Primaquine is presently the only drug available as anti-hypnozoites in the treatment of malaria caused by Plasmodium vivax. Due to its hydrophilic properties, it was estimated that the uptake of primaquine to its target (liver) to be very difficult. This study was aimed to understand the mechanism of primaquine uptake to the hepatocytes through the transport protein, OCT1 (organic cationic transporter 1). This was an in vitro experiment in HepG2 cells. The HepG2 cells were propagated in vitro following the procedure published previously. The intracellular concentrations of primaquine were quantified using HPLC coupled with photodiode array detection (HPLC-PDA). The mRNA expression of OCT1 was determined using quantitative RT-PCR. To determine whether the uptake of primaquine to the hepatocytes was transported by OCT1, we quantify intracellular primaquine concentrations and analyze the mRNA OCT1 expressions in the cells treated with primaquine +/- OCT1 inhibitor (quinidine). OCT1 inhibitor (quinidine) decreased the intracellular levels of primaquine significantly in almost all the concentrations investigated. The exposure of primaquine with quinidine consistently reduced the expression of OCT1 mRNA compared with primaquine alone. In conclusion, primaquine is efficiently transported by OCT1 in HepG2 cells. OCT1 is thought to be one of the target protein to increase the uptake of primaquine to the hepatocytes.