The action of ethyl-N-(2-amino-6-(4-fluorophenylmethylamino) pyridin - 3 - yl) carbamate (flupirtine, D 9998), a recently synthesized analgesic, on prostaglandin formation and platelet aggregation was studied in vitro. Flupirtine was found to significantly inhibit the basal prostaglandin I2 formation in preparations of the rat aorta as well as the arachidonic acid-stimulated prostaglandin release form the Langendorff-perfused guinea pig heart. The IC50 amounted to 5-50 mumol/l in these systems and was more than one order of magnitude higher than indometacin (0.5-1 mumol/l). Flupirtine was found to inhibit dose-dependently the collagen - but not the primary adenosine diphosphate-induced aggregation of human platelets, being again 1 order of magnitude less potent than indometacin (IC50: 4.0 vs. 0.6 mumol/l). Interestingly there was no inhibition of arachidonic acid-induced thromboxane formation of human platelets by flupirtine in concentrations up to 23 mumol/l. These data suggest a weak inhibition of prostaglandin formation by flupirtine. There may also exist a weak local anaesthetic activity of the agent, demonstrated here on the rabbit cornea, that aids the observed decrease in sensitivity of smooth muscle preparations and might help to explain the inhibition of collagen-induced platelet aggregation in absence of diminished thromboxane formation. It is concluded that these modifications of prostaglandin formation by flupirtine are probably of minor importance for an analgesic action of the compound in vivo.