Key result
GPVI-targeting drugs show potential as safe antithrombotics by blocking GPVI-mediated platelet activation.
Why the study?
GPVI targeted antiplatelet therapy is investigated as a means to redress the balance between antithrombotic efficacy and bleeding risk.
Answers are grounded in this paper and cite their sources.
GPVI-targeted therapies represent a novel class of antithrombotics that may decouple antithrombotic efficacy from bleeding risk.
GPVI targeted antiplatelet therapy as a means to redress the balance between antithrombotic efficacy and bleeding risk. Collagen binds to the platelet GPVI receptor and triggers platelet activation via the Fc receptor γ (FcRγ) chain which contains an immunoreceptor tyrosine-based activation motif (ITAM). Mechanisms of action of different GPVI-targeting drug candidates: Revacept, a recombinant GPVI-Fc fusion protein acts as a competitive GPVI antagonist and blocks potential collagen-binding sites. Glenzocimab, a humanised anti-GPVI antibody blocks the collagen binding site of GPVI. EMA601, a novel high-affinity, humanised anti-GPVI antibody blocks GPVI-mediated platelet activation, but partially retains platelet adhesion on exposed collagen.
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McFadyen et al. (2024) conducted a review in Thrombosis. GPVI-targeting drug candidates (Revacept, Glenzocimab, EMA601) was evaluated. GPVI-targeting drug candidates (Revacept, Glenzocimab, EMA601) offer potential as safe antithrombotic therapies by blocking collagen-binding sites or GPVI-mediated platelet activation.
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