It also boosts the specificity on the target and could be involved in the binding of the alpha unit. The whole complex is slightly acidic with a pH(I) of 5, but under a lower pH and/or high ionic strength the subunits dissociate. Just as the PLA2 enzyme the PLA2 toxin is Ca2+ dependent for hydrolysing fatty acyl ester bonds at the sn-2 position of glycerol-phospholipids. Depending on disulphide bridge positions and lengths of C-termini these PLA2 enzymes/PLA2 toxins are categorized into three classes. These classes are also an indication of the toxicity of PLA2/PLA2, as PLA2s from pancreatic secretions, bee venom or the weak elapid venoms are grouped into class I, whereas PLA2s from the more potent viperid venoms which causes inflammatory exudate's are grouped into class II. However most snake venoms are capable of more than one toxic activity, such as cytotoxicity, myotoxicity, neuro-toxicity, anticoagulant activity and hypotensive effects. Taipoxin can be purified from the venom of the coastal taipan by gel filtration chromatography. In addition to taipoxin, the venom consists of many different components, responsible for the complex symptoms. In the beginning Taipoxin was thought to be only neurotoxic. Studies showed an increase in acetylcholine release, indicating a presynaptic activity. Further experiments showed that Taipoxin inhibited the responses to electrical stimuli greater than the reaction to additionally administered acetylcholine. This led to the conclusion that Taipoxin has pre- and postsynaptic effects. Additional to the increased acetylcholine release it inhibits the vesicular recycling. More recent studies showed that the toxin has a myotoxic effect as well. The injection of Taipoxin into the hind limbs of rats leads to oedema formation and muscle degeneration. The study also supports the findings by Fohlman, that the α subunit yields the PLA2 potency, which is similar to the potency of notexin. Even so, the full potential of the raw toxin is only reached by the combination of the α and γ subunits. A similar experiment has been done refocusing on the neural compounds. 24 hours after the injection the innervation was compromised to the extent of being unable to identify intact axons. This showed that Taipoxin like toxins lead to the depletion of transmitters from the nerve terminals and lead to the degeneration of nerve terminal and intramuscular axons.