Noribogaine

Noribogaine at a Glance

Noribogaine is the long-lived metabolite of ibogaine, the principal alkaloid of the West African shrub Tabernanthe iboga. It is not present in the plant. It is made in the body, by the liver enzyme CYP2D6, which strips a methyl group from ibogaine within minutes of a dose ^{8,12Reference 8Litjens RP · 2016ReviewHow toxic is ibogaine? — reviewView study →Reference 12Mash DC · 2023ReviewIUPHAR invited review — ibogaine: a legacy within the current renaissance of psychedelic therapy — reviewView study →}.

That relationship inverts what usually matters about a plant compound. Blood levels of noribogaine after an ibogaine dose exceed those of ibogaine itself, and where ibogaine is cleared within roughly a day, noribogaine persists at clinically relevant concentrations for days ^{3,8Reference 3Baumann MH et al. · 2000AnimalNoribogaine (12-hydroxyibogamine): a biologically active metabolite of the antiaddictive drug ibogaine — animal modelView study →Reference 8Litjens RP · 2016ReviewHow toxic is ibogaine? — reviewView study →}. Its own pharmacology is also different in kind: it is a G-protein-biased kappa-opioid agonist and about ten times more potent than ibogaine as an indirect serotonin agonist, while producing none of the tremor that ibogaine causes in animals ^{1,2Reference 1Maillet EL et al. · 2015In vitroNoribogaine is a G-protein biased κ-opioid receptor agonist — in vitroView study →Reference 2Baumann MH et al. · 2001AnimalIn vivo neurobiological effects of ibogaine and its O-desmethyl metabolite, 12-hydroxyibogamine (noribogaine), in ratsView study →}.

It is the most plausible carrier of the part of the iboga effect that has always been hardest to explain — the reduction in craving and drug-seeking that outlasts the drug experience by days or weeks. It is also, unhelpfully, a hERG channel blocker in its own right, so the cardiac liability does not end when the trip does ^{6Reference 6Alper K et al. · 2016In vitrohERG blockade by iboga alkaloids — in vitroView study →}.

A Metabolite, Not a Plant Compound

Noribogaine is not a phytochemical, and treating it as one produces two specific errors.

There is no plant concentration, no extract standardisation and no source ranking for noribogaine, because no plant contains it. Any product claiming to supply it from a botanical source is either mislabelled or supplying ibogaine.

And exposure is set by the person, not by the dose. CYP2D6 is one of the most genetically variable drug-metabolising enzymes in humans, and in patients given a single 10 mg/kg dose of ibogaine, plasma pharmacokinetics were highly variable and significantly correlated with CYP2D6 genotype — ibogaine clearance rose by about 30.7 L/h for every point of CYP2D6 activity score, from a baseline of 0.82 L/h in a person with no functional enzyme ^{7Reference 7Knuijver T et al. · 2024Clinical trialThe pharmacokinetics and pharmacodynamics of ibogaine in opioid use disorder patients — clinical studyView study →}. A poor metaboliser and an ultrarapid metaboliser given the same milligram dose do not experience the same drug, and they do not make the same amount of this metabolite.

The practical version: the same dose is not the same exposure, and the variable is the person’s liver.

Why the Effect Outlasts the Drug

The reason noribogaine matters is a timing problem. Ibogaine’s acute effects — the oneirogenic state, the tremor, the ataxia — resolve within about a day. The reduction in opioid withdrawal and craving that people seek ibogaine for is reported to persist well beyond that ^{11,12Reference 11Mash DC et al. · 2018Clinical trialIbogaine detoxification transitions opioid and cocaine abusers between dependence and abstinence: clinical observations and treatment outcomes — open-label clinical studyView study →Reference 12Mash DC · 2023ReviewIUPHAR invited review — ibogaine: a legacy within the current renaissance of psychedelic therapy — reviewView study →}.

Two mechanisms plausibly bridge the gap, and they are not exclusive. Ibogaine is sequestered in fat and released slowly, continuing to generate metabolite ^{9Reference 9Glick SD · 1998ReviewMechanisms of antiaddictive actions of ibogaine — reviewView study →}. And noribogaine itself has a half-life of 24–49 hours ^{4,5Reference 4Glue P et al. · 2015RCTAscending-dose study of noribogaine in healthy volunteers: pharmacokinetics, pharmacodynamics, safety, and tolerability — randomised placebo-controlled trialView study →Reference 5Glue P et al. · 2016RCTAscending single-dose, double-blind, placebo-controlled safety study of noribogaine in opioid-dependent patients — randomised placebo-controlled trialView study →} — an order of magnitude longer than the parent’s — so a single ibogaine dose leaves a metabolite steadily present for the better part of a week.

The direct animal test supports this reading. Noribogaine, given on its own, decreases morphine and cocaine self-administration in rats for several days, as ibogaine does ^{9Reference 9Glick SD · 1998ReviewMechanisms of antiaddictive actions of ibogaine — reviewView study →}. It binds kappa-opioid, NMDA and serotonin-uptake sites at low micromolar affinity, the same target set implicated in ibogaine’s anti-addictive action ^{10Reference 10Glick SD · 2000ReviewDevelopment of novel medications for drug addiction: the legacy of an African shrub — reviewView study →}.

What is not established is that this is the whole explanation. Ibogaine also raises GDNF and BDNF in the ventral tegmental area, which is a mechanism for a lasting change that does not require the drug to still be present at all. Noribogaine is a strong candidate for the delayed phase; it is not a proven one.

What It's Used For

Noribogaine’s pharmacology is unusually well characterised for a metabolite — it has been through two Phase I human trials in its own right — and the results are more sobering than the enthusiasm around iboga suggests.

Evidence by IndicationStrength of support · Beta

01Opioid Withdrawal & DetoxificationShaky36%Two Phase I trials of noribogaine itself — safe and PK-clean, but only a non-significant trend on withdrawal scores ^{4,5Reference 4Glue P et al. · 2015RCTAscending-dose study of noribogaine in healthy volunteers: pharmacokinetics, pharmacodynamics, safety, and tolerability — randomised placebo-controlled trialView study →Reference 5Glue P et al. · 2016RCTAscending single-dose, double-blind, placebo-controlled safety study of noribogaine in opioid-dependent patients — randomised placebo-controlled trialView study →}

02Reducing Drug Self-AdministrationShaky30%Rat morphine and cocaine self-administration reduced for several days by the metabolite alone ^{9,10Reference 9Glick SD · 1998ReviewMechanisms of antiaddictive actions of ibogaine — reviewView study →Reference 10Glick SD · 2000ReviewDevelopment of novel medications for drug addiction: the legacy of an African shrub — reviewView study →}

03Analgesia & Opioid-Tolerance ModulationShaky20%Predicted from biased kappa agonism and animal tolerance modulation; human pharmacodynamic tests were negative ^{1,4Reference 1Maillet EL et al. · 2015In vitroNoribogaine is a G-protein biased κ-opioid receptor agonist — in vitroView study →Reference 4Glue P et al. · 2015RCTAscending-dose study of noribogaine in healthy volunteers: pharmacokinetics, pharmacodynamics, safety, and tolerability — randomised placebo-controlled trialView study →}

04Mood & Anxiety (Dynorphin Antagonism)Shaky14%A mechanistic hypothesis from the β-arrestin inhibition data; never tested behaviourally or clinically ^{1Reference 1Maillet EL et al. · 2015In vitroNoribogaine is a G-protein biased κ-opioid receptor agonist — in vitroView study →}

Mechanisms

The two rows that define this molecule are the kappa bias and the hERG block. The first is why it might work; the second is why its long half-life is a liability rather than a convenience.

Pharmacokinetics

Noribogaine’s kinetics are the whole reason it has a page. It is formed by CYP2D6 O-demethylation of ibogaine during first-pass metabolism, fast enough that peak blood levels of the metabolite exceed those of the parent ^{2,3,12Reference 2Baumann MH et al. · 2001AnimalIn vivo neurobiological effects of ibogaine and its O-desmethyl metabolite, 12-hydroxyibogamine (noribogaine), in ratsView study →Reference 3Baumann MH et al. · 2000AnimalNoribogaine (12-hydroxyibogamine): a biologically active metabolite of the antiaddictive drug ibogaine — animal modelView study →Reference 12Mash DC · 2023ReviewIUPHAR invited review — ibogaine: a legacy within the current renaissance of psychedelic therapy — reviewView study →}.

Given directly by mouth in healthy volunteers at 3, 10, 30 or 60 mg, noribogaine was rapidly absorbed with peak concentrations at 2–3 hours, showed dose-linear AUC and Cmax, and was slowly eliminated with mean half-lives of 28–49 hours. Its apparent volume of distribution was very large — 1,417 to 3,086 L across dose groups — consistent with extensive tissue distribution ^{4Reference 4Glue P et al. · 2015RCTAscending-dose study of noribogaine in healthy volunteers: pharmacokinetics, pharmacodynamics, safety, and tolerability — randomised placebo-controlled trialView study →}. In opioid-dependent patients at 60–180 mg the mean half-life ran 24–30 hours ^{5Reference 5Glue P et al. · 2016RCTAscending single-dose, double-blind, placebo-controlled safety study of noribogaine in opioid-dependent patients — randomised placebo-controlled trialView study →}. Ibogaine, for comparison, is cleared within about a day, so noribogaine is present at clinically relevant concentrations long after the parent has gone ^{8Reference 8Litjens RP · 2016ReviewHow toxic is ibogaine? — reviewView study →}.

The genotype effect is the practical one. In 14 patients given 10 mg/kg ibogaine, plasma pharmacokinetics were highly variable and significantly correlated with CYP2D6 genotype (p < 0.001) — clearance of 0.82 L/h at an activity score of 0, rising 30.7 L/h per activity-score point ^{7Reference 7Knuijver T et al. · 2024Clinical trialThe pharmacokinetics and pharmacodynamics of ibogaine in opioid use disorder patients — clinical studyView study →}. Ibogaine is also sequestered in fat and released slowly, which prolongs metabolite generation beyond what the parent’s plasma curve suggests ^{9Reference 9Glick SD · 1998ReviewMechanisms of antiaddictive actions of ibogaine — reviewView study →}.

Clinical Trials

Two Phase I trials of noribogaine itself have been completed; both were safety and pharmacokinetic studies, and no efficacy trial has followed. Development was pursued commercially and did not reach a controlled efficacy stage.

Last checked: September 2026.

Isolate vs. Plant Studies

This molecule has no plant studies, and that is the informative part.

Every noribogaine study is an isolate study, because noribogaine only exists as an isolate or as something the body makes. The two Phase I trials dosed synthesised noribogaine directly ^{4,5Reference 4Glue P et al. · 2015RCTAscending-dose study of noribogaine in healthy volunteers: pharmacokinetics, pharmacodynamics, safety, and tolerability — randomised placebo-controlled trialView study →Reference 5Glue P et al. · 2016RCTAscending single-dose, double-blind, placebo-controlled safety study of noribogaine in opioid-dependent patients — randomised placebo-controlled trialView study →}; the rat self-administration and neurochemistry studies injected it intravenously ^{2,9Reference 2Baumann MH et al. · 2001AnimalIn vivo neurobiological effects of ibogaine and its O-desmethyl metabolite, 12-hydroxyibogamine (noribogaine), in ratsView study →Reference 9Glick SD · 1998ReviewMechanisms of antiaddictive actions of ibogaine — reviewView study →}; the receptor and channel work is cell-based ^{1,6Reference 1Maillet EL et al. · 2015In vitroNoribogaine is a G-protein biased κ-opioid receptor agonist — in vitroView study →Reference 6Alper K et al. · 2016In vitrohERG blockade by iboga alkaloids — in vitroView study →}.

Everything about iboga root bark is a different subject. The traditional Bwiti preparation and the clinics that administer flood doses give ibogaine, and the human outcome literature — including the 191-person open-label case series — describes people who took ibogaine and then made noribogaine themselves, in amounts nobody measured or controlled ^{11Reference 11Mash DC et al. · 2018Clinical trialIbogaine detoxification transitions opioid and cocaine abusers between dependence and abstinence: clinical observations and treatment outcomes — open-label clinical studyView study →}. Attributing those outcomes to noribogaine specifically is an inference, and a reasonable one given the timing, but it is not a finding.

The one bridge between them is the CYP2D6 correlation ^{7Reference 7Knuijver T et al. · 2024Clinical trialThe pharmacokinetics and pharmacodynamics of ibogaine in opioid use disorder patients — clinical studyView study →}, and it points the wrong way for the plant: it means that the whole-plant dose does not determine the metabolite exposure, so no root-bark quantity can be mapped onto the doses in the noribogaine trials.

Prevalence in Nature

Noribogaine does not occur in Tabernanthe iboga, or in any other plant so far reported. It is a mammalian metabolite, generated by hepatic CYP2D6 from ingested ibogaine ^{8,12Reference 8Litjens RP · 2016ReviewHow toxic is ibogaine? — reviewView study →Reference 12Mash DC · 2023ReviewIUPHAR invited review — ibogaine: a legacy within the current renaissance of psychedelic therapy — reviewView study →}.

The plant makes the precursor set instead: ibogaine, the dominant root-bark alkaloid ^{12Reference 12Mash DC · 2023ReviewIUPHAR invited review — ibogaine: a legacy within the current renaissance of psychedelic therapy — reviewView study →}, alongside ibogamine, ibogaline, tabernanthine and the biosynthetic precursor voacangine. Noribogaine appears only downstream of that, in the person who swallowed it — so no plant-material quantity corresponds to a noribogaine exposure, and no content-by-source comparison is possible.

The link between noribogaine and iboga is metabolic, not botanical.

Discovery & Synthesis

Noribogaine entered the literature in the 1990s as O-desmethylibogaine, when it became clear that ibogaine given to primates and humans was rapidly demethylated and that the metabolite reached higher blood levels than the parent ^{3Reference 3Baumann MH et al. · 2000AnimalNoribogaine (12-hydroxyibogamine): a biologically active metabolite of the antiaddictive drug ibogaine — animal modelView study →}. Its systematic in-vivo characterisation came from Baumann, Mash and colleagues in 2000–2001, who established that it was independently biologically active — raising extracellular serotonin more potently than ibogaine while producing none of ibogaine’s tremor or forepaw treading, and concluding that the metabolite “may be a safer alternative for medication development” ^{2,3Reference 2Baumann MH et al. · 2001AnimalIn vivo neurobiological effects of ibogaine and its O-desmethyl metabolite, 12-hydroxyibogamine (noribogaine), in ratsView study →Reference 3Baumann MH et al. · 2000AnimalNoribogaine (12-hydroxyibogamine): a biologically active metabolite of the antiaddictive drug ibogaine — animal modelView study →}.

Its naming is inconsistent in the literature and worth flagging: the same molecule is written 12-hydroxyibogamine by Baumann and Mash and 10-hydroxyibogamine in some toxicology reviews, reflecting two numbering conventions for the ibogamine skeleton ^{2,8Reference 2Baumann MH et al. · 2001AnimalIn vivo neurobiological effects of ibogaine and its O-desmethyl metabolite, 12-hydroxyibogamine (noribogaine), in ratsView study →Reference 8Litjens RP · 2016ReviewHow toxic is ibogaine? — reviewView study →}.

Manufacture is by chemistry, not extraction — there is nothing to extract it from. It is prepared by O-demethylation of ibogaine, itself obtainable either from T. iboga root bark or by semisynthesis from voacangine sourced from Voacanga africana ^{6Reference 6Alper K et al. · 2016In vitrohERG blockade by iboga alkaloids — in vitroView study →}. Noribogaine was developed as a drug candidate in its own right, on the reasoning that giving the metabolite directly would skip the parent’s psychoactivity, tremor and much of its acute cardiac effect. The two Phase I trials were run on that basis; nothing further has been reported ^{4,5Reference 4Glue P et al. · 2015RCTAscending-dose study of noribogaine in healthy volunteers: pharmacokinetics, pharmacodynamics, safety, and tolerability — randomised placebo-controlled trialView study →Reference 5Glue P et al. · 2016RCTAscending single-dose, double-blind, placebo-controlled safety study of noribogaine in opioid-dependent patients — randomised placebo-controlled trialView study →}.

More recently the same logic has been pushed further into chemistry: the oxa-iboga analogues, redesigned rather than purified, disrupt opioid use in animal models without the cardiac risk ^{13Reference 13Havel V et al. · 2024AnimalOxa-iboga alkaloids lack cardiac risk and disrupt opioid use in animal modelsView study →}.

Patents: not yet researched.

Toxicity & Safety

Noribogaine’s safety story is dominated by one channel and one number.

It blocks the hERG (IKr) potassium channel with an IC50 of about 2.86 µM — more potently than ibogaine itself (3.53 µM extracted, 4.09 µM semisynthetic) and comparably to voacangine (2.25 µM) ^{6Reference 6Alper K et al. · 2016In vitrohERG blockade by iboga alkaloids — in vitroView study →}. That places the cardiac liability in the iboga scaffold, not in ibogaine alone. The synthetic congener 18-methoxycoronaridine, by contrast, binds hERG with similar affinity but produces an IC50 above 50 µM — showing the block is separable from the chemistry by design ^{6Reference 6Alper K et al. · 2016In vitrohERG blockade by iboga alkaloids — in vitroView study →}.

The human number follows from it. In opioid-dependent patients, noribogaine produced a concentration-dependent QTc increase of 0.17 ms per ng/mL, with mean effects of about 16, 28 and 42 ms at 60, 120 and 180 mg respectively ^{5Reference 5Glue P et al. · 2016RCTAscending single-dose, double-blind, placebo-controlled safety study of noribogaine in opioid-dependent patients — randomised placebo-controlled trialView study →}. A 42 ms mean prolongation is well into the range that regulators treat as a clinical signal.

Safety at a Glance

⚠️ Moderate toxicity

• No euphoria, no tremor, no psychedelic effect. In trials the notable subjective effects were non-euphoric changes in light perception, headache and nausea — quite unlike ibogaine.
• hERG blockade and dose-dependent QT prolongation. Mean QTc +42 ms at 180 mg in patients; the same channel block that underlies ibogaine’s documented arrhythmias and deaths.
• The cardiac exposure outlasts the experience by days. A 24–49 hour half-life means QT effects persist long after ibogaine’s acute effects have resolved — a plausible explanation for delayed arrhythmias reported days after an ibogaine dose.
• CYP2D6 genotype changes the exposure more than the dose does. Poor metabolisers and people taking CYP2D6 inhibitors are not comparable to others on the same milligram dose.
• No efficacy has been demonstrated. Both human trials were safety studies; the withdrawal benefit was a non-significant trend.

Full Safety & Interactions Detail

Cardiac. The iboga alkaloids block hERG as a class, with voltage-dependent, low-affinity kinetics; measured IC50 values are 2.25 µM for voacangine, 2.86 µM for noribogaine, 3.53 µM for plant-extracted ibogaine and 4.09 µM for semisynthetic ibogaine ^{6Reference 6Alper K et al. · 2016In vitrohERG blockade by iboga alkaloids — in vitroView study →}. Ibogaine has been associated with QT prolongation, torsades de pointes and fatalities ^{8Reference 8Litjens RP · 2016ReviewHow toxic is ibogaine? — reviewView study →}. The authors of the hERG study make the specific point that noribogaine’s extended half-life may explain observations of persistent QT prolongation and arrhythmia days after an ibogaine dose ^{6Reference 6Alper K et al. · 2016In vitrohERG blockade by iboga alkaloids — in vitroView study →} — the cardiac risk window is set by the metabolite, not by the acute experience.

One important nuance runs the other way. In the 14-patient pharmacokinetic study, QTc prolongation and cerebellar ataxia correlated significantly with ibogaine concentrations and not with noribogaine concentrations, leading those authors to conclude the acute cardiac and cerebellar effects are more likely driven by the parent ^{7Reference 7Knuijver T et al. · 2024Clinical trialThe pharmacokinetics and pharmacodynamics of ibogaine in opioid use disorder patients — clinical studyView study →}.

Both readings can be true: the parent may dominate the acute peak while the metabolite sustains a lower, longer effect. What neither supports is treating noribogaine as cardiac-neutral — it produced 42 ms of QTc prolongation on its own in a placebo-controlled trial ^{5Reference 5Glue P et al. · 2016RCTAscending single-dose, double-blind, placebo-controlled safety study of noribogaine in opioid-dependent patients — randomised placebo-controlled trialView study →}.

Neurological. Noribogaine notably does not reproduce ibogaine’s tremor or forepaw treading in rats, and is a weaker stimulator of corticosterone secretion ^{2,3Reference 2Baumann MH et al. · 2001AnimalIn vivo neurobiological effects of ibogaine and its O-desmethyl metabolite, 12-hydroxyibogamine (noribogaine), in ratsView study →Reference 3Baumann MH et al. · 2000AnimalNoribogaine (12-hydroxyibogamine): a biologically active metabolite of the antiaddictive drug ibogaine — animal modelView study →}. Ibogaine’s neurotoxicity — Purkinje-cell degeneration in rats, mediated by inferior-olive stimulation — is attributed to sigma-2 activity that noribogaine does not share to the same degree ^{8,9Reference 8Litjens RP · 2016ReviewHow toxic is ibogaine? — reviewView study →Reference 9Glick SD · 1998ReviewMechanisms of antiaddictive actions of ibogaine — reviewView study →}.

Interactions. The dominant interaction is metabolic and it concerns the parent drug: anything that inhibits CYP2D6 — including many SSRIs, bupropion and quinidine — reduces conversion of ibogaine and shifts the exposure profile ^{7,8Reference 7Knuijver T et al. · 2024Clinical trialThe pharmacokinetics and pharmacodynamics of ibogaine in opioid use disorder patients — clinical studyView study →Reference 8Litjens RP · 2016ReviewHow toxic is ibogaine? — reviewView study →}. For noribogaine given directly, the mechanistic concerns are additive QT prolongation with other QT-prolonging drugs, and serotonergic interaction, since it inhibits serotonin reuptake ^{2Reference 2Baumann MH et al. · 2001AnimalIn vivo neurobiological effects of ibogaine and its O-desmethyl metabolite, 12-hydroxyibogamine (noribogaine), in ratsView study →}. No dedicated human interaction studies exist for the metabolite.

Reproductive. No reproductive or developmental toxicity data are available for noribogaine. That is an absence of study, not a clearance.

Legal. Ibogaine is a Schedule I controlled substance in the United States and controlled in a number of other countries; noribogaine has been handled as an investigational drug rather than as a controlled substance in the trials described here, but legal status varies and should be checked locally.

Dosage

There is no approved or established dose of noribogaine. The only human figures come from the two Phase I trials:

Indirect exposure — the way essentially everyone actually encounters this molecule — comes from an ibogaine dose, typically around 10 mg/kg in the clinical study cited here ^{7Reference 7Knuijver T et al. · 2024Clinical trialThe pharmacokinetics and pharmacodynamics of ibogaine in opioid use disorder patients — clinical studyView study →} and higher in flood-dose protocols. That exposure cannot be converted into a noribogaine dose, because the conversion depends on the individual’s CYP2D6 activity, which varied enough in a 14-person study to change clearance by more than an order of magnitude ^{7Reference 7Knuijver T et al. · 2024Clinical trialThe pharmacokinetics and pharmacodynamics of ibogaine in opioid use disorder patients — clinical studyView study →}.

These are research doses and are not a personal recommendation.

References

1. Maillet EL, Milon N, Heghinian MD, et al. (2015). Noribogaine is a G-protein biased κ-opioid receptor agonist — in vitro. Neuropharmacology. https://pubmed.ncbi.nlm.nih.gov/26302653/
2. Baumann MH, Rothman RB, Pablo JP, et al. (2001). In vivo neurobiological effects of ibogaine and its O-desmethyl metabolite, 12-hydroxyibogamine (noribogaine), in rats. Journal of Pharmacology and Experimental Therapeutics. https://pubmed.ncbi.nlm.nih.gov/11303040/
3. Baumann MH, Pablo JP, Ali SF, et al. (2000). Noribogaine (12-hydroxyibogamine): a biologically active metabolite of the antiaddictive drug ibogaine — animal model. Annals of the New York Academy of Sciences. https://pubmed.ncbi.nlm.nih.gov/11085335/
4. Glue P, Lockhart M, Lam F, et al. (2015). Ascending-dose study of noribogaine in healthy volunteers: pharmacokinetics, pharmacodynamics, safety, and tolerability — randomised placebo-controlled trial. Journal of Clinical Pharmacology. https://pubmed.ncbi.nlm.nih.gov/25279818/
5. Glue P, Cape G, Tunnicliff D, et al. (2016). Ascending single-dose, double-blind, placebo-controlled safety study of noribogaine in opioid-dependent patients — randomised placebo-controlled trial. Clinical Pharmacology in Drug Development. https://pubmed.ncbi.nlm.nih.gov/27870477/
6. Alper K, Bai R, Liu N, et al. (2016). hERG blockade by iboga alkaloids — in vitro. Cardiovascular Toxicology. https://pubmed.ncbi.nlm.nih.gov/25636206/
7. Knuijver T, Ter Heine R, Schellekens AFA, et al. (2024). The pharmacokinetics and pharmacodynamics of ibogaine in opioid use disorder patients — clinical study. Journal of Psychopharmacology. https://pubmed.ncbi.nlm.nih.gov/38519421/
8. Litjens RP, Brunt TM (2016). How toxic is ibogaine? — review. Clinical Toxicology. https://pubmed.ncbi.nlm.nih.gov/26807959/
9. Glick SD, Maisonneuve IS (1998). Mechanisms of antiaddictive actions of ibogaine — review. Annals of the New York Academy of Sciences. https://pubmed.ncbi.nlm.nih.gov/9668680/
10. Glick SD, Maisonneuve IM (2000). Development of novel medications for drug addiction: the legacy of an African shrub — review. Annals of the New York Academy of Sciences. https://pubmed.ncbi.nlm.nih.gov/10911925/
11. Mash DC, Duque L, Page B, et al. (2018). Ibogaine detoxification transitions opioid and cocaine abusers between dependence and abstinence: clinical observations and treatment outcomes — open-label clinical study. Frontiers in Pharmacology. https://pubmed.ncbi.nlm.nih.gov/29922156/
12. Mash DC (2023). IUPHAR invited review — ibogaine: a legacy within the current renaissance of psychedelic therapy — review. Pharmacological Research. https://pubmed.ncbi.nlm.nih.gov/36907284/
13. Havel V, Kruegel AC, Bechand B, et al. (2024). Oxa-iboga alkaloids lack cardiac risk and disrupt opioid use in animal models. Nature Communications. https://doi.org/10.1038/s41467-024-51856-y

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