American Society of Hirudotherapy

Calin from Hirudo medicinalis, an inhibitor of von Willebrand factor binding to collagen under static and flow conditions

Research article published in Blood (1995)

Last Updated: June 18, 2026Reviewed by: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: Research reportSalivary PharmacologyDrug DevelopmentHarsfalvi J et al. · Blood, 1995

Abstract

Calin from the saliva of the medicinal leech, Hirudo medicinalis, is a potent inhibitor of collagen mediated platelet adhesion and activation. In addition to inhibition of the direct platelet-collagen interaction, we presently demonstrate that binding of von Willebrand to coated collagen can be prevented by Calin, both under static and flow conditions in agreement with the occurrence of binding of Calin to collagen, confirmed by Biospecific Interaction Analysis. To define whether Calin acted by inhibiting the platelet-collagen or the platelet-von Willebrand factor (vWF)-collagen-mediated thrombus formation, platelet adhesion to different types of collagens was studied in a parallel-plate flow chamber perfused with whole blood at different shear rates. Calin dose-dependently prevented platelet adhesion to the different collagens tested both at high- and low-shear stress. The concentration of Calin needed to cause 50% inhibition of platelet adhesion at high-shear stress was some fivefold lower than that needed for inhibition of vWF-binding under similar conditions, implying that at high-shear stress, the effect of Calin on the direct platelet-collagen interactions, suffices to prevent thrombus formation. Platelet adhesion to extracellular matrix (ECM) of cultured human umbilical vein endothelial cells was only partially prevented by Calin, and even less so at a high-shear rather than a low-shear rate, whereas the platelet binding to coated vWF and fibrinogen were minimally affected at both shear rates. Thus, Calin interferes with both the direct platelet-collagen interaction and the vWF-collagen binding. Both effects may contribute to the inhibition of platelet adhesion in flowing conditions, although the former seems to predominate.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Publication typeJournal ArticleResearch Support, Non-U.S. Gov't
Indexed MeSH termsAnimalsCollagenDose-Response Relationship, DrugHumansInvertebrate HormonesKineticsLeechesPlatelet AdhesivenessPlatelet Aggregation InhibitorsProtein BindingSalivary Proteins and PeptidesStress, Mechanical

Summary

Calin from Hirudo medicinalis prevents binding of von Willebrand factor to coated collagen under static and flow conditions; interferes with platelet-collagen and vWF-collagen interactions.

Why This Matters for Hirudotherapy

This in vitro study characterized Calin, a salivary protein from Hirudo medicinalis, as an inhibitor of collagen-mediated platelet adhesion and von Willebrand factor (vWF) binding to collagen under both static and flow conditions. Using a parallel-plate flow chamber perfused with whole blood, the authors showed Calin dose-dependently prevented platelet adhesion to various collagens at high- and low-shear stress, with the direct platelet-collagen interaction appearing to predominate over vWF-binding inhibition at high shear. This work is relevant to ASH's domain as it elucidates a mechanism by which a leech salivary constituent may prevent thrombus formation. The honest caveat is that this is a preclinical in vitro study with no in vivo or clinical data presented, so no therapeutic or efficacy claims can be inferred from the abstract.

Citation

Calin from Hirudo medicinalis, an inhibitor of von Willebrand factor binding to collagen under static and flow conditions.

Harsfalvi J et al. · Blood, 1995

Added to ASH library: May 27, 2026 · Site last updated: June 18, 2026

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