Harmane
PubChem records this structure as Harman.
Also known asHarman · 1-Methyl-9H-pyrido[3,4-b]indole · Aribine · Locuturine · Loturine · Aribin · Locuturin · Passiflorin
1-methyl-9H-pyrido[3,4-b]indole
- PubChem CID
- 5281404
- ChEMBL
- CHEMBL12014
- Measurements
- 14
- InChIKey
- PSFDQSOCUJVVGF-UHFFFAOYSA-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
Harman is an indole alkaloid fundamental parent with a structure of 9H-beta-carboline carrying a methyl substituent at C-1. It has been isolated from the bark of Sickingia rubra, Symplocus racemosa, Passiflora incarnata, Peganum harmala, Banisteriopsis caapi and Tribulus terrestris, as well as from tobacco smoke. It is a specific, reversible inhibitor of monoamine oxidase A. It has a role as an EC 1.4.3.4 (monoamine oxidase) inhibitor, an anti-HIV agent and a plant metabolite. It is an indole alkaloid fundamental parent, an indole alkaloid and a harmala alkaloid.
harman has been reported in Cribricellina cribraria, Polygala tenuifolia, and other organisms with data available.
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 Harmane 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 Harmane 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.
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.
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 — 14 measurements in this archive, equilibrium constants kept apart from functional readouts.
- Toxicology — nothing published for Harmane. 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 Harmane 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.
- Formula
- C12H10N2R
- Molecular weight
- 182.23g/molR
- Exact mass
- 182.0844DaR
- cLogP
- 3.02R
- TPSA
- 28.7ŲR
- H-bond donors
- 1R
- H-bond acceptors
- 1R
- Rotatable bonds
- 0R
- Aromatic rings
- 3R
- Heavy atoms
- 14R
- Fraction sp³
- 0.083R
- Formal charge
- 0R
Computed with RDKit 2025.09.2 from the SMILES returned by PubChem. Audit run 26/09/2026.
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
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.
No half-life is published for this compound in the sources this site reads.
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.
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 0 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
basal ganglia: drawn as the caudate nucleus, putamen and globus pallidus.
Measured but not drawn — this anatomogram has no outline for them: midbrain 47.7, retina 24.3, spinal cord 14.4, pituitary gland 6.4.
Body
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.
hypothalamus
103.9 nTPMcerebellum
59.1 nTPMmidbrain
47.7 nTPMbasal ganglia
38.3 nTPMretina
24.3 nTPMcerebral cortex
23.4 nTPMamygdala
21.5 nTPMhippocampal formation
14.8 nTPMspinal cord
14.4 nTPMpituitary gland
6.4 nTPM
Peripheral & autonomic
Tissues outside the CNS expressing the same targets — where a compound's bodily effects become possible.
liver
3367.1 nTPMsmall intestine
754.5 nTPMduodenum
713.0 nTPMskeletal muscle
152.9 nTPMthyroid gland
105.7 nTPMcolon
104.7 nTPMkidney
69.7 nTPMsalivary gland
66.9 nTPMurinary bladder
61.9 nTPMlung
56.9 nTPMstomach 1
50.0 nTPMheart muscle
44.8 nTPMpancreas
35.0 nTPMadrenal gland
24.9 nTPMsmooth muscle
21.4 nTPMspleen
5.6 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.
1 of this compound’s targets could not be resolved to a gene and are absent from both columns: GABAA.
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 5 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.
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.
Cytochrome P450 inhibition 2
Inhibition of a drug-metabolising enzyme, which is how interactions arise — the harmala alkaloids' MAO inhibition is the same kind of fact, and appears with the measurements above.
