Whether epibatidine occurs naturally remains controversial due to challenges in conclusively identifying the compound from the limited samples collected by Daly.

By the time that high-resolution spectrometry was used in 1991, there remained less than one milligram of extract from Daly's samples, raising concerns about possible contamination.

It was isolated from the skin of Epipedobates anthonyi frogs collected by Daly and colleague, Charles Myers.

[5] The structure of epibatidine was elucidated in 1992, an effort hindered by E. anthonyi gaining IUCN protected status in 1984.

[11] A number of approaches to discovering structural analogs of epibatine that maintain analgesics effects, but without the toxicity, have been attempted.

Specifically, the analgesic property of epibatidine is believed to take place by its binding to the α4/β2 subtype of nicotinic receptors.

This signal will ultimately induce release of dopamine and norepinephrine, resulting in an antinociceptive effect on the organism.

While this may be a potential therapeutic advantage over morphine, epibatidine has not entered clinical trials because even very small doses are lethal to rodents.

Empirically proven effects include splanchnic sympathetic nerve discharge and increased arterial pressure.

[23] The nerve discharge effects can cause antinociception partially mediated by agonism of central nicotinic acetylcholine receptors at low doses of epibatidine; 5 μg/kg.

[28] At higher doses, however, epibatidine will cause paralysis and loss of consciousness, coma and eventually death.

In research on mice, administration of doses greater than 5 μg/kg of epibatidine caused a dose-dependent paralyzing effect on the organism.

With doses over 5 μg/kg, symptoms included hypertension (increased blood pressure), paralysis in the respiratory system, seizures, and, ultimately, death.

[10] As the compound was not addictive nor did it cause habituation,[citation needed], it was initially thought to be very promising to replace morphine as a painkiller.

This means that even at a therapeutic dose (5 μg/kg[28]), some epibatidine might bind to the muscarinic acetylcholine receptors and cause adverse effects, such as hypertension, bradycardia and muscular paresis.

Currently, only rudimentary research into epibatidine's effects has yet been performed; the drug has been administered only to rodents for analysis at this time.