Objective：To assess the variability and reproducibility of patch clamp platforms/sites for defining clinical drug effects on human ether-à-go-go related gene（hERG） currents across and between platforms and sites and to investigate the blocking effect of nine clinical drugs that have high（bepridil，quinidine，sotalol），intermediate（ondansetron，cisapride，terfenadine）and low（ranolazine，verapamil and mexiletine）torsade de pointes risk（TdP）on hERG potassium channel. Methods：The whole-cell patch clamp technique was used to record the change in hERG potassium current（IKr）on HEK293 cells that stably expressed hERG potassium channel（hERG-HEK293 steady-state cells），which was treated with four test concentrations of bepridil，quinidine，sotalol，ondansetron，cisapride，terfenadine，ranolazine，verapamil and mexiletine，to study the concentration-dependence of the effects on IKr and the half maximal inhibitory concentration（IC50）. Resuts：All of the nine clinical drugs tested produced a concentration-dependent reduction of hERG current. The IC50 values of bepridil and quinidine（high TdP risk clinical drugs） were about 98.32 nmol/L and 1.95 μmol/L，respectively，and the IC50 values of sotalol was >300 μmol/L. The IC50 values of ondansetron，cisapride，terfenadine（intermediate TdP risk clinical drugs）were 0.94 μmol/L，39.10 nmol/L，128.58 nmol/L，respectively. The IC50 values of ranolazine，verapamil and mexiletine（low TdP risk clinical drugs）were 9.94 μmol/L，235.49 nmol/L and 65.56 μmol/L，respectively. The IC50 values for the nine clinical drugs corresponded well to those published within the literature. Conclusion：The risk of drug-induced TdP is closely related to the block of the hERG channel，but the hERG channel block is lack of specificity as a predictor of TdP，which is also associated with multiple ion channel effects. Some clinical drugs also block Nav1.5-late and/or Cav1.2 currents，which can reduce the risk of TdP caused by hERG block. The data obtained by this method is reliable，which provides a reference for the hERG block test performed by domestic GLP laboratories and can be used for the safety evaluation of drug cardiac toxicity.