Anthopleurin is a toxin from the venom of the sea anemones Anthopleura xanthogrammica and Anthopleura elegantissima. These anemones use anthopleurin as a pheromone to quickly withdraw their tentacles in the presence of predators. Anthopleurin has four isoforms (Anthopleurin-A, -B, -C, and -Q). Their working mechanism is based on binding to sodium channels, which leads to increased excitation especially in cardiac myocytes. Function in sea anemones Anthopleurin functions both as a toxin as well as a pheromone. When a predator approaches the anemone, their reaction is to withdraw their tentacles and oral disc. These are the preferred attack sites for predators, because the concentration of anthopleurin is the lowest in these sites. The body region of the sea-anemone that is exposed to the predator contains the highest concentration of anthopleurin. After consuming the sea-anemone, the predator travels through the water and actually helps to spread the anthopleurin. This functions as an alarm pheromone for the other anemones, so they can hide certain body parts and defend themselves. Sources Anthopleura xanthogrammica (Giant green anemone) and Anthopleura elegantissima (Aggregating anemone) are named after the terrestrial anemone flower and are typically found along rocky, tidy shores in the Pacific Ocean. Molecular structure Anthopleurins are water-soluble proteins. They are built of four short strands of antiparallel beta-sheets, and contain three disulfide bridges. Mode of action Anthopleurins bind to the extracellular site-3 of mammalian sodium channels. Anthopleurins can affect cardiac myocytes by binding to the cardiac isoform of the sodium channel, RT4-B. Anthopleurins slow down inactivation of the sodium channels As a result, they can have positive inotropic effects on the whole heart. Pre-treatment with AP-Q has an effect on hepatocytes in CCl4-induced acute liver injury, decreasing the activity of aspartate transaminase (AST) and alanine transaminase (ALT) in the liver. Potency All different forms of anthopleurin are potent toxins. Anthopleurin A and C show effect at concentrations of 50 nM, Anthopleurin B at 3 nM and AP-Q at 30 nM. Mechanism of toxin action Anthopleurin can bind to the extracellular site of voltage-gated sodium channels. This results in slower inactivation, which has a positive inotropic effect on the heart. Anthopleurin has no effect on heart rate and blood pressure when given in concentrations of normal range. When the concentration of anthopleurin gets too high, arrhythmia of the heart can occur and this can cause serious damage or even death. Intoxication in humans is very rare. Therapeutic