Abstract
Two novel nonsteroidal anti-inflammatory drugs (NSAID), R-805 (4-nitro-2-phenoxymethane sulfonanilide) and R-807 (3-benzoyldinuoromethane sultonanilide, diflumidonel, inhibit the biosynthesis of prostaglandin by bovine seminal vesicle microsomes and arachidonic acid-induced aggregation of human platelets in a concentration-dependent manner. Comparison of these sulfonanilides with NSAID indicates the following order of potency: (1) vs prostaglandin synthetase: indomethacin > flufenamic acid > R-807 > R-805 > phenylbutazone ⪢ aspirin and (2) vs platelet aggregation: indomethacin > R-807 > R-805 > flufenamic acid > phenylbutazone ⪢ aspirin. Time-dependent, irreversible inhibition of prostaglandin synthetase can be demonstrated for both R-805 and R-807. These compounds also inhibit equally the formation of PGE 2 and PGF 2α, which suggests blockade of endoperoxide formation. This is the first report of inhibition of prostaglandin synthetase and platelet aggregation by drugs of this class.
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