Why the study?
Current antithrombotic therapies reduce thrombotic events but are limited by bleeding risk; selective BTK degradation may provide antithrombotic benefits without affecting hemostasis.
Does selective degradation of platelet BTK by PROTAC NX-5948 reduce thrombosis without affecting hemostasis in preclinical models?
Population
In vitro human platelets and in vivo mouse model
Comparison
BTK degraders NX-2127 and NX-5948 vs control
Design
Preclinical experimental study
Key result
The BTK degrader NX-5948 selectively degraded platelet BTK and markedly reduced in vivo arterial thrombosis in mice without increasing bleeding time.
Authors
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Hypothesis-generating for antithrombotic therapy sparing hemostasis; human trials needed before any clinical consideration.
Does selective degradation of platelet BTK by PROTAC NX-5948 reduce thrombosis without affecting hemostasis in preclinical models?
Selective degradation of platelet BTK by NX-5948 offers a promising antithrombotic strategy that decouples thrombosis prevention from bleeding risk.
May et al. (2026) studied Thrombosis. NX-5948 was evaluated on Arterial thrombosis and bleeding time. The BTK degrader NX-5948 selectively degraded platelet BTK and markedly reduced in vivo arterial thrombosis in mice without increasing bleeding time.
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