Abstract: To study the transport mechanisms of drugs for transplacental treatment of fetal tachyarrhythmia, MDCKII-BCRP and MDCKII cell models was used. MDCKII-BCRP and MDCKII cell monolayer model was used to investigate the bi-direction transport of sotalol, propranolol, propafenone, procainamide and flecainide. Drug concentrations were measured by HPLC-UV or chemiluminescence. The apparent permeability coefficient (P_app), efflux rate (R_E) and net efflux rate (R_net) were calculated. Drugs with R_net greater than 1.5 were further investigated using cellular accumulation experiments with or without a BCRP inhibitor. The R_net of sotalol, propranolol, propafenone and procainamide were less than 1.5, while R_net of flecainide with concentrations of 20 and 5 μmol·L^-1 were 1.6 and 1.9, respectively. The results showed that the transport of flecainide on MDCKII- BCRP cell monolayer could be mediated by BCRP; and the affinity increased when the concentration of flecainide decreased. Cellular accumulation experiments further suggested that accumulation of flecainide in MDCKII-BCRP cells was significantly lower than that in MDCKII cells in a concentration-dependent manner. BCRP inhibitor quercetin (50 μmol·L^-1) significantly increased the accumulation of flecainide in MDCKII- BCRP cells (P < 0.05). Our preliminary data showed that flecainide but not sotalol, propranolol, propafenone or procainamide can be a substrate of BCRP. Thus the effect of flecainide may be affected by the BCRP in the maternal placental trophoblast membrane layer when treating fetal tachyarrhythmia.