Cannabidiol
Also known as(-)-Cannabidiol · (-)-trans-Cannabidiol · Epidiolex · delta1(2)-trans-Cannabidiol · cannabidiolum · NanoCDB · Melody Cloverstrip · CBD Oil
2-[(1R,6R)-3-methyl-6-prop-1-en-2-ylcyclohex-2-en-1-yl]-5-pentylbenzene-1,3-diol
- PubChem CID
- 644019
- ChEMBL
- CHEMBL190461
- Measurements
- 35
- InChIKey
- QHMBSVQNZZTUGM-ZWKOTPCHSA-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
Cannabidiol is an cannabinoid that is cyclohexene which is substituted by a methyl group at position 1, a 2,6-dihydroxy-4-pentylphenyl group at position 3, and a prop-1-en-2-yl group at position 4. It has a role as an antimicrobial agent and a plant metabolite. It is a member of resorcinols, a phytocannabinoid and an olefinic compound.
Cannabidiol, or CBD, is one of at least 85 active cannabinoids identified within the Cannabis plant. It is a major phytocannabinoid, accounting for up to 40% of the Cannabis plant's extract, that binds to a wide variety of physiological targets of the endocannabinoid system within the body. Although the exact medical implications are currently being investigated, CBD has shown promise as a therapeutic and pharmaceutical drug target. In particular, CBD has shown promise as an analgesic, anticonvulsant, muscle relaxant, anxiolytic, antipsychotic and has shown neuroprotective, anti-inflammatory, and antioxidant activity, among other currently investigated uses. CBD's exact place within medical…
The mechanism of action of cannabidiol is as a Cytochrome P450 2C8 Inhibitor, and Cytochrome P450 2C9 Inhibitor, and Cytochrome P450 2C19 Inhibitor, and UGT1A9 Inhibitor, and UGT2B7 Inhibitor, and Cytochrome P450 1A2 Inhibitor, and Cytochrome P450 2B6 Inhibitor, and Cytochrome P450 2B6 Inducer.
Cannabidiol (CBD) is a non-psychoactive component of Cannabis sativa (marijuana), one of more than 80 cannabinoids identified in the plant, and the second most common constituent after Δ9-tetrahydrocannabinol (THC), the major psychoactive component. Cannabidiol is available as an FDA approved prescription medication (Epidiolex) used in moderately high doses for severe forms of epilepsy, but it is also widely available as over-the-counter CBD oils, gummies, topical creams or vaping solutions. High daily doses of cannabidiol are associated with frequent serum enzyme elevations during therapy, but has not been linked to cases of clinically apparent liver injury with jaundice. The lower doses of…
Recognized use
When used in combination with delta-9-tetrahydrocannabinol as the product Sativex, cannabidiol was given a standard marketing authorization (ie. a Notice of Compliance (NOC)) by Health Canada for the following indications: 1) as adjunctive treatment for symptomatic relief of spasticity in adult patients with multiple sclerosis (MS) who have not responded adequately to other therapy and who demonstrate meaningful improvement during an initial trial of therapy; Due to the need for confirmatory studies to verify the clinical benefit coupled with the promising nature of the clinical evidence, Sativex was also given a Notice of Compliance with Conditions (NOC/c) by Health Canada for the followi…
How it acts
- Cannabinoid CB1 receptor negative allosteric modulatorNEGATIVE ALLOSTERIC MODULATORPMID 26218440
The exact mechanism of action of CBD and THC is not currently fully understood. However, it is known that CBD acts on cannabinoid (CB) receptors of the endocannabinoid system, which are found in numerous areas of the body, including the peripheral and central nervous systems, including the brain. The endocannabinoid system regulates many physiological responses of the body including pain, memory, appetite, and mood. More specifically, CB1 receptors can be found within the pain pathways of the brain and spinal cord where they may affect CBD-induced analgesia and anxiolysis, and CB2 receptors have an effect on immune cells, where they may affect CBD-induced anti-inflammatory processes. CBD h…
Although the exact mechanism and magnitude of effects of THC and CBD are not fully understood, CBD has been shown to have analgesic, anticonvulsant, muscle relaxant, anxiolytic, neuroprotective, anti-oxidant, and anti-psychotic activity. This wide variety of effects is likely due to it's complex pharmacological mechanisms. In addition to binding to CB1 and CB2 receptors of the endocannabinoid system, there is evidence that CBD activates 5-HT1A serotonergic and TRPV1–2 vanilloid receptors, antagonizes alpha-1 adrenergic and µ-opioid receptors, inhibits synaptosomal uptake of noradrenaline, dopamine, serotonin and gaminobutyric acid and cellular uptake of anandamide, acts on mitochondria Ca2 s…
Behavior carries the pharmacological classes and the acute-effect durations, with plasma half-life kept separate from duration of effect.
In the body
Following a single buccal administration, maximum plasma concentrations of both CBD and THC typically occur within two to four hours. When administered buccally, blood levels of THC and other cannabinoids are lower compared with inhalation of smoked cannabis. The resultant concentrations in the blood are lower than those obtained by inhaling the same dose because absorption is slower, redistribution into fatty tissues is rapid and additionally some of the THC undergoes hepatic first pass metabolism to 11-OH-THC, a psycho-active metabolite. The CBD component of sublingual Sativex was found to have a Tmax of 1.63hr and a Cmax of 2.50ng/mL, while buccal Sativex was found to have a Tmax of 2.8…
Absorption, Distribution and Excretion
Elimination from plasma is bi-exponential with an initial half-life of one to two hours. The terminal elimination half-lives are of the order of 24 to 36 hours or longer. Sativex is excreted in the urine and faeces.
Absorption, Distribution and Excretion
Cannabinoids are distributed throughout the body; they are highly lipid soluble and accumulate in fatty tissue. The release of cannabinoids from fatty tissue is responsible for the prolonged terminal elimination half-life.
Absorption, Distribution and Excretion
THC and CBD are metabolized in the liver by a number of cytochrome P450 isoenzymes, including CYP2C9, CYP2C19, CYP2D6 and CYP3A4. They may be stored for as long as four weeks in the fatty tissues from which they are slowly released at sub-therapeutic levels back into the blood stream and metabolized via the renal and biliary systems. The main primary metabolite of CBD is 7-hydroxy-cannabidiol.
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 Cannabidiol 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 Cannabidiol 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 — 35 measurements in this archive, equilibrium constants kept apart from functional readouts.
- Toxicology — 1 published passage, plus any assay in this archive bearing on toxicity.
- 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 Cannabidiol 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
- C21H30O2R
- Molecular weight
- 314.47g/molR
- Exact mass
- 314.2246DaR
- cLogP
- 5.85R
- TPSA
- 40.5ŲR
- H-bond donors
- 2R
- H-bond acceptors
- 2R
- Rotatable bonds
- 6R
- Aromatic rings
- 1R
- Heavy atoms
- 23R
- Fraction sp³
- 0.524R
- 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 Cannabidiolic acid, Cannabidivarin. 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
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.
The CBD component of sublingual Sativex was found to have a half life (t1/2) of 1.44hr, while buccal Sativex was found to have a half life (t1/2) of 1.81hr.
DrugBank
Primary pharmacological drivers
- Cannabinoid CB1 receptor negative allosteric modulator26218440
Mechanism, as published
Quoted verbatim from the