ATX activates voltage-gated sodium channels, which can cause cell depolarisation, NMDA-receptor overactivity, excess calcium influx and neuronal necrosis.

[2] The three dimensional NMR study of this toxin showed that it consists of a tripeptide glycine-N-methylvaline-alanine, a hydroxycarboxylic acid and a 9-t-butyl-6,8-dimethyl-6,8-diene attached to the C5 atom of the cyclic peptide backbone.

Structures that added a bulky side group to the C5 position also showed dramatic decreases in toxicity, including loss of activity.

After transformation into the phenylselenyl derivative, alkaline cleavage, allyl esterification and coupling with the tripeptide yields the ester.

[8] Antillatoxin is a sodium channel gating modifier with special efficacy in cells expressing rNav1.2, rNav1.4 and rNav1.5 α subunits.

[9] The exact mechanism is still unclear, as antillatoxin’s effect on the membrane potential is not sufficient to relieve the NMDA receptor block by magnesium.

[11] Aside from toxic effects, ATX seems to enhance neurite outgrowth in developing immature neurons, depending on sodium influx, NMDA receptor activity, voltage-gated calcium channels and the calmodulin-kinase pathway.

[14] Other voltage gated sodium channel antagonists also inhibit the effects of antillatoxin, such as lidocaine, lamotrigine, phenytoin, carbamazepine, riluzole, and SKA-19.