Guanitoxin (GNT), formerly known as anatoxin-a(S) "Salivary"[a],[1] is a naturally occurring cyanotoxin commonly isolated from cyanobacteria (specifically of the genus Anabaena).

Guanitoxin was first structurally characterized in 1989, and consists of a cyclic N-hydroxyguanidine organophosphate with a phosphate ester moiety.

[2] The main mechanism of action for guanitoxin is by irreversibly inhibiting the active site of acetylcholinesterase leading to excess acetylcholine in the parasympathetic and peripheral nervous systems; inducing poisoning via nicotinic and muscarinic cholinergic receptor stimulation.

[3] The clinical signs of high level guanitoxin exposure consists mainly of excessive salivation, lacrimation, chromodacryorrhea (in rats), urinary incontinence, muscular weakness, muscle twitching, convulsion, including opisthotonus, and respiratory distress and/or failure, and death.

[4][5] Treatment of afflicted case by atropine has attested to suppress the muscarinic mediated toxicity; which prevents the namesake salivation that similarly reacts to prevent the toxin's other poisoning symptoms which include lacrimation, urinary incontinence and defecation.