These toxins are often found in the venom of vipers for example the Fer-de-lance snake (Bothrops atrox), they work by disrupting the sequence of clotting within their prey, which is advantageous to the snake during digestion. Snake venom contains two main types of haemotoxin; homeostatic and anti-thrombitic. As shown in the diagram these proteins interfere with the clotting process at various different stages.

These toxins have been found to be extremely useful as scientific tools not only in laboratory but also within medical science. For example using the thrombin-like enzymes found in Central American pit viper Bothrops moojeni, scientists are able to determine the levels of fibrinogen in a blood sample, by there conversion into fibrin, which can then be evaluated³.

Snake venom can also contain haemolytic enzymes which cause the haemorrhage of red blood cells, this is another way of digesting the prey internally for the snake. The Russell's viper (Daboia russelli) has been used to treat patients suffering from haemophilia in the past due to to its potent coagulative properties. Which shows that snake haemotoxins have huge potential use within the treatment of blood and cardiac conditions in general.

α-Bungarotoxins work by acting as an antagonist at the neuromuscular nicotinc receptors, the stimulation of these receptors is crucial to movement and breathing, by blocking these receptors acetylcholine (the bodies natural chemical for neurotransmission) is blocked and no transmission can occur. This causes the prey to become paralysed and leads to their eventual asphyxiation as diaphragm is unable to move which stops breathing. The effect of α-Bungarotoxin is quicker than that of the pre-synaptic toxins as it is able to act instantly at the synapse, thus it tends to induce paralysis much quicker, it is however generally more treatable than pres-synaptic toxins as it can be overcome by increasing the acetylcholine levels. This is achieved by treatment with anticholinesterase such as neostigmine.

Dendrotoxin
Dendrotoxins act on the pre-synaptic neuron by preventing the release of potassium ions through blockade of ion channels. This in turn stimulates the increased release of acetylcholine from the pre-synaptic neuron causing an initial stimulation, however the pre-synaptic neuron is then unable to depolarise and hence signals are blocked. This blockade leads to paralysis and eventual death if left untreated.

β-Bungarotoxin
β-Bungarotoxin binds to the pre-synaptic terminal axon, it then damages it in turn making neurotransmission impossible. The mechanism by which it damages the axon is not definitely known however it is thought to prevent

                             
                    Image taken from http://www-  nmr.cabm.rutgers.edu/photogallery/structures/html/page9.html