Enzymatic anticoagulant proteins |
|
|
|
1. Phospholipase A2 enzymes |
Strongly anticoagulant |
Inhibits activation of FX to FXa by extrinsic tenase complex |
By both enzymatic and non-enzymatic mechanisms; target protein not known |
|
|
Inhibits activation of prothrombin to thrombin by prothrombinase complex |
By non-enzymatic mechanism; binds to FXa and interferes in the prothrombinase complex formation |
|
Weakly anticoagulant |
Inhibits activation of FX to FXa by extrinsic tenase complex |
By non-enzymatic mechanism through hydrolysis of phospholipids |
2. Metalloproteinases (α-fibrinogenase) |
|
Weaker soft clot formation due to physical destruction of fibrinogen |
By cleaving Aα-chain of fibrinogen |
3. Serine proteinases |
Protein C activators |
Inactivation of cofactors FVa and FVIIIa degradation |
Directly activate protein C |
|
Thrombin-like enzymes |
Deplete fibrinogen in the plasma |
Releases either fibrinopeptide A or B; fibrin clots are removed leading to depletion of fibrinogen content |
|
Fibrinogenases |
Physical destruction of fibrinogen |
Mechanism not known |
4. L-Amino acid oxidase |
|
Inhibits FIX activity |
Mechanism not known |
Non-enzymatic anticoagulant proteins |
|
|
|
1. C-type lectin related proteins |
FX and FIX binding proteins |
Inhibit the formation of coagulation complexes |
Bind to the Gla domain of FIX and FX, and interfere in their binding to phospholipids |
|
Bothrojaracin, bothroalternin |
Inhibit the activity of thrombin |
Bind to α-thrombin at both exosite-1 and exosite-2 |
2. Three-finger toxin |
Cardiotoxins from Naja nigricollis crawshawii venom |
Act on the extrinsic pathway of the clotting cascade |
Mechanism not known |
|
Hemextin A and hemextin AB complex from Hemachatus haemachatus venom |
Prevents clot initiation by inhibiting extrinsic tenase activity |
Specifically binds to FVIIa |