Key result
Monoclonal antibodies JAQ2 and JAQ3 deplete GPVI in vivo as effectively as JAQ1.
Why the study?
The mechanism by which monoclonal antibodies induce in vivo down-regulation of GPVI, specifically whether targeting the collagen-binding site is essential, was unclear.
Population
Mouse model and in vitro platelet studies
Comparison
Monoclonal antibodies JAQ2 and JAQ3 versus JAQ1 against different GPVI epitopes
Design
Preclinical experimental study
Authors
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In vitro GPVI mAb data support ligand-binding mechanism; leaves open translation to clinical antithrombotic use.
Anti-GPVI antibodies induce in vivo down-regulation of the GPVI receptor irrespective of their specific binding site or Fc involvement, suggesting a general mechanism for this potential antithrombotic strategy.
Schulte et al. (2003) studied this question. Monoclonal antibodies against different epitopes on GPVI (JAQ2, JAQ3) vs. JAQ1 was evaluated on Depletion of GPVI in vivo. Injection of monoclonal antibodies against different epitopes on GPVI (JAQ2, JAQ3) induced depletion of GPVI with the same efficacy and kinetics as JAQ1 in vivo.
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