Related Experiment Video
Updated: May 15, 2026

Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Prasugrel reduces agonists' inducible platelet activation and leukocyte-platelet interaction more efficiently than
Thomas Gremmel1, Roza Badr Eslam, Renate Koppensteiner
1Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Aims:
The antiplatelet effects of clopidogrel and prasugrel have mainly been compared using different platelet reactivity tests. Further, data on the impact of both drugs on thrombin-inducible platelet activation are scarce. We therefore investigated the influence of clopidogrel and prasugrel on different flow cytometric parameters of platelet activation as well as on platelet function assessed by leukocyte-platelet interaction.
Methods:
Baseline, ADP and thrombin receptor-activating peptide (TRAP)-6 inducible P-selectin expression, activation of glycoprotein (GP) IIb/IIIa and monocyte-platelet aggregate (MPA) formation were determined by flow cytometry in 84 clopidogrel- and 21 prasugrel-treated patients undergoing percutaneous coronary intervention with stent implantation.
Results:
Baseline expressions of P-selectin and activated GPIIb/IIIa did not differ significantly between clopidogrel- and prasugrel-treated patients (both P > 0.2). After activation with ADP or TRAP-6, patients with clopidogrel therapy exhibited significantly higher platelet surface expressions of P-selectin and activated GPIIb/IIIa than prasugrel-treated patients (all P ≤ 0.001). Further, high P-selectin and high GPIIb/IIIa were significantly more frequent in clopidogrel-treated patients than in patients on prasugrel therapy (all P = 0.01). Likewise, the formation of MPA without addition of agonists did not differ significantly between patients receiving clopidogrel and patients on prasugrel therapy (P = 0.2). After activation with ADP or TRAP-6, clopidogrel-treated patients showed a significantly more pronounced formation of MPA than patients-receiving prasugrel (both P = 0.02).
Conclusions:
Prasugrel reduces ADP and TRAP-6 inducible platelet activation, and leukocyte-platelet interaction more efficiently than clopidogrel.
More Related Videos
Related Concept Videos
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
GPCR Desensitization
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Drug-Receptor Interaction: Agonist
Agonists can bind to receptors in different ways. Some agonists bind directly to the receptor's active site, mimicking the endogenous ligand's action.

