IT has been reported that prostaglandin endoperoxides (PGG2 and PGH2), possible intermediates in the biosynthesis of PGE2 and PGF2α from arachidonic acid, may be mediators of platelet aggregation1–3. Kloeze reported4 that neither PGE2 nor PGF2α cause platelet aggregation or ADP release, and Willis5 stated that prostaglandins themselves cannot induce platelet aggregation. But we have found that three synthetic prostaglandins, Wy-16, 991, Wy-17, 185 and Wy-17, 186, induce platelet aggregation in vitro, and two of them, Wy-17, 185 and Wy-17, 186, significantly shorten the Lee White clotting time in rats. The most active of the three, Wy-17, 186, exerts a haemostatic effect on a bleeding wound surface.