The Other Alkaloids of Iboga

Every page on this site that discusses dose, risk or effect is really discussing ibogaine, because that is what the literature measures. This page is about everything else in the plant, and about how little is known concerning any of it.

The short version: the plant is a mixture, the extract is a different mixture, the purified powder is very nearly one compound but not quite, and the pharmacology of the mixture has essentially never been studied in a human being.

What is actually in the root bark

The botanical monograph says “about 20 have been identified so far”, and that the highest concentrations sit in the root bark. Only seven are securely identified for this species, which the species page sets out along with the forty-eight peaks a 2018 analysis could not assign at all.

Where numbers exist, they come from a 2021 review that compiled isolation yields across the family. Its figures for Tabernanthe iboga are these, as a percentage of the weight of the plant material:

Read the second row against the first. The range reported for ibogamine overlaps the range for ibogaine and, at its upper end, exceeds it.

Two things stop that from being a headline. These are isolation yields, not content: what a chemist recovered, which is never more than what was there and is often a good deal less. And the ranges come from different laboratories using different material, so the top of one and the bottom of another may not describe any single plant.

Ibogamine keeps turning up

Of all the compounds on this page, one appears again and again in places nobody looks for it.

It is the precursor of ibogaine inside the plant. The 2018 paper that identified the final steps of the biosynthesis found the plant makes ibogaine from noribogaine, by way of an enzyme it names noribogaine 10-O-methyltransferase. The ibogan skeleton is assembled first and decorated afterwards.

It is more potent than ibogaine at the receptor the field cares about. The alpha3beta4 nicotinic acetylcholine receptor is the target most often nominated for the anti-addictive effect. A 2015 study measured the whole family against the human receptor, and the order it reports is:

Ibogamine is first and ibogaine is third. Noribogaine, the metabolite that circulates for days and carries much of the explanation for the drug’s duration, is last by a factor of ten.

It was the best performer in the only study that ranked the alkaloids in animals. A 1994 rat study gave eight iboga alkaloids and reported that all of them dose-dependently reduced morphine and cocaine self-administration, and that one produced next-day effects “more consistently than any of the other alkaloids”. That one was ibogamine.

That study needs a caveat, and it is a serious one. The 2021 review argues that the compounds the 1994 paper labelled as R and S enantiomers were probably something else, since no asymmetric synthesis of them existed at the time, and that they “are more likely the exo and endo epimers”. The one experiment that ranked these molecules against each other may have mislabelled what it ranked.

And it is in the powder sold as pure ibogaine. See below.

What is actually in what people buy

One published study has assayed commercial iboga products. It analysed sixteen samples bought from five vendors across nine countries between 2006 and 2013. This site already uses its ibogaine column on forms of iboga. The rest of the table has not been published here before.

Mean content by mass, with the number of samples in which each compound was detected:

Three things fall out of that table.

Extraction changes the mixture, it does not merely concentrate it. Every one of the five total alkaloid samples contained all five compounds. Root bark contained voacangine once in six and iboluteine never. The extract is not bark with the inert matter removed; the ratios are different.

One extract was 39 per cent ibogamine by alkaloid content. A sample bought in New Zealand in May 2012, sold as “35% ibogaine”, assayed at 25.4 per cent ibogaine and 16.4 per cent ibogamine.

Every sample sold as ibogaine hydrochloride contained ibogamine, between 2.1 and 8.7 per cent, and one contained 7.2 per cent ibogaline. The authors suggest some may have been mislabelled extract. They also note that material purified to 95 to 99.6 per cent for scientific use has shown traces of the same compounds, and that “traces of ibogamine or ibogaline are to be expected in ibogaine isolated from the Tabernanthe iboga plant”. Purity here is a matter of degree.

Two cardiac mechanisms that are not ibogaine’s

Cardiac risk is the central safety question for ibogaine, and it is described entirely in terms of one molecule blocking one channel. Two other compounds have their own cardiac pharmacology.

