Multiplate® TRAPtest

Multiplate® TRAPtest frontview

Multiplate TRAPtest

Assay for the quantitative in vitro determination of platelet function triggered by TRAP-6. Thrombin receptor activating peptide-6 (TRAP-6) is a potent platelet activator and stimulates platelet aggregation via the thrombin receptor PAR-1.


Thrombin is capable of activating platelets, which is mediated primarily by the hydrolysis of a G-protein-coupled receptor on the platelet membrane, referred to as protease-activated receptor 1 (PAR-1) and a second receptor (PAR-4) that expresses a lower sensitivity to thrombin.1 Activation by thrombin results in cross linked platelet aggregation as fibrinogen strands bind to glycoprotein IIb/IIIa receptors. Upon activation the components of the GPIIb/IIIa receptors physically alter their conformation producing the high affinity fibrinogen binding site GPIIb/IIIa on the platelet membrane. In order to analyze platelet function triggered via the thrombin receptor commonly a peptide, which stimulates the PAR-1 receptor is used (SFLLRN = TRAP-6).2 This allows to test for platelet function activated by the PAR-1 receptor, without triggering fibrin formation in the sample, which would happen if thrombin was used as the agonist. TRAP-6 induced platelet aggregation may be reduced or absent in the presence of GPIIb/IIIa antagonists3 or in deficiency states of GpII/bIIIa receptors (Glanzman trombasthenia).4,5 TRAP-6 induced aggregation displays only a minor sensitivity for the inhibiting effects of acetylsalicylic acid 6,7,8 or ADP receptor antagonists.8,9,10,11


1. Khan, M.L., Zheng, Y.-W., Huang W, et al. (1998). A dual thrombin receptor system for platelet activation. Nature.;394:690–694.
2. Kinlough-Rathbone, R.L., Perry, D.W., Guccione, M.A., et al. (1993). Degranulation of human platelets by the thrombin receptor peptide SFLLRN: comparison with degranulation by thrombin. Thromb Haemost. Dec 20;70(6):1019-23.
3. Desch, S., Siegemund, A., Scholz, U., et al. (2011). Platelet inhibition and GP IIb/IIIa receptor occupancy by intracoronary versus intravenous bolus administration of abciximab in patients with ST-elevation myocardial infarction. Clin Res Cardiol. Oct 21.
4. Halimeh, S. et al. (2010). Multiplate Whole Blood Impedance Point of Care Aggregometry : Preliminary Reference Values in Healthy Infants, Children, and Adolescents. Klin Padiatr; 222: 158-163.
5. Penz, S., Perchuc, A., Calatzis, A., et al. (2010). Effects of GpIIbIIIa and GpIb blockade on multiple electrode aggregometry (MEA). GTH; Abstract P10-13.
6. Jámbor, C., Weber, C.F., Gerhardt, K., et al. (2009). Whole blood multiple electrode aggregometry is a reliable point-of-care test of acetylsalicylic acid-induced platelet dysfunction. Anesth Analg Jul;109(1):25-31.
7. von Pape, K.W., Dzijan-Horn, M., Bohner, J., et al. (2007). Control of acetylsalicylic acid effect in chronic cardiovascular patients using two whole blood platelet function assays. PFA-100 and Multiplate. Hamostaseologie. Aug;27(3):155-60.
8. Velik-Salchner, C., Maier, S., Innerhofer, P., et al. (2008). Point-of-care whole blood impedance aggregometry versus classical light transmission aggregometry for detecting acetylsalicylic acid and clopidogrel: the results of a pilot study. Anesth Analg. Dec;107(6):1798-806
9. Johnson, A., Dovlatova, N., Heptinstall, S. (2008). Multiple electrode aggregometry and P2Y(12) antagonists. Thromb Haemost. Jun;99(6):1127-9.
10. Sibbing, D., Stegherr, J., Braun, S., et al. (2010). A double-blind, randomized study on prevention and existence of a rebound phenomenon of platelets after cessation of clopidogrel treatment. Am Coll Cardiol Feb 9;55(6):558-65.
11. Djukanovic, N., Todorovic, Z., Obradovic, S., et al. (2011). Abrupt Cessation of One-Year Clopidogrel Treatment Is Not Associated With Thrombotic Events. J Pharmacol Sci.;117(1):12-8.