently found that nifekalant not only inhibited the hERG current but also increased the current in a membrane voltage-dependent manner. How such a current increasing effect by hERG channel inhibitors, which referred to as a facilitation effect, affect the AP of cardiomyocytes is not yet fully understood. We constructed an I_Kr current model based on the voltage-clamp experiment of hERG channel expressed in HEK293 cells and macroscopic current recordings under the administration of nifekalant. Our constructed I_Kr current model was constrained by current recorded from HEK293 cells expressing hERG channels. Furthermore, we performed AP simulation with a human ventricular myocyte model replaced with our I_Kr model and found that the I_Kr facilitation prevents early afterdepolarization developments as compared to drugs without the facilitation effect. A specific hERG inhibitor with facilitation effect may contribute positively to suppress drug arrhythmogenicity.