Anticoagulation & Antiplatelet Compounds
Beyond hirudin — multiple anticoagulation strategies working synergistically
Last updated: March 14, 2026
Hirudin gets the headlines, but leech SGS deploys multiple anticoagulation strategies simultaneously — a redundant, synergistic system that ensures blood remains liquid throughout feeding and post-detachment bleeding.
Calin — Platelet Adhesion Inhibitor
Calin is a ~65 kDa glycoprotein that inhibits collagen-mediated platelet adhesion and von Willebrand factor (vWF) binding. Unlike hirudin, which targets thrombin, calin prevents platelets from adhering to damaged tissue in the first place.
Clinical significance: Calin is responsible for the prolonged post-detachment bleeding phase (the "passive bleed") that can last 4 to 24 hours after the leech is removed. This sustained bleeding is therapeutically valuable in venous congestion management.
Apyrase — ADP Antagonist
Apyrase is an ATP-diphosphohydrolase that hydrolyzes ADP (adenosine diphosphate) — a key platelet aggregation agonist released during the coagulation cascade.
By degrading ADP, apyrase blocks ADP-dependent platelet aggregation. It works synergistically with calin: calin prevents initial adhesion, apyrase prevents subsequent aggregation — two distinct targets, same outcome.
Saratin — Anti-Adhesion Peptide
Saratin is a ~12 kDa peptide that inhibits platelet-collagen adhesion through a mechanism distinct from calin. While calin targets vWF binding, saratin directly blocks the platelet collagen receptor (GPVI).
Saratin has been investigated as a standalone antiplatelet agent in preclinical research, though no pharmaceutical product has reached clinical trials.
Factor Xa Inhibitors
Leech saliva contains antistatin (originally identified in Haementeria leeches, with homologs in Hirudo) — a peptide that blocks factor Xa in the coagulation cascade.
Factor Xa inhibition represents yet another anticoagulation mechanism, complementing the direct thrombin inhibition (hirudin) and platelet-targeted strategies (calin, apyrase, saratin).
Synergistic Strategy
Summary Table
| Compound | Target | Mechanism | Clinical Significance |
|---|---|---|---|
| Hirudin | Thrombin | Direct inhibition (active site + exosite I) | Prevents fibrin formation |
| Calin | Platelet adhesion | Blocks vWF binding and collagen adhesion | Prolonged post-detachment bleeding (4 to 24 hours) |
| Apyrase | ADP | Hydrolyzes ADP (ATP-diphosphohydrolase) | Prevents ADP-dependent platelet aggregation |
| Saratin | GPVI receptor | Directly blocks platelet-collagen interaction | Redundant anti-adhesion mechanism |
| Antistatin | Factor Xa | Blocks factor Xa in coagulation cascade | Upstream coagulation inhibition |