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PsychedeliaDokholyan Laboratory
Plate 467 of 545Verified

Noribogaine

PubChem records this structure as (-)-Noribogaine.

Also known as(-)-Noribogaine · Ibogamin-12-ol · 12-hydroxy-ibogamine · 12-Hydroxyibogamine · 12-OH-ibogamine · O-Demethylibogaine · O-Noribogaine · O-desmethylibogaine

(1R,15R,17S,18S)-17-ethyl-3,13-diazapentacyclo[13.3.1.02,10.04,9.013,18]nonadeca-2(10),4(9),5,7-tetraen-7-ol

PubChem CID
3083548
Measurements
1
InChIKey
RAUCDOKTMDOIPF-RYRUWHOVSA-N

I · Summary

What is known

Published passages, each quoted whole and attributed to the database that published it. Two blocks are written here rather than quoted, and both say so where they stand: the synthesized summary at the top, which may draw only on the passages beneath it, and the history note, which cites the works it came from. Every claim in either carries a marker to its source.

What it is

  • Noribogaine is an organic heteropentacyclic compound that is ibogamine in which the indole hydrogen para to the indole nitrogen has been replaced by a hydroxy group. It is the primary (and long-lived) metabolite of ibogaine, the psychoactive indole alkaloid found in the African rainforest shrub Tabernanthe iboga. It has a role as a psychotropic drug, a serotonin uptake inhibitor, a kappa-opioid receptor agonist and a NMDA receptor antagonist. It is an organic heteropentacyclic compound, a secondary amino compound, a tertiary amino compound and a monoterpenoid indole alkaloid. It is functionally related to an ibogaine. It is a conjugate base of a noribogaine(1+).

    ChEBI

History, discovery and cultural use

— Not in this archive. PubChem, ChEMBL and the Human Protein Atlas publish pharmacology, regulation and toxicology, and none of them publishes a heading for when Noribogaine was first made, by whom, or how it has been used. That is a gap in the databases this site reads and not a gap in the literature — the history of these compounds is written, at length and under peer review, in the works below. This site does not summarize them; it says where they are. Where a published passage above happens to touch origin or traditional use, it appears inside the entry that carries it.

Histories of this field

Scholarship on psychedelics generally, not on Noribogaine specifically. Whether any of these treats this compound is a question for the book, not for this page.

  • Mescaline: A Global History of the First Psychedelic

    Traces mescaline and the peyote and San Pedro cacti from pre-Columbian ritual use through nineteenth-century chemistry to twentieth-century psychiatry and the counterculture.

    Jay M. Mescaline: A Global History of the First Psychedelic. Yale University Press, New Haven and London; 2019. ISBN 9780300231076.

  • Expanding Mindscapes: A Global History of Psychedelicsopen access

    Essays on the international and cross-cultural history of psychedelic science, deliberately decentring the standard North American and European account.

    Dyck E, Elcock C, editors. Expanding Mindscapes: A Global History of Psychedelics. The MIT Press, Cambridge MA; 2023. ISBN 9780262546935 (paper), 9780262376891 (open access). doi:10.7551/mitpress/14417.001.0001.

  • Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers

    Botany, ethnography and chemistry of the principal hallucinogenic plants, by the founder of modern ethnobotany and the chemist who first synthesized LSD.

    Schultes RE, Hofmann A, Rätsch C. Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers. 2nd ed. Healing Arts Press, Rochester VT; 2001. ISBN 9780892819799.

  • Psychonauts: Drugs and the Making of the Modern Mind

    The tradition of scientific self-experimentation with psychoactive drugs, and its part in the emergence of psychology and of modernism.

    Jay M. Psychonauts: Drugs and the Making of the Modern Mind. Yale University Press, New Haven; 2023. ISBN 9780300257946.

  • Ancient Psychoactive Substances

    Archaeological and bioarchaeological evidence for psychoactive plant use across the ancient world.

    Fitzpatrick SM, editor. Ancient Psychoactive Substances. University Press of Florida, Gainesville; 2018. ISBN 9780813056708.

  • History and Current Status of Psychedelics and Entactogens for the Treatment of Psychiatric Disorders

    A chapter tracing psychedelic and entactogen research from earlier ritual use through the mid-century research period to current clinical trials.

    Stroud C, Posey Norris SM, Matney C, editors. History and Current Status of Psychedelics and Entactogens for the Treatment of Psychiatric Disorders. In: Exploring Psychedelics and Entactogens as Treatments for Psychiatric Disorders: Proceedings of a Workshop. National Academies Press, Washington DC; 2022. NBK587225.