- Cytochrome P450 3A4Potency3,981nMCHEMBL1613886
- Cytochrome P450 2D6Potency10,000nMCHEMBL1614110
Published toxicology
— None. The toxicology databases this site reads — HSDB, RTECS and LiverTox, by way of PubChem — hold no record for Harmane. 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 2
Ki and Kd — a concentration at equilibrium. Directly comparable across rows at the same target.
| Target | Class | Type | Value (nM) | pX | Organism | Assay |
|---|---|---|---|---|---|---|
| Unchecked | Unclassified | Ki | 54.00 | 7.27 | — organism not recorded | CHEMBL897567 |
| GABAA | GABA receptors | Ki | 12,400 | 4.91 | Rattus norvegicus | CHEMBL652562 |
Functional readouts 12
IC₅₀, EC₅₀, AC₅₀ and potency. Assay-dependent, and not interchangeable with a binding constant.
| Target | Class | Type | Value (nM) | pX | Organism | Assay |
|---|---|---|---|---|---|---|
| Amine oxidase [flavin-containing] A | Enzymes | IC50 | 29.00 | 7.54 | Homo sapiens | CHEMBL5235559 |
| GABAA | GABA receptors | IC50 | 2,500 | 5.60 | Homo sapiens | CHEMBL5235566 |
| Cytochrome P450 3A4 | Enzymes | Potency | 3,981 | 5.40 | Homo sapiens | CHEMBL1613886 |
| Tryptophan 2,3-dioxygenase | Unclassified | IC50 | 6,310 | 5.20 | Homo sapiens | CHEMBL5142248 |
| Cytochrome P450 2D6 | Enzymes | Potency | 10,000 | 5.00 | Homo sapiens | CHEMBL1614110 |
| GABAA | GABA receptors | IC50 | 12,303 | 4.91 | Homo sapiens | CHEMBL650075 |
| Unchecked | Unclassified | IC50 | 12,303 | 4.91 | — organism not recorded | CHEMBL1005398 |
| Unchecked | Unclassified | IC50 | 12,303 | 4.91 | — organism not recorded | CHEMBL3057670 |
| GABAA | GABA receptors | IC50 | 12,388 | 4.91 | Rattus norvegicus | CHEMBL651677 |
| GABAA | GABA receptors | IC50 | 12,388 | 4.91 | Rattus norvegicus | CHEMBL858255 |
| GABAA | GABA receptors | IC50 | 12,400 | 4.91 | Rattus norvegicus | CHEMBL650289 |
| Acetylcholinesterase | Enzymes | IC50 | 20,910 | 4.68 | Electrophorus electricus | CHEMBL2020010 |
- 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.
— No registered study names Harmane as an intervention. That is an absence of registered research, not evidence about the compound. Most of this archive has never been the subject of a registered trial.
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 Harmane · Locuturine · Passiflorin. Run this search at the registry.
A registered trial is a protocol somebody filed with the registry. It is not a result, and nothing on this plate says whether Harmane worked.
X · Legal
Controlled-substance status
United States federal scheduling, read from the DEA records this archive holds. Not legal advice, and an absent record is not a finding that a compound is uncontrolled.
Other regulatory records
Registers outside the DEA that hold an entry for Harmane — chemical-safety and national inventories, each naming itself. They are not scheduling decisions.
9H-Pyrido3,4-bindole, 1-methyl-: Does not have an individual approval but may be used under an appropriate group standard
An absent DEA record is not a finding that Harmane is legal. It means this archive holds no DEA passage for it. The Controlled Substances Analogue Enforcement Act reaches substances that appear on no schedule by name, and many compounds here are ring-substituted analogues of scheduled drugs. Nothing on this plate should be read as saying a compound may lawfully be made, held or supplied.
United States federal status only. State law differs, and so does the law of every other country — none of it is represented here. Scheduling changes, and this reflects the DEA records held by PubChem descriptive sections when the monograph was last harvested, not necessarily today. This is a record of what a database publishes, not legal advice.
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.
No reference is recorded against any value for this compound. Its measurements come from ChEMBL assay records that carry an assay identifier but no publication, so there is no paper to cite here — an absence in the upstream record, not a judgment about the evidence. The assay identifiers in Every measurement resolve to the records the values were read from.