Wolfgang Miesbach: How Does Protein S Inhibition Restore Hemostasis in von Willebrand Disease?
Wolfgang Miesbach, Professor of Medicine at Frankfurt University Hospital, shared a post on LinkedIn about a recent article by Yumiko Sakurai, published in Blood:
“How Does Protein S Inhibition Restore Hemostasis in von Willebrand Disease?
At EAHAD2026, fascinating microfluidics data from Emory University shed light on VGA039’s mechanism in VWD.
The connection isn’t immediately obvious:
VWD stems from insufficient platelet adhesion due to low or dysfunctional VWF.
Protein S is a cofactor for activated protein C, regulating thrombin generation.
Findings from the Ex Vivo Model, The haemostasis-on-a-chip data demonstrated that VGA039:
- Significantly shortened bleeding times in VWD patient blood
- Accelerated platelet deposition (p<0.004)
- Enhanced fibrin accumulation (p<0.008)
- Restored haemostasis through dual inhibition of TFPI and aPC pathways
The Mechanistic Insight:
The answer lies at the microvascular level.
By neutralizing Protein S’s dual activities (cofactor for protein C and TFPI inhibitor), VGA039 allows enhanced local thrombin generation specifically at microvascular sites – precisely where VWF normally enables platelet adhesion and where most bleeding occurs in VWD patients.
Congratulations to Yumiko Sakurai and co-authors.”
Title: A protein S-targeting monoclonal antibody, VGA039, improves both primary and secondary hemostatic activity of von Willebrand disease patient blood in an ex vivo vascularized hemostasis-on-a-chip
Authors: Yumiko Sakurai, Megan Brown, Yongzhi Qiu, Elaissa Hardy, Tony Byun, Sandip Panicker, Wilbur Lam
Read the Full Article on Blood
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