Abstract1A single oral dose (50 mg) of quinidine significantly increased the debrisoquine metabolic ratio in six healthy volunteers. For four of the volunteers the metabolic ratio changed to that typical of the poor metaboliser (PM) phenotype.2The effect of quinidine in producing debrisoquine oxidation “poor metaboliser” phenocopies persisted for at least 3 days but had disappeared by 1 week.3The debrisoquine metabolic ratios for the same six subjects were not significantly altered by the oral administration of quinine (200 or 400 mg), the dia‐stereoisomer of quinidine.4The plasma pharmacokinetic parameters of both nortriptyline and desipramine in healthy volunteers were all changed to those more typical of the debrisoquine PM phenotype following the concomitant administration of quinidine (50 mg).5It is concluded that quinidine, but not its diastereoisomer quinine, is a potent selective inhibitor of thein vivooxidation of debrisoquine and can produce an artifactual PM phenocopy in persons who are phenotypically extensive metaboliser (EM) phenotype status. The clinical implications of this observation are disc