Sociedad Americana de Hirudoterapia

The Antithrombotic Effect of Recombinant Neorudin on Thrombi

Animal model study published in Drug Design Development and Therapy (2022)

Última actualización: June 18, 2026Revisado por: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: In vitro / laboratoryDesarrollo de fármacosEnsayos clínicosLiu YB et al. · Drug Design Development and Therapy, 2022

Abstract

INTRODUCTION: Recombinant neorudin (EPR-hirudin, EH) was developed through the addition of an EPR (Glu-Pro-Arg) peptide to the amino terminus of hirudin, which can be recognized and cut by coagulation factors XIa (FXIa) and/or Xa (FXa). In this study, the low-bleeding antithrombotic effects of EH were evaluated utilizing experimental models of thrombosis in rabbits and rats to provide a test basis for clinical trials. METHODS: The bleeding risks of EH and hirudin were first compared in mice by the tail-clipping method, and then the antithrombotic activity of EH was investigated in a rabbit model of arteriovenous bypass thrombosis and a rat model of thrombotic cerebral infarction. RESULTS: In mice, intravenous administration of EH at 1.5 mg/kg and 3 mg/kg did not affect the bleeding time compared with normal saline, while the administration of hirudin at 1.5 mg/kg prolonged the bleeding time by over 3 times the administration of normal saline. Furthermore, intravenous administration of EH had a significant dose-dependent inhibitory effect on the formation and development of arteriovenous bypass thrombosis and thrombotic cerebral infarction. Compared with an equimolar dose of hirudin, the antithrombotic effect of EH was similar, while the bleeding side effects were significantly attenuated. Moreover, when the antithrombotic effects were similar, EH had a shorter bleeding time and was associated with less bleeding than low molecular weight heparin (LMWH). EH had a therapeutic effect on thrombotic cerebral infarction without increasing the occurrence of cerebral hemorrhage. CONCLUSION: The findings from the preclinical animal models used in this study showed that EH could not only effectively inhibit thrombus formation but also reduce the risk of bleeding.

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

Publication typeJournal Article
Indexed MeSH termsAnimalsCerebral InfarctionFibrinolytic AgentsHemorrhageHeparin, Low-Molecular-WeightHirudinsMiceRabbitsRatsRecombinant ProteinsSaline SolutionThrombosis

Resumen

EPR-hirudin (neorudin) inhibited arteriovenous bypass thrombosis and cerebral infarction in rabbits and rats without prolonging mouse tail bleeding time at therapeutic doses, even at 3x the classic hirudin dose — demonstrating an engineered safety advantage.

Por qué esto importa para la hirudoterapia

This study evaluated recombinant neorudin (EPR-hirudin, EH)—an engineered hirudin with an EPR peptide cleavable by FXIa/FXa—across multiple animal thrombosis models. In mice, EH at 1.5 and 3 mg/kg intravenously did not prolong bleeding time versus saline, while native hirudin at 1.5 mg/kg prolonged it over threefold; EH showed dose-dependent inhibition of arteriovenous bypass thrombosis in rabbits and thrombotic cerebral infarction in rats, with similar antithrombotic efficacy but significantly attenuated bleeding compared to equimolar hirudin or LMWH. For ASH, this is relevant as it advances engineered hirudin derivatives toward clinical translation with an improved safety profile. CAVEAT: All data are from preclinical animal models (mice, rats, rabbits); no human clinical trials are reported, and the abstract does not specify randomization, blinding, or full statistical methods.

Citación

The Antithrombotic Effect of Recombinant Neorudin on Thrombi.

Liu YB et al. · Drug Design Development and Therapy, 2022

Contexto clínico relacionado

Añadido a la biblioteca ASH: May 27, 2026 · Última actualización del sitio: June 18, 2026

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