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Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice

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Interleukin-10 does not modulate clopidogrel platelet response in mice.

Q Yin¹, T Tai¹, J-Z Ji¹

¹General Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.

Journal of Thrombosis and Haemostasis : JTH

|December 30, 2015

Summary

Interleukin-10 (IL-10) does not affect the maximum levels of clopidogrel active metabolite (CAM) or its antiplatelet effects. CAM’s maximum concentration, not its overall exposure, is key to clopidogrel

Keywords:

clopidogrel hemostasis interleukin-10 mice platelet aggregation

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Area of Science:

Pharmacology and Toxicology
Immunology
Drug Metabolism

Background:

Elevated interleukin-10 (IL-10) levels correlate with reduced clopidogrel response in patients.
Clopidogrel requires hepatic bioactivation to exert its antiplatelet effects.
No prior data existed on the direct association between IL-10 and clopidogrel metabolism or efficacy.

Purpose of the Study:

To investigate the impact of IL-10 gene expression on clopidogrel active metabolite (CAM) formation.
To determine if IL-10 influences the antiplatelet response to clopidogrel.
To compare clopidogrel pharmacokinetics and pharmacodynamics in IL-10 knockout and wild-type mice.

Main Methods:

Administered a single oral dose of clopidogrel to IL-10 knockout and wild-type mice.
Quantified clopidogrel and CAM pharmacokinetic parameters, including area under the curve (AUC) and maximum concentration (Cmax).
Assessed adenosine diphosphate-induced platelet aggregation to measure antiplatelet effects.

Main Results:

Wild-type mice showed lower CAM AUC and shorter half-life compared to IL-10 knockout mice.
Clopidogrel AUC was higher in wild-type mice, indicating slower clearance.
Despite differences in CAM AUC, antiplatelet effects did not significantly differ due to comparable CAM Cmax between groups.

Conclusions:

IL-10 influences the overall exposure (AUC) of clopidogrel active metabolite (CAM), but not its peak concentration (Cmax).
The maximum concentration (Cmax) of CAM is the primary determinant of clopidogrel's antiplatelet activity in mice.
IL-10 status does not significantly alter the therapeutic efficacy of clopidogrel in this mouse model.