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Related Concept Videos

Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants01:18

Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants

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Anticoagulant Drugs: Low-Molecular-Weight Heparins

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Related Experiment Video

Updated: Jun 12, 2026

Determination of the Procoagulant Activity of Extracellular Vesicle (EV) Using EV-Activated Clotting Time (EV-ACT)
04:56

Determination of the Procoagulant Activity of Extracellular Vesicle (EV) Using EV-Activated Clotting Time (EV-ACT)

Published on: August 4, 2023

Cell-dependent antithrombotic effect of tranexamic acid.

Kata Balog Virág1,2, Petra Csikós1,2, Alexandra Raska1,2

  • 1Department of Biochemistry, Institute of Biochemistry and Molecular Biology, Semmelweis University, Budapest, Hungary.

Frontiers in Immunology
|June 11, 2026
PubMed
Summary

Tranexamic acid (TXA) reduces venous clot formation by inhibiting leukocyte-associated plasmin activity, without increasing bleeding risk. This study clarifies TXA

Keywords:
antithrombotic actionfibrinolysisimmunothrombosisplasminogentranexamic acid

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Last Updated: Jun 12, 2026

Determination of the Procoagulant Activity of Extracellular Vesicle (EV) Using EV-Activated Clotting Time (EV-ACT)
04:56

Determination of the Procoagulant Activity of Extracellular Vesicle (EV) Using EV-Activated Clotting Time (EV-ACT)

Published on: August 4, 2023

Rapid Point-of-Care Assay of Enoxaparin Anticoagulant Efficacy in Whole Blood
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Rapid Point-of-Care Assay of Enoxaparin Anticoagulant Efficacy in Whole Blood

Published on: October 12, 2012

Area of Science:

  • Biochemistry
  • Hematology
  • Pharmacology

Background:

  • Tranexamic acid (TXA) is a lysine analog that inhibits fibrinolysis.
  • While effective in reducing bleeding mortality, its prophylactic benefits and effects on thrombus formation are context-dependent.
  • TXA may have cell-dependent effects beyond antifibrinolysis due to plasmin(ogen)'s interactions with cellular components.

Purpose of the Study:

  • To investigate how cellular elements influence TXA's impact on thrombus formation.
  • To determine if TXA's antithrombotic effects are cell-dependent.

Main Methods:

  • Utilized an *in vivo* murine venous thrombosis model (IVC stenosis) without endothelial injury.
  • Assessed thrombin generation in whole blood and platelet-rich plasma to evaluate cell dependence.
  • Quantified leukocyte-associated plasminogen activation and measured plasma VWF:Ag and MCP-1 levels.

Main Results:

  • TXA significantly reduced venous thrombus initiation by 90% but did not affect existing clot mass.
  • TXA decreased thrombin generation in whole blood, but not in platelet-rich plasma, indicating a cellular requirement.
  • TXA inhibited leukocyte surface-mediated plasminogen activation and suppressed stenosis-induced MCP-1 increase.

Conclusions:

  • TXA is not prothrombotic in venous stasis; it reduces thrombus initiation without impairing primary hemostasis.
  • This study demonstrates TXA's cell-dependent modulation of thrombin generation, linked to inhibiting leukocyte-associated plasmin activity.