It is the N,N,N-trimethyl derivative of the well-known biogenic amine tyramine, and, being a natural product with a positively charged nitrogen atom in its molecular structure, it is classed as an alkaloid.

Candicine is toxic after parenteral administration, producing symptoms of neuromuscular blockade; further details are given in the "Pharmacology" section below.

The presence of the phenolic group would make aqueous solutions of candicine salts weakly acidic, but no pKa seems to have been recorded.

[11] After Reti's discovery (and naming) of candicine as a natural product,[12] a series of pharmacological investigations was carried out on this alkaloid by Luduena.

In Luduena's experiments, candicine first stimulated, then blocked ganglionic transmission; its effects were not altered by yohimbine, cocaine, or atropine, but completely counteracted by sparteine or tetrapropylammonium iodide.

Taking additional observations into account, these researchers concluded that the effects on frog tissue of candicine most closely resembled those of the well-known depolarizing neuromuscular-blocking drug decamethonium.

[4] Following their experiments on frogs, the Japanese group carried out a series of classical pharmacological investigations of candicine on cats and rabbits, and on various isolated animal organs/tissues.

A concentration of 0.012 mg/mL applied to the isolated guinea pig atrium caused a decrease in the amplitude and rate of contractions, these effects being enhanced by eserine, but inhibited by atropine pre-treatment.

Concentrations of 3-6 μg/mL produced contractions of the isolated guinea pig ileum which were inhibited by pre-treatment with atropine, hexamethonium, tubocurarine or cocaine, but were not affected by the presence of pyribenzamine or chlorpheniramine.

Summarizing the results of these and other observations, the authors concluded that: candicine was primarily a stimulant of autonomic ganglia; it liberated catecholamines from the adrenal medulla; it showed muscarine-like and sympathomimetic effects in some assays, and it was a neuromuscular blocker of the depolarizing type.