    Workshop proceedings record what participants said; they are not a consensus statement of the National Academies.

  • Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions

    Peer-reviewed review covering the isolation, synthesis, pharmacology and ritual use of peyote and mescaline.

    Dinis-Oliveira RJ, Pereira CL, da Silva DD. Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions. Current Molecular Pharmacology 12(3):184–194; 2019. doi:10.2174/1874467211666181010154139.

Institutional archives

  • Heffter Research Institute Funds and coordinates clinical research on psilocybin, and keeps records of the studies it has supported since 1993. Sponsors the research it archives.
  • Multidisciplinary Association for Psychedelic Studies (MAPS) Sponsors clinical research, chiefly on MDMA-assisted therapy, and publishes an archive of historical and contemporary documents. A sponsor and an advocacy organization, not a disinterested archive; its clinical programme has a commercial arm.

The rest of this dossier

  • Affinity — 1 measurement in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — nothing published for Noribogaine. An absent record is an absence of study, not evidence of safety.
  • Legal — no DEA record is held here — which is not a finding that this compound is uncontrolled.
  • Systems — where this compound’s targets are transcribed, by brain region and tissue.

Passages via PubChem descriptive sections, aggregating DrugBank, LiverTox, FDA, DEA, HSDB, EPA. Each is quoted whole and attributed to the database that published it. The only prose written here about Noribogaine is the history note, which says so on its face and carries a reference for every claim in it.

II · Identity

Structure and descriptors

Descriptors are computed here with RDKit from the structure PubChem returns — not from the archive's stored copy, so an edited local structure cannot reach this table.

2D structural depiction of Noribogaine
Depiction served by PubChem for CID 3083548. Not redrawn here, so the picture and the identity come from the same record.
Formula
C19H24N2OR
Molecular weight
296.41g/molR
Exact mass
296.1889DaR
cLogP
3.63R
TPSA
39.3ŲR
H-bond donors
2R
H-bond acceptors
2R
Rotatable bonds
1R
Aromatic rings
2R
Heavy atoms
22R
Fraction sp³
0.579R
Formal charge
0R

Computed with RDKit 2025.09.2 from the SMILES returned by PubChem. Audit run 26/09/2026.

Bemis–Murcko scaffold

c1ccc2c3c([nH]c2c1)[C@@H]1C[C@H]2CC[C@@H]1N(CC3)C2

Shared with Ibogaine, Ibogaline, Ibogamine, Tabernanthine. All families

III · Behavior

Behavioral summary

Class, mechanism, and the duration of acute effects — each quoted from the record or trial that publishes it. Duration of effects and plasma half-life are shown separately, because they are different quantities and diverge by a factor of three or four.

Classification

MeSH indexes no pharmacological class for this compound.

Duration of acute subjective effects

—

No controlled human trial reporting a duration for this compound is cited here. The archive does hold onset and duration ranges for it, inherited from an earlier build, but their source column is empty and so they cannot be shown. A duration is not inferred from a chemical relative.

Plasma elimination half-life

How fast the body clears the drug — not how long the effects last. The two diverge sharply: LSD is cleared with a half-life of about 2.6 h while its subjective effects run 8–12 h.

28–49 h

“The drug was slowly eliminated, with mean half-life estimates of 28-49 hours across dose groups”
Glue P et al., Journal of clinical pharmacology 2015. PMID 25279818

Primary pharmacological drivers

ChEMBL holds no curated mechanism-of-action record for this compound. The measured affinities below are the evidence this archive has for what it binds.

Nothing about this compound’s pharmacology is published with a citation in the sources this site reads. The measured binding data below is what the archive can show.

IV · Clinical

Clinical description

Where this compound's substance class sits in ICD-11 and DSM-5-TR, and how much of the recorded literature speaks to each domain of a mental status examination.

No diagnostic chapter is shown for this compound. Either PubChem records no MeSH pharmacological class for it, or the class it records is not one of the substance classes ICD-11 gives a chapter to. Inferring a chapter from the compound’s name or its binding profile would be a diagnosis this archive is in no position to make.

How much has been written about each domain

The clinical domains, and how many of the records this archive holds for this compound say something under each. What the terms mean, and the word list behind every spoke, are set out in the method.

None of the 1 records this archive holds for this compound uses a term from any of the clinical domains. That is a statement about the literature recorded here, not about the compound.

