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Suppression of niacin-induced vasodilation with an antagonist to prostaglandin D2 receptor subtype 1.

Author(s): Lai E, De Lepeleire I, Crumley TM, Liu F, Wenning LA, Michiels N, Vets E, O'Neill G, Wagner JA, Gottesdiener K

Affiliation(s): Department of Clinical Pharmacology, Merck Research Laboratories, Rahway, New Jersey, USA. eseng_lai@merck.com

Publication date & source: 2007-06, Clin Pharmacol Ther., 81(6):849-57. Epub 2007 Mar 28.

Publication type: Randomized Controlled Trial; Research Support, Non-U.S. Gov't

Niacin (nicotinic acid) reduces cardiovascular events in patients with dyslipidemia. However, symptoms associated with niacin-induced vasodilation (e.g., flushing) have limited its use. Laropiprant is a selective antagonist of the prostaglandin D(2) receptor subtype 1 (DP1), which may mediate niacin-induced vasodilation. The aim of this proof-of-concept study was to evaluate the effects of laropiprant (vs placebo) on niacin-induced cutaneous vasodilation. Coadministration of laropiprant 30, 100, and 300 mg with extended-release (ER) niacin significantly lowered flushing symptom scores (by approximately 50% or more) and also significantly reduced malar skin blood flow measured by laser Doppler perfusion imaging. Laropiprant was effective after multiple doses in reducing symptoms of flushing and attenuating the increased malar skin blood flow induced by ER niacin. In conclusion, the DP1 receptor antagonist laropiprant was effective in suppressing both subjective and objective manifestations of niacin-induced vasodilation.

Page last updated: 2007-08-04

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