The thioether metabolite of sulphinpyrazone is between 8 and 13 times more potent than the parent compound as a competitive inhibitor of human, guinea pig and rabbit platelet aggregation induced by sodium arachidonate. Of the other known metabolites, the sulphone is approximately equipotent and the p-hydroxy compounds are much less potent that sulphinpyrazone itself. Malondialdehyde biosynthesis from sodium arachidonate by washed human platelets and collagen-induced aggregation of all three species is also inhibited by the thioether. It is 10 times more potent than sulphinpyrazone. ADP-induced aggregation is not affected by sulphinpyrazone, its thioether metabolite, nor the other metabolites. After intravenous administration of the thioether metabolite to groups of guinea pigs the inhibitory effect on sodium arachidonate-induced platelet aggregation ex vivo was long lasting (up to 24 h). In view of the recent information about the metabolism of sulphinpyrazone to its thioether in guinea pigs, we conclude that the thioether metabolite is the substance responsible for the prolonged effect of sulphinpyrazone on platelet fuction in this species and in man.