V · Systems

Systems physiology

Where the targets this compound binds are transcribed — brain regions on the left, peripheral and autonomic tissues on the right. A join of two measurements, not a claim about what the compound does to either.

Brain

cerebral cortex — 10.0 nTPM, from KCNH2cerebellum — 32.4 nTPM, from KCNH2hippocampal formation — 8.9 nTPM, from KCNH2amygdala — 7.5 nTPM, from KCNH2hypothalamus — 14.4 nTPM, from KCNH2thalamus — no resolved target expressed herebasal ganglia — 14.0 nTPM, from KCNH2medulla oblongata — no resolved target expressed here

basal ganglia: drawn as the caudate nucleus, putamen and globus pallidus.

Measured but not drawn — this anatomogram has no outline for them: pituitary gland 41.5, midbrain 6.7, retina 5.3, spinal cord 4.0.

Body

heart — 28.4 nTPM, from KCNH2smooth muscle — 7.0 nTPM, from KCNH2lung — 1.8 nTPM, from KCNH2liver — 0.2 nTPM, from KCNH2kidney — 1.1 nTPM, from KCNH2stomach — 10.6 nTPM, from KCNH2duodenum — 2.4 nTPM, from KCNH2small intestine — 8.1 nTPM, from KCNH2colon — 36.0 nTPM, from KCNH2adrenal gland — 3.4 nTPM, from KCNH2thyroid gland — 0.1 nTPM, from KCNH2pancreas — 3.2 nTPM, from KCNH2urinary bladder — 13.4 nTPM, from KCNH2skeletal muscle — 0.2 nTPM, from KCNH2spleen — 1.7 nTPM, from KCNH2salivary gland — 0.9 nTPM, from KCNH2
042 nTPM

Square-root ramp · shared scale across both plates

Shading is transcript level — not affinity, and not affinity combined with expression. Outlined but unshaded organs hold none of this compound’s resolved targets above the atlas’s detection threshold. Anatomy from EMBL-EBI Anatomogram (Apache License 2.0); regions identified by Uberon (uberon.org), CC BY 3.0.

Brain regions

Regions where this compound's measured targets are transcribed. Linked from the plate above.

  1. pituitary gland

    41.5 nTPM

  2. cerebellum

    32.4 nTPM

  3. hypothalamus

    14.4 nTPM

  4. basal ganglia

    14.0 nTPM

  5. cerebral cortex

    10.0 nTPM

  6. hippocampal formation

    8.9 nTPM

  7. amygdala

    7.5 nTPM

  8. midbrain

    6.7 nTPM

  9. retina

    5.3 nTPM

  10. spinal cord

    4.0 nTPM

Peripheral & autonomic

Tissues outside the CNS expressing the same targets — where a compound's bodily effects become possible.

  1. colon

    36.0 nTPM

  2. heart muscle

    28.4 nTPM

  3. urinary bladder

    13.4 nTPM

  4. stomach 1

    10.6 nTPM

  5. small intestine

    8.1 nTPM

  6. smooth muscle

    7.0 nTPM

  7. adrenal gland

    3.4 nTPM

  8. pancreas

    3.2 nTPM

  9. duodenum

    2.4 nTPM

  10. lung

    1.8 nTPM

  11. spleen

    1.7 nTPM

  12. kidney

    1.1 nTPM

  13. salivary gland

    0.9 nTPM

  14. liver

    0.2 nTPM

  15. skeletal muscle

    0.2 nTPM

  16. thyroid gland

    0.1 nTPM

Each row joins two published measurements and nothing else: the affinity this archive holds for the compound at that target, and the transcript level the Human Protein Atlas reports for that target’s gene in that region. Bars scale with expression only. Expression is not activation — a receptor transcribed in a region is a receptor available to be bound there, which is a weaker and more defensible claim than saying the region is affected.

Expression data from Human Protein Atlas (CC BY-SA 3.0), RNA expression, nTPM (normalized transcripts per million), consensus tissue dataset. Uhlén M, et al. Tissue-based map of the human proteome. Science. 2015;347(6220):1260419.

VI · Profile

Affinity rosette

The strongest measurement at each of 1 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.

hERG — Ki 5.71 pXhERG579
Fig. Radius is pX = −log₁₀(value in M), that is 9 − log₁₀(value in nM), computed from the normalized measurement. Hatched wedges are equilibrium binding constants (Ki, Kd); dashed outlines are functional readouts (IC₅₀, EC₅₀, AC₅₀, potency), which answer a different question and are not pooled with them. Rings mark whole pX units from 5 to 10, labeled every second ring in the gutter at the top. Where a target carries several measurements, the strongest is drawn.

