The name "methyl-lycaconitine" was assigned by John Goodson, working at the Wellcome Chemical Research Laboratories in London, England, when he isolated the alkaloid, in purer form, from seeds of Delphinium elatum, L. in 1943.

[10] A more modern isolation procedure is described by Pelletier and his co-workers, who used seeds of the "garden larkspur", Consolida ambigua (also referred to as Delphinium ajacis) as their plant source.

[12] This structure, supported in part by X-ray crystallography (considered usually to be a "definitive" analytical technique) of a chemical derivative of MLA performed by Maria Przybylska,[13] was accepted as correct until the early 1980s.

[10] Although commonly referred to as a "diterpenoid" alkaloid, MLA is, strictly speaking, a nor-diterpenoid, since its carbon skeleton only contains 19 C atoms, one having been deleted somewhere during its biosynthesis.

The "curare-like" properties of MLA seem to have been first mentioned in 1958 by Kuzovkov and Bocharnikova,[20] working at the Ordzhinikidze All-Union Institute for Scientific Research in Pharmaceutical Chemistry, in the former USSR.

A detailed paper on the pharmacology of MLA (in the form of its hydriodide salt, given the drug name "mellictine") in classical animal preparations was published from the same Institute in the following year by Dozortseva.

Ganglion-blocking effects of MLA were observed using the cat nictitating membrane preparation: complete inhibition of the response was produced by 4 mg/kg of "mellictine" given intravenously.

No significant effects were produced by the drug in smooth muscle preparations from rabbit, guinea pig or cat, indicating the lack of activity at typically muscarinic sites.

A more detailed summary of the above data, together with much related material, may be found in a review written by Kip Panter and collaborators at USDA-ARS laboratories in Utah and California.

Doses large enough to produce collapse also caused an increase in heart and respiration rates, as well as tremor, with significant convulsions evident in mice and rats, but not in cattle or sheep.

[21][22] It is worth noting that although a LD50 for man is not available, the clinical studies of Kabelyanskaya showed that an oral dose of 0.02 g of MLA hydriodide ("mellictine") might be given to patients up to 5 times per day, over the course of 1 month.

[6] The earliest observation on a relationship between the molecular structure of MLA and a biological activity concerned the effect of the C-18 ester group on acute toxicity.

[30] When compared with MLA in the rat phrenic nerve-diaphragm assay, lycoctonine-18-O-benzoate was also about 10x less potent, and a similar reduction in potency was observed in an electrophysiological study involving frog extensor muscle.

However, this suggestion was apparently based only on work by Solinas et al.[35] who showed that doses of 0.3-5.6 mg/kg, i.p., in rats, dose-dependently antagonized the discriminative-stimulus effects of 3 mg/kg THC.

Given that the early Soviet work[6] with "mellictine" indicated that as little as ~0.2-0.3 mg/kg, orally, in man (assuming a weight of 60–70 kg, for the sake of making the dose conversion) could produce symptoms of toxicity, and that oral administration of most drugs typically requires more drug than parenteral administration, it is uncertain if MLA will prove to be a practical treatment for either nicotine or cannabis addiction, based on the effective doses required in the rat experiments.