The effects of 14 b-carbolines on human platelet aggregability were comparatively studied, and the effects on lipid membranes were determined. Several b-carbolines inhibited platelet aggregation induced by collagen, epinephrine, adenosine 5’-diphosphate, platelet-activating factor and thrombin. This activity was structure-dependent. Of all the compounds examined, 1-methyl-1,2,3,4tetrahydro-b-carboline was the most potent. Treatment with 15–177 μM 1-methyl-1,2,3,4-tetrahydro-b-carboline inhibited the aggregation responses to different stimulants by up to 50%. Its potency was comparable to or greater than that of the antiplatelet reference, aspirin. The next most effective compound was 1-methyl-3,4-dihydro-b-carboline. The structure-antiplatelet activity relationship indicated that this activity is reduced by oxidation to 1-methyl-b-carboline, by demethylation to 1,2,3,4-tetrahydro-b-carboline and by 6-hydroxylation, 7-hydroxylation and 3-carboxylation. Active 1-methyl-1,2,3,4-tetrahydro-b-carboline fluidized biomimetic membranes at 25–250 μM which corresponded to the antiaggregatory concentrations, although relatively inactive 6-hydroxy-1-methyl-1,2,3,4-tetrahydro-b-carboline showed no significant effects on the membranes. b-Carbolines are considered to be effective antiplatelet agents that inhibit human platelet aggregation by interacting with lipid membranes to modify fluidity.