VII · Toxicology

Toxicological profile

What has been measured, and what has been published — kept apart, and neither scored. There is no risk rating on this page; the archive once carried one, identical for every compound, produced by a stub.

Measured in this archive

Assays that bear on toxicity, drawn from the same ChEMBL records as everything else on this page. They are measurements of what a compound binds or does to cells — not verdicts about what it does to a person.

hERG / cardiac ion channel 1

Block of the hERG potassium channel (KCNH2) is the standard in-vitro flag for QT prolongation. A measured affinity is not an arrhythmia risk, and this archive does not convert one into the other.

  • hERGKi1,960nMno origin

Published toxicology

— None. The toxicology databases this site reads — HSDB, RTECS and LiverTox, by way of PubChem — hold no record for Noribogaine. They index compounds that have been studied for decades, so most of this archive has no entry. An absent record is an absence of study, not evidence of safety.

Published passages via PubChem toxicology sections, aggregating Hazardous Substances Data Bank (HSDB), RTECS, LiverTox. No figure on this page is scored, ranked or combined into a risk level.

VIII · Evidence

Every measurement

One row per published value. The identifier in the last column resolves to the ChEMBL assay record it was read from.

Equilibrium binding constants 1

Ki and Kd — a concentration at equilibrium. Directly comparable across rows at the same target.

TargetClassTypeValue (nM)pXOrganismAssay
hERGIon channelsKi1,9605.71HAMSTERPMID 25636206
P
PubChem
C
ChEMBL
R
Computed here with RDKit
D
Derived here from the stored measurement

IX · Trials

Registered clinical trials

Studies filed with ClinicalTrials.gov that name this compound as an intervention. A registered trial is a protocol, not a result — status and enrollment are printed beside every row, and withdrawn studies are counted rather than hidden.

1T

Registered studies

0T

Open or ongoing

1T

With a phase recorded

By phase

A study may carry two phase codes at once, so these count studies bearing each phase and do not sum to the total.

  • Phase 11

By status

The registry’s own status for each record. Withdrawn and terminated studies are counted here rather than hidden — a stopped trial is part of what is known.

  • Completed1

Every matched study

Newest first by start date. Each identifier opens the registry record it came from; the title is the sponsor’s own, quoted.

  • NCT06480981Completed · Phase 1

    Multiple Ascending Dose Noribogaine PK/PD in Healthy Volunteers

    Enrollment
    55Tactual
    Started
    2024-06-20
    Sponsor
    DemeRx NB

    Conditions Pharmacokinetics

    Matched “Noribogaine” in the study’s intervention “Noribogaine”

Records from ClinicalTrials.gov (U.S. National Library of Medicine, NIH), API v2. A study is listed against a compound only when a verified name for that compound appears as a whole word in one of the study's own intervention names. A short code must appear as written, and a name the registry uses for something else (Aleph, a vaccine maker) is not matched. Title matches are not accepted. The matched name and the intervention text it matched are shown with every row.

Searched as Noribogaine · (-)-Noribogaine · Ibogamin-12-ol. Run this search at the registry — it returns the unfiltered result, including studies this page rejected as belonging to a different molecule.

A registered trial is a protocol somebody filed with the registry. It is not a result, and nothing on this plate says whether Noribogaine worked.

XI · Literature

Sources behind this dossier

The papers this compound's values were read from, ranked by what each contributed. Not a review of the field.

Every paper below is one some value on this page came from — a binding constant, a passage of pharmacology or toxicology, or a measured duration. Each entry says what this archive took from it. Nothing else is claimed about any of them: the title is the study’s own account of itself, and a summary written here would be an assertion with no source behind it.

  1. 01

    hERG Blockade by Iboga Alkaloids

    Alper K, Bai R, Liu N et al. · Cardiovascular toxicology 2016

    • · 1 measurement at 1 target (Ki), strongest hERG at 5.71 pX

    PMID 25636206

  2. 02

    Ascending-dose study of noribogaine in healthy volunteers: pharmacokinetics, pharmacodynamics, safety, and tolerability

    Glue P, Lockhart M, Lam F et al. · Journal of clinical pharmacology 2015

    • · Plasma elimination half-life

    PMID 25279818