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Chinensinaphthol methyl ether prevents thrombosis by inhibiting the intrinsic pathway of coagulation through

Hui Zhang1, Ting Zhang2, Panyao Zhou1

  • 1Faculty of Pharmacy, Hubei University of Chinese Medicine, Wuhan, 430065, China; Key Laboratory of Traditional Chinese Medicine Resources and Chemistry of Hubei Province, Wuhan, 430065, China.

Phytomedicine : International Journal of Phytotherapy and Phytopharmacology
|April 5, 2026
PubMed
Summary

Chinensinaphthol methyl ether (CME) effectively inhibits thrombosis by targeting coagulation factor ⅩⅡ (F12). This natural lignan offers dual antithrombotic effects with a low bleeding risk, presenting a promising therapeutic candidate for thrombotic disorders.

Keywords:
Antiendogenous coagulationAntiplatelet aggregationChinensinaphthol methyl etherCoagulation factor ⅩⅡProteomicsRostellularia procumbens (L.) Nees

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Area of Science:

  • Pharmacology
  • Biochemistry
  • Molecular Biology

Background:

  • Thrombotic disorders are a major global health burden.
  • Dysregulated coagulation and platelet aggregation drive thrombus formation.
  • Targeting both pathways is crucial for effective antithrombotic therapy.

Purpose of the Study:

  • To investigate the antithrombotic mechanism of Chinensinaphthol methyl ether (CME).
  • To identify the molecular target of CME in coagulation.
  • To evaluate CME as a potential therapeutic agent for thrombotic diseases.

Main Methods:

  • In vivo antithrombotic assays.
  • Platelet, liver, and plasma proteomics.
  • Molecular docking, DSF, BLI, molecular dynamics, and mutation studies.
  • Evaluation of Rostellularia procumbens (L.) Nees lignan.

Main Results:

  • CME significantly inhibited platelet aggregation and the intrinsic coagulation pathway.
  • Proteomic analyses revealed down-regulation of complement-coagulation cascade proteins.
  • Coagulation factor ⅩⅡ (F12) was identified as the primary target.
  • CME binds to F12's FnI domain, inhibiting its activation to F12a.

Conclusions:

  • This study elucidates CME's novel antithrombotic mechanism targeting F12.
  • CME demonstrates dual antithrombotic effects with a low bleeding risk.
  • CME represents a promising small-molecule drug candidate for thrombotic diseases.