Cannabidivarin
Also known asCannabidivarol · CBDV · CBD-V · CBDV compound · Cannabidivarin (CBDV) · (-)-cannabidivarin · cannabidivarine · CANNABIDIVARIN [NFLIS-DRUG]
2-[(1R,6R)-3-methyl-6-prop-1-en-2-ylcyclohex-2-en-1-yl]-5-propylbenzene-1,3-diol
- PubChem CID
- 11601669
- ChEMBL
- CHEMBL2387742
- Measurements
- 19
- InChIKey
- REOZWEGFPHTFEI-JKSUJKDBSA-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
Cannabidivarin, also known as cannabidivarol or CBDV, is a non-psychoactive cannabinoid found within [DB14009]. It is one of over 100 cannabinoids identified from the Cannabis plant that can modulate the physiological activity of cannabis, or marijuana. Compared to its homolog, [DB09061], CBDV is shortened by two methyl (CH2) groups on its side chain. Notably, both [DB09061] and CBDV have demonstrated anticonvulsant activity in animal and human models and are demonstrating promising clinical trial results. Other cannabinoids with some evidence of anti-epileptic activity include [DB11755] (THCV) and Δ9-tetrahydrocannabinolic acid. While the primary components of cannabis, CBD and THC, have b…
Cannabidivarin has been reported in Cannabis sativa with data available.
Recognized use
Cannabidivarin does not currently have any FDA or Health Canada approved indications, however in October 2017 CBDV was given orphan designation by the European Medicines Agency for use in Rett Syndrome and again in February 2018 for treatment of Fragile X Syndrome.
How it acts
The anti-epileptic activity of CBD and CBDV is thought to be modulated by their effects on transient receptor potential cation channel subfamily V member 1 (TRPV1), also known as the capsaicin receptor, which is part of a large family of ion channels that are involved in the onset and progression of several types of epilepsy. CBD and CBDV have been shown to dose-dependently activate and then desensitize TRPV1 as well as TRPV2 and TRPA1 channels. Desensitization of these ion channels is a potential mechanism by which these molecules cause a reduction of neuronal hyperexcitability that contributes to epileptic activity and seizures. CBDV has also been shown to inhibit the activity of diacyl…
Behavior carries the pharmacological classes and the acute-effect durations, with plasma half-life kept separate from duration of effect.
In the body
Like Δ9-THC, CBDV has low water solubility and poor oral bioavailability (~6% in humans), making oral administration an unfavourable method of delivery. Despite this, CBDV has relatively rapid absorption with peak concentrations seen around 2 h after oral administration in animal pharmacokinetic studies. Orally administered CBDV in mice was found to have a plasma Cmax of 0.47ug/mL and Tmax of 30 minutes, and a brain Cmax of 0.94ug/mL and Tmax of 60 minutes.
Absorption, Distribution and Excretion
Due to its lipophilicity, CBDV has been shown to cross the blood brain barrier.
Absorption, Distribution and Excretion
Significant first-pass metabolism by the liver results in erratic absorption from the GI tract, low bioavailability, and unreliable pharmacokinetics.
Metabolism/Metabolites
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 Cannabidivarin 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 Cannabidivarin 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 — 19 measurements in this archive, equilibrium constants kept apart from functional readouts.
- Toxicology — nothing published for Cannabidivarin. 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 Cannabidivarin 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
- C19H26O2R
- Molecular weight
- 286.41g/molR
- Exact mass
- 286.1933DaR
- cLogP
- 5.07R
- TPSA
- 40.5ŲR
- H-bond donors
- 2R
- H-bond acceptors
- 2R
- Rotatable bonds
- 4R
- Aromatic rings
- 1R
- Heavy atoms
- 21R
- Fraction sp³
- 0.474R
- Formal charge
- 0R
Computed with RDKit 2025.09.2 from the SMILES returned by PubChem. Audit run 26/09/2026.
Bemis–Murcko scaffold
C1=C[C@@H](c2ccccc2)CCC1
Shared with Cannabidiol, Cannabidiolic acid. 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 holds no other record of one either. 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.
Orally administered CBDV in mice was found to have a plasma elimination half life of 222 minutes, and a brain elimination half life of 204 minutes.
DrugBank
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.
Mechanism, as published
Quoted verbatim from the database named after each passage, never summarized.
The anti-epileptic activity of CBD and CBDV is thought to be modulated by their effects on transient receptor potential cation channel subfamily V member 1 (TRPV1), also known as the capsaicin receptor, which is part of a large family of ion channels that are involved in the onset and progression of several types of epilepsy. CBD and CBD…
DrugBank
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 2 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: retina 12.0, midbrain 6.6, spinal cord 6.4, pituitary gland 5.0.
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.
cerebellum
12.1 nTPMretina
12.0 nTPMmidbrain
6.6 nTPMspinal cord
6.4 nTPMhippocampal formation
6.3 nTPMcerebral cortex
5.8 nTPM- Transient receptor potential cation channel subfamily V member 1TRPV15.4 pX5.8
- Cytochrome P450 1A1CYP1A15.8 pX0.7
- Transient receptor potential cation channel subfamily V member 3TRPV35.8 pX0.4
- Cytochrome P450 2B6CYP2B65.9 pX0.1
- Transient receptor potential cation channel subfamily V member 4TRPV46.0 pX0.1
amygdala
5.8 nTPMhypothalamus
5.6 nTPMbasal ganglia
5.6 nTPMpituitary gland
5.0 nTPM
Peripheral & autonomic
Tissues outside the CNS expressing the same targets — where a compound's bodily effects become possible.
liver
549.6 nTPMurinary bladder
59.6 nTPMduodenum
30.5 nTPMsmall intestine
18.6 nTPMsalivary gland
18.1 nTPM- Transient receptor potential cation channel subfamily V member 4TRPV46.0 pX18.1
- Transient receptor potential cation channel subfamily V member 1TRPV15.4 pX3.7
- Cytochrome P450 1A1CYP1A15.8 pX1.6
- Cytochrome P450 2C19CYP2C195.9 pX0.2
- Transient receptor potential cation channel subfamily V member 3TRPV35.8 pX0.2
- and 1 more
kidney
14.4 nTPMheart muscle
10.8 nTPMlung
9.9 nTPMspleen
8.4 nTPMpancreas
6.7 nTPMskeletal muscle
6.0 nTPMstomach 1
5.2 nTPM- Transient receptor potential cation channel subfamily V member 1TRPV15.4 pX5.2
- Cytochrome P450 2C19CYP2C195.9 pX2.8
- Cytochrome P450 1A1CYP1A15.8 pX1.6
- Transient receptor potential cation channel subfamily V member 3TRPV35.8 pX0.9
- Transient receptor potential cation channel subfamily V member 4TRPV46.0 pX0.6
- and 2 more
colon
5.1 nTPM- Transient receptor potential cation channel subfamily V member 1TRPV15.4 pX5.1
- Cytochrome P450 2B6CYP2B65.9 pX4.7
- Cytochrome P450 1A1CYP1A15.8 pX2.1
- Transient receptor potential cation channel subfamily V member 3TRPV35.8 pX0.8
- Transient receptor potential cation channel subfamily V member 4TRPV46.0 pX0.4
- and 2 more
adrenal gland
4.4 nTPMthyroid gland
4.1 nTPMsmooth muscle
1.5 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.
3 of this compound’s targets could not be resolved to a gene and are absent from both columns: Transient receptor potential cation channel subfamily A member 1, Transient receptor potential cation channel subfamily M member 8, Transient receptor potential cation channel subfamily V member 2.
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 10 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 6
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 1A1IC5060.00nMCHEMBL5096651
- Cytochrome P450 2B6Ki1,300nMCHEMBL5096654
- Cytochrome P450 2C19Ki1,400nMCHEMBL5096658
- Cytochrome P450 1A1Ki1,600nMCHEMBL5096652
- Cytochrome P450 2C19IC503,700nMCHEMBL5096657
- Cytochrome P450 2B6IC507,400nMCHEMBL5096653
Published toxicology
— None. The toxicology databases this site reads — HSDB, RTECS and LiverTox, by way of PubChem — hold no record for Cannabidivarin. 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 4
Ki and Kd — a concentration at equilibrium. Directly comparable across rows at the same target.
| Target | Class | Type | Value (nM) | pX | Organism | Assay |
|---|---|---|---|---|---|---|
| CB2 | Cannabinoid receptors | Ki | 574 | 6.24 | Homo sapiens | CHEMBL6080628 |
| Cytochrome P450 2B6 | Enzymes | Ki | 1,300 | 5.89 | Homo sapiens | CHEMBL5096654 |
| Cytochrome P450 2C19 | Enzymes | Ki | 1,400 | 5.85 | Homo sapiens | CHEMBL5096658 |
| Cytochrome P450 1A1 | Enzymes | Ki | 1,600 | 5.80 | Homo sapiens | CHEMBL5096652 |
Functional readouts 15
IC₅₀, EC₅₀, AC₅₀ and potency. Assay-dependent, and not interchangeable with a binding constant.
- 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.
3T
Registered studies
1T
Open or ongoing
3T
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 22
- Not applicable1
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.
- Terminated1
- Recruiting1
- 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.
- NCT03848481Terminated · Phase 2
CBDV vs Placebo in Children and Adults up to Age 30 With Prader-Willi Syndrome (PWS)
- Enrollment
- 6Tactual
- Started
- 2020-11-23
- Sponsor
- Eric Hollander
Conditions Prader-Willi Syndrome
Matched “CBDV compound” in the study’s intervention “CBDV Compound”
- NCT03202303Recruiting · Phase 2
Cannabidivarin (CBDV) vs. Placebo in Children With Autism Spectrum Disorder (ASD)
- Enrollment
- 100Testimated
- Started
- 2019-04-12
- Sponsor
- Montefiore Medical Center
Conditions Autism Spectrum Disorder
Matched “Cannabidivarin” in the study’s intervention “Cannabidivarin”
- NCT03537950Completed · Not applicable
Shifting Brain Excitation-Inhibition Balance in Autism Spectrum Disorder
- Enrollment
- 38Tactual
- Started
- 2016-08-22
- Sponsor
- King's College London
Conditions Autism Spectrum Disorder
Matched “CBDV” in the study’s intervention “CBDV”
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 Cannabidivarin · Cannabidivarol · CBDV compound. 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 Cannabidivarin 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.
An absent DEA record is not a finding that Cannabidivarin 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.