[2] The name notexin comes from the fact that this toxin was first found to be the major component in the venom of the tiger snake.

[4] The toxin was first purified more than a hundred years later in 1972 by Karlsson et al.[3][5] This prompted more research into notexin.

Also the active site seems to be similar enough to that of other PLA2s in order to use their model building studies when discussing enzymatic properties.

Notexin does deviate significantly from other PLA2s due to different main chain lengths and its conformation in the 69th amino acid residue.

This lethal effect is the result of a presynaptic blockade of transmission across neuromuscular junctions of the breathing muscles, causing asphyxiation.

[8] Notexin causes an indirect reduction or complete end of the release of acetylcholine in the affected nerve terminals.

[13][16] Research [16] showed that neurons, after treatment with notexin, had strongly reduced numbers of synaptic vesicles.

[13][16][17] Like in muscle cells, the Ca2+ influx in neurons also leads to reduced mitochondrial functionality and the activation of calpains and endogenous Ca2+-dependent PLA2s.

A study[18] showed that depending on the dose, there was renal tubular and glomerular damage within 24 hours.

[19][20][21] In a certain study, mice become resistant to notexin, similar isoforms of the toxin and other venoms from the same origin.

Notexin causes pain at the site of the bite followed by excessive salivation, weakness, drowsiness, difficulty breathing, decreased blood pressure and paralysis of lips, larynx, tongue and facial muscles.

[22][23] There has been no research on the reaction of notexin in humans, however it is known that upon injection with the toxin, muscle damage and myoglobinuria will follow.

[23][25] There have also been researches into functional and morphological properties of regrowing mouse extensor digitorum longus (EDL) muscles after a notexin injection.