Voacangine blocks hERG more potently than ibogaine does. In a 2016 study of the whole family in human embryonic kidney cells, voacangine gave the lowest inhibitory concentration of any compound tested, 2.25 micromolar, against 3.53 for plant-derived ibogaine. The 18-MC page carries that full table, because the striking result there is that 18-MC barely blocks the channel at all.

Two things restrain the conclusion. Voacangine was detected in one root-bark sample out of six, at 0.2 per cent, and in extract at 0.1 to 0.6 per cent, so it is present in far smaller quantity than ibogaine. And nobody has ever tested ibogamine, ibogaline, coronaridine or iboluteine against hERG at all, so the compounds present in the largest amounts after ibogaine are simply unmeasured.

Tabernanthine has a different mechanism entirely, and it was abandoned in 1985. A small French literature from the 1980s reports that tabernanthine is a calcium entry blocker that also affects cellular calcium metabolism, and that the bradycardia it produces is not inhibited by vagotomy, atropine or propranolol. Separate work attributes its tremor to inverse agonism at the benzodiazepine receptor.

That is a cardiac depressant mechanism with nothing to do with hERG, in a compound present in iboga root, described forty years ago and never followed up. No page on this site mentioned tabernanthine before this one.

The human evidence

There is almost none, and the shape of the almost is worth stating precisely.

For ibogamine, tabernanthine, coronaridine and voacangine there is no human study of effect at all. Not a trial, not a cohort, not a case series.

For ibogaline there is exactly one, published in German in 1967 and indexed as a controlled clinical trial of ibogaline hydrochloride. It has no abstract in the database and we could not obtain the paper. We know it exists, we know its subject, and we do not know what it found. We are not going to characterise it from its indexing terms.

The only way any of these compounds has been measured in a human body is after death. A 2006 forensic analysis of a fatal iboga poisoning detected four compounds besides ibogaine and noribogaine, identified one of them as ibogamine, and could not identify three “because of the unavailability of reference substances”. A 2013 case, which deaths describes, quantified ibogaine and ibogamine in the powder and in post-mortem tissue.

Why so little is known

The gap is not mysterious, and three concrete facts explain most of it.

There were no reference standards. A forensic laboratory in 2006 could not name three of the compounds it had detected in a dead man because pure samples to compare them against did not exist.

There was no way to make two of them. The first total syntheses of tabernanthine and ibogaline were published in 2024. Both were available by isolation from plant material before that, which is how the 1980s French work was done, but no route independent of the plant existed until two years ago.

The one comparative animal study is disputed, on the identity of the compounds it compared, by a review published twenty-seven years later.

A field cannot accumulate pharmacology on molecules that are hard to obtain, hard to identify and hard to make.

What we could not establish

What the 1967 ibogaline study found. Not available in any repository we could reach.

Whether ibogaine really is about 0.3 per cent of root bark, as the 2021 review states, against every higher figure in the literature. The disagreement is unresolved and not, as far as we can tell, addressed anywhere.

Whether the mixture behaves differently from the molecule in a person. No trial, cohort or case series has compared total alkaloid extract against ibogaine hydrochloride in humans. The only basis for expecting a difference is the laboratory data above, and laboratory potency is not clinical effect.

The source of the most-repeated claim that the mixture matters. The botanical monograph states that root extract is a hundred times stronger than ibogaine as a cholinesterase inhibitor, “because of the additional effects of the alkaloids tabernanthine, ibogamine and the more distantly related iboluteine”. It gives no citation, and we could not trace the claim to any primary paper. We repeat it here as a claim the monograph makes, because it is the single assertion most often used to argue that whole plant differs from isolated compound, and it rests on nothing a reader can check.

Any measurement of how the alkaloid profile varies by geography, variety or individual plant. Three separate literature searches returned nothing. That gap, noted on the species page as well, is the one most worth closing.