Snake venom metalloproteinases (SVMPs) induces local and systemic effects on patients suffering from snakebite, degrading extracellular matrix (ECM) proteins such as collagen, gelatin, elastin, laminin, fibronectin, nidogen (entactin), and thrombospondin that cause local hemorrhage and tissue damage. They cleave or activate coagulation factors such as
fibrinogen, fibrin, prothrombin, factor V, factor IX, factor X and protein C that bring about systemic coagulopathy. SVMPs and
their truncated forms cleave or interfere with platelet adhesive proteins such as vWF, fibrinogen and collagen, and cleave or
interfere with platelet receptors such as GPVI, alpha2beta1, GPIb, GPIX, and GPIIbIIIa that result in platelet aggregation
defect. SVMPs induce cancer cell line to form morphological changes and apoptosis in vitro concordant with skin necrosis
after snakebite in some cases. These local effects caused by SVMPs have no certain treatments, even with commercial antivenom. SVMPs researches are focusing on their inhibitors, measurement and replacement of blood coagulation factor
defects, or anti-cancer drug.

Keywords: Snake venom metalloproteinase (SVMP), Extracellular matrix (ECM), Coagulation factor, Platelet aggregation, Anti-cancer drug