Abstract
Although proquazone is not an acid, its action on platelets is similar to that of a typical acidic non steroidal antiinflammatory drug: it inhibits the release reaction and associated production of malonidaldehyde without affecting primary aggregation caused by ADP or epinephrine, and it fails to inhibit the collagen-induced release which remains after maximal inhibition by aspirin. It is unusually active; it may have an effect in vitro at 11 nM, and is at least 50 times more active than indomethacin in preventing collagen-induced release from human platelets.