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Thrombolysis by chemically modified coagulation factor Xa.

E L G Pryzdial1,2, S C Meixner3,4, K Talbot3,4

  • 1Centre for Blood Research and Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada. ed.pryzdial@blood.ca.

Journal of Thrombosis and Haemostasis : JTH
|July 1, 2016
PubMed
Summary
This summary is machine-generated.

A novel dual-acting molecule, Xai-K, acts as both a non-enzymatic thrombolytic agent and an anticoagulant. This improved thrombolytic therapy shows potential for enhanced safety and efficacy in treating blood clots.

Keywords:
factor Xafibrinolysisplasmintherapeutic thrombolysistissue plasminogen activator

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Area of Science:

  • Biochemistry
  • Pharmacology
  • Hematology

Background:

  • Enzymatic thrombolysis using recombinant tissue plasminogen activator (rtPA) risks hemorrhage and requires anticoagulants.
  • Existing thrombolytic agents may cause systemic side effects due to non-specific activation.
  • There is a need for safer and more effective thrombolytic strategies.

Purpose of the Study:

  • To develop and evaluate a novel dual-functioning molecule, Xai-K, with both thrombolytic and anticoagulant properties.
  • To assess the safety and efficacy of Xai-K compared to existing thrombolytic therapies.
  • To investigate Xai-K's mechanism of action in clot dissolution and hemostasis.

Main Methods:

  • Chemical modification of clotting factor Xa (FXa) to create non-enzymatic Xai-K.
  • In vitro assessment of Xai-K's fibrinolytic activity using turbidity, thromboelastography, and chromogenic assays.
  • In vivo evaluation of Xai-K in a murine model of carotid thrombosis and hemostatic models.
  • Assessment of anticoagulant properties in plasma clotting and bleeding models.

Main Results:

  • Xai-K demonstrated potent, tissue plasminogen activator (tPA)-dependent enhancement of plasma clot dissolution in vitro (~7-fold).
  • Xai-K alone achieved therapeutic thrombolysis in a murine carotid artery thrombosis model.
  • Co-administration of Xai-K significantly reduced the required dose of Tenecteplase (TNK) for reperfusion.
  • Xai-K did not induce systemic fibrinolysis markers observed with TNK and exhibited anticoagulant activity.

Conclusions:

  • Xai-K represents a promising novel agent for thrombolytic therapy, functioning as both a thrombolytic and anticoagulant.
  • Xai-K may offer an improved safety profile compared to conventional rtPA therapies by minimizing systemic fibrinolysis.
  • Xai-K holds potential as a primary therapeutic agent or as an adjunctive therapy with tPA variants like TNK.