Calin from Hirudo medicinalis, an inhibitor of platelet adhesion to collagen, prevents platelet-rich thrombosis in hamsters
Research article published in Blood (1995)
Abstract
Interaction between exposed collagen and platelets and/or von Willebrand factor is believed to be one of the initiating events for thrombus formation at sites of damaged endothelium. Interference with this mechanism may provide an anti-thrombotic potential. Calin, a product from the saliva of the leech Hirudo medicinalis, was tested in vitro and for its in vivo activity in a thrombosis model in hamsters. Calin specifically and dose dependently (IC50:6.5 to 13 micrograms/mL) inhibited human platelet aggregation induced by collagen. In addition, specific platelet adhesion onto microtiter wells coated with collagen and detected with a monoclonal antiglycoprotein IIb/IIIa antibody-conjugated with horseradish peroxidase, could be completely prevented with Calin (IC50:22 micrograms/mL). A dose-response curve was constructed in groups of six hamsters in whom a standardized trauma was induced on the femoral vein. Thrombus formation was followed continuously using video recording and processing of the image obtained upon transillumination of the vessel. Intravenous Calin dose-dependently inhibited platelet-rich thrombus formation in this model with an ED50 of 0.07 mg/kg and complete inhibition with 0.2 mg/kg. No effects were seen on coagulation tests or bleeding times, whereas ex vivo aggregation induced by collagen was inhibited dose dependently. Local application of leech saliva, Calin, hirudin, or the combination of the latter two into the bleeding time wound of hamsters resulted in a mild prolongation of the bleeding time (twofold to threefold). A similar experiment in baboons did not cause any prolongation of the bleeding time. This is in sharp contrast with the long-lasting bleeding after a leech bite itself in both species. Calin from the leech Hirudo medicinalis is able, by binding to collagen, to effectively interfere with platelet-collagen interaction, which results in an antithrombotic effect observed in a platelet-rich thrombosis model in hamsters.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Resumen
Calin inhibits collagen-induced platelet aggregation (IC50 6.5-13 microg/mL) and prevents platelet-rich thrombosis in hamster femoral vein model with ED50 of 0.07 mg/kg.
Por qué esto importa para la hirudoterapia
Este estudio examinó Calin, una proteína salival de Hirudo medicinalis, tanto in vitro como en un modelo de trombosis de la vena femoral en hámster, demostrando una inhibición dependiente de la dosis de la agregación plaquetaria humana inducida por colágeno (CI50 ~6,5–13 µg/mL) y la prevención completa de la adhesión plaquetaria a superficies recubiertas de colágeno (CI50 ~22 µg/mL). La administración intravenosa de Calin inhibió de forma dosis-dependiente la formación de trombos ricos en plaquetas en hámsteres (DE50 ~0,07 mg/kg, completa a 0,2 mg/kg) sin efectos sobre las pruebas de coagulación ni sobre los tiempos de sangría, aunque la aplicación local en heridas de tiempo de sangrado prolongó levemente el sangrado en hámsteres pero no en babuinos. Estos hallazgos son pertinentes para el ámbito de ASH, ya que demuestran un efecto antitrombótico in vivo de un compuesto salival definido de sanguijuela. La advertencia es que se trata de un estudio en modelo animal con datos limitados a pocas especies; la discrepancia observada entre el sangrado por mordedura de sanguijuela y los efectos de la administración de Calin subraya que los hallazgos podrían no representar plenamente la acción completa del secretoma de la sanguijuela en humanos.
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Añadido a la biblioteca ASH: May 27, 2026 · Última actualización del sitio: 18 de junio de 2026