[1] Taipoxin like many other pre-synaptic neurotoxins are phospholipase A2 (PLA2) toxins, which inhibit/complete block the release of the motor transmitter acetylcholine and lead to death by paralysis of the respiratory muscles (asphyxia).
[6] However it is thought that under strict evolution selection pressures of prey immobilisation and therefore extended feeding lead to the PLA2 enzyme losing its so called pancreatic loop and mutations for the toxin binding with pre-synaptic membranes of motor neuron end plates.
[7] The α and β complex consist of 120 amino acid residues which are cross linked by 7 disulfide bridges.
The gamma subunit also seems to function as a protector of the alpha complex, preventing fast renal clearance or proteolytic degradation.
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.
[1] Further experiments showed that Taipoxin inhibited the responses to electrical stimuli greater than the reaction to additionally administered acetylcholine.
The injection of taipoxin into the hind limbs of rats leads to oedema formation and muscle degeneration.
[20][21] The toxicity of Taipoxin or other PLA2 toxins are often measured with their ability to cut short chain phospholipids or phospholipids-analogues.
[23][24][25] The treatment of choice is an antivenom produced by CSL Ltd in 1956 in Australia on the basis of immunised horse plasma.
[26] After being bitten the majority of patients will develop systemic envenoming of which clinical evidence is usually present within two hours.