Key result
A series of synthesized 8-acetyl- (or 1-hydroxyethyl-) 12-hydroxy-13-aryloxytridecanoic acids and their sulfonamide isosteres were found to be potent inhibitors of collagen-induced blood platelet aggregation in guinea pigs upon oral administration.
Why the study?
Do 8-acetyl- (or 1-hydroxyethyl-) 12-hydroxy-13-aryloxytridecanoic acids and their sulfonamide isosteres inhibit collagen-induced blood platelet aggregation in guinea pigs?
Do 8-acetyl- (or 1-hydroxyethyl-) 12-hydroxy-13-aryloxytridecanoic acids and their sulfonamide isosteres inhibit collagen-induced blood platelet aggregation in guinea pigs?
The synthesized 11,12-secoprostaglandin derivatives demonstrate potent inhibition of platelet aggregation in a guinea pig model.
These guinea pig data support preclinical lead optimization; leaves open human translation for oral antiplatelet therapy.
The synthesis of a series of 8-acetyl- (or 1-hydroxyethyl-) 12-hydroxy-13-aryloxytridecanoic acids and their sulfonamide isosteres is described. These compounds are formally derived from members of earlier reported series of modified secoprostaglandins by replacing the omega-butyl chain termini by substituted aryloxy groups. A number of these compounds are potent inhibitors of collagen-induced blood platelet aggregation in guinea pigs on oral administration.
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Bicking et al. (1978) studied collagen-induced blood platelet aggregation. 8-acetyl- (or 1-hydroxyethyl-) 12-hydroxy-13-aryloxytridecanoic acids and their sulfonamide isosteres was evaluated on collagen-induced blood platelet aggregation. A series of synthesized 8-acetyl- (or 1-hydroxyethyl-) 12-hydroxy-13-aryloxytridecanoic acids and their sulfonamide isosteres were found to be potent inhibitors of collagen-induced blood platelet aggregation in guinea pigs upon oral administration.
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