This study was designed to test the allitridum (All) activity in correction of sodium current decrease caused by SCN5A-F1473S mutation in HEK293 cells. The result may provide a theoretical basis for screening of new drugs in the treatment of Brugada syndrome. We transferred SCN5A-F1473S channel plasmids into HEK293 cells in a transient transfection. All was administrated acutely and chronically using extracellular irrigation flow and co-culture model. The concentration of All was 30 μmol·L(-1). We used whole cell patch clamp technique in voltage clamp mode to record current and gating kinetics. In order to explore the rescue function of All on decreased sodium peak current, we used confocal microscopy and Western blot to detect the expression of channel proteins in the cell membrane. We found a significant increase in sodium peak current of the 30 μmol·L(-1) All HEK293 cells (269.8 ± 16.6 pA/pF, P < 0.01), almost closed to the current density of the control group（298.2 ± 17.5 p A/p F, P < 0.01）. All allowed the steady-state inactivation of the channel to move toward a more positive direction (V(1/2, inact) returns to -79.5 ± 2.4 mV, P < 0.01). It also slowed the intermediate state inactivation of the channel (inactivation prolongated to 598.1 ± 22.6 ms, P < 0.01). Meanwhile, All increased distribution and expression of the channel protein in the cell membrane (compared to F1473S, P < 0.01). All caused an increase of current in SCN5A-F1473S mutation cells. We consider that the main mechanism may be related to the reduced channel inactivation by the drug with an improvement of the migration barrier of the mutational channel.