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Because PGD<jats:sub>2<\/jats:sub>has been reported to inhibit platelet aggregation in vitro, it has been speculated that antagonism of DP1 may enhance platelet reactivity. Three clinical studies evaluated the potential effect of laropiprant, with or without coadministration of ER niacin, on in vivo platelet function in healthy subjects and hypercholesterolemic or diabetic subjects by measuring urinary levels of 11\u2010dehydrothromboxane B<jats:sub>2<\/jats:sub>(11\u2010dTxB<jats:sub>2<\/jats:sub>), a marker of in vivo platelet activation. Following 7 days of multiple\u2010dose administration, coadministration of laropiprant with ER niacin did not increase urinary 11\u2010dTxB<jats:sub>2<\/jats:sub>levels compared to ER niacin alone in healthy, hypercholesterolemic, or diabetic subjects. In hypercholesterolemic and diabetic subjects, laropiprant did not increase urinary 11\u2010dTxB<jats:sub>2<\/jats:sub>levels compared to placebo. These results demonstrate that laropiprant does not enhance in vivo platelet reactivity, either alone or in combination with niacin.<\/jats:p>","DOI":"10.1177\/0091270009339593","type":"journal-article","created":{"date-parts":[[2009,10,16]],"date-time":"2009-10-16T01:11:10Z","timestamp":1255655470000},"page":"1426-1435","source":"Crossref","is-referenced-by-count":11,"title":["Laropiprant in Combination With Extended\u2010Release Niacin Does Not Alter Urine 11\u2010Dehydrothromboxane B<sub>2<\/sub>, a Marker of In Vivo Platelet Function, in Healthy, Hypercholesterolemic, and Diabetic 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