Amerikanische Gesellschaft für Hirudotherapie

New derivative of staphylokinase SAK-RGD-K2-Hirul exerts thrombolytic effects in the arterial thrombosis model in rats

Comparative study published in Pharmacological reports : PR (2011)

Zuletzt aktualisiert: June 18, 2026Geprüft von: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: Observational studyArzneimittelentwicklungSzemraj J et al. · Pharmacological reports : PR, 2011

Abstract

SAK-RGD-K2-Hir and SAK-RGD-K2-Hirul are recombinant proteins that are derivatives of r-SAK (recombinant staphylokinase). They are characterized by their fibrin-specific plasminogen activation properties and their antithrombin and antiplatelet activities. The difference between these proteins is the presence of the antithrombotic fragment (hirudin or hirulog) in the C-terminal portion of the r-SAK. The aim of the present study was to examine the thrombolytic potentials of SAK-RGD-K2-Hir and SAK-RGD-K2-Hirul in an electrically induced carotid artery thrombosis model in rats and to compare the potentials to that of r-SAK. We determined that a bolus injection of SAK-RGD-K2-Hirul was more effective than one of r-SAK in the improvement and maintenance of carotid patency and in arterial thrombus weight reduction; however, it had the same potency as SAK-RGD-K2-Hir. The bleeding time, prothrombin time and activated partial thromboplastin time were significantly prolonged in the animals that were treated with either dose (1.5 or 3.0 mg/kg) of SAK-RGD-K2-Hir or SAK-RGD-K2-Hirul, whereas no changes were observed in the plasma fibrinogen concentration or the α2 plasmin inhibitor level. r-SAK alone did not change the bleeding time or coagulation parameters. In conclusion, our findings demonstrate the thrombolytic activity of intravenous bolus injection of the novel thrombolytic agent SAK-RGD-K2-Hirul in rats. Although this protein compares favorably with r-SAK, we were unable to show the presence of any beneficial effects of SAK-RGD-K2-Hirul over those of SAK-RGD-K2-Hir. Furthermore, our results suggest that high doses of SAK-RGD-K2-Hirul bear the risk of bleeding.

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

Publication typeComparative StudyJournal ArticleResearch Support, Non-U.S. Gov't
Indexed MeSH termsAnimalsBleeding TimeBlood CoagulationCarotid Artery ThrombosisDisease Models, AnimalDose-Response Relationship, DrugFibrinolytic AgentsHirudinsInjections, IntravenousMaleMetalloendopeptidasesRats

Zusammenfassung

SAK-RGD-K2-Hir and SAK-RGD-K2-Hirul are recombinant proteins that are derivatives of r-SAK (recombinant staphylokinase).

Warum dies für die Hirudotherapie relevant ist

This study examined the thrombolytic potential of a recombinant staphylokinase derivative, SAK-RGD-K2-Hirul, which incorporates a hirulog (hirudin-derived) antithrombotic fragment, in an electrically induced carotid artery thrombosis model in rats. A bolus injection of SAK-RGD-K2-Hirul was more effective than r-SAK alone in improving carotid patency and reducing thrombus weight, comparable to the hirudin-fragment-containing SAK-RGD-K2-Hir, but high doses carried bleeding risk. This demonstrates the functional contribution of a hirudin-derived peptide within a multimodal thrombolytic fusion protein, relevant to hirudin-based antithrombotic drug design. Caveat: this is an animal (rat) study of a recombinant fusion protein, not natural hirudin or live leech therapy, and no advantage over the hirudin-fragment variant was shown.

Zitation

New derivative of staphylokinase SAK-RGD-K2-Hirul exerts thrombolytic effects in the arterial thrombosis model in rats

Szemraj J et al. · Pharmacological reports : PR, 2011

DOI

Verwandter klinischer Kontext

Erfahren Sie, wie diese Forschung mit der klinischen Praxis verknüpft ist

Drug PipelineDrug DevelopmentDirect Thrombin InhibitorsHirudinAnticoagulation CompoundsHemostasisOtolaryngology

Zur ASH-Bibliothek hinzugefügt: May 27, 2026 · Letzte Aktualisierung der Website: June 18, 2026

Diese Website stellt Bildungsinformationen bereit und ist weder eine medizinische Beratung noch eine Diagnose oder Behandlungsempfehlung. Die medizinische Blutegeltherapie ist mit klinisch relevanten Risiken verbunden und sollte ausschließlich von qualifizierten Klinikerinnen und Klinikern unter institutionell genehmigten Protokollen durchgeführt werden. Die FDA-510(k)-Zulassung für medizinische Blutegel ist auf bestimmte Indikationen beschränkt; experimentelle und Off-Label-Diskussionen werden entsprechend gekennzeichnet. Für patientenspezifische Beratung wenden Sie sich an eine qualifizierte Gesundheitsfachkraft.