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Laropiprant attenuates EP3 and TP prostanoid receptor-mediated thrombus formation
Sonia Philipose1, Viktoria Konya, Mirjana Lazarevic
1Institute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.
Plos One
|August 8, 2012
Summary
Niacin-induced flushing can be reduced by laropiprant. However, laropiprant may affect platelet function and increase thrombotic risk in cardiovascular disease patients.
Area of Science:
- Pharmacology
- Cardiovascular Research
- Biochemistry
Background:
- Niacin, a lipid-lowering agent, causes flushing mediated by prostaglandin D2 (PGD2).
- Laropiprant, a PGD2 receptor antagonist, is used to prevent niacin-induced flushing.
- PGD2 inhibits platelet aggregation, raising concerns about atherothrombotic risk with laropiprant use.
Purpose of the Study:
- To investigate the in vitro effects of laropiprant on platelet function.
- To assess the potential impact of laropiprant on thrombotic events in cardiovascular disease.
Main Methods:
- In vitro platelet assays measuring aggregation, Ca2+ flux, P-selectin expression, glycoprotein IIb/IIIa activation, and thrombus formation.
- Testing laropiprant's effects in combination with PGD2, acetylsalicylic acid, and niacin.
- Evaluating laropiprant's effects on platelet activation via thromboxane (TP), E-type prostanoid (EP)-3, EP4, and I-type prostanoid (IP) receptors.
Main Results:
- Laropiprant prevented PGD2-mediated inhibition of platelet function.
- Laropiprant did not inhibit thrombus formation induced by acetylsalicylic acid or niacin.
- At higher concentrations, laropiprant attenuated platelet activation via TP and EP-3 receptors but not EP4 or IP receptors.
Conclusions:
- Niacin/laropiprant combination may have a favorable profile regarding platelet function.
- The findings suggest a potentially beneficial effect on thrombotic events in vascular disease.
- Further research is warranted to confirm these in vitro findings in clinical settings.
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