Purpose: The failure to cure persons with cancer is caused primarily by the development of drug resistance by overexpression of p-glycoprotein. Diverse groups of drugs have been identified, including cyclosporine A, which can reverse drug resistance by inhibiting P-glycoprotein transport. Tc-99m sestamibi is a substrate for P-glycoprotein. P-glycoprotein is normally expressed in biliary canalicular surfaces of hepatocytes and is responsible for the excretion of cationic metabolites from the liver. The aim of the current study was to evaluate the effect of cyclosporine A on the biological distribution of Tc-99m sestamibi in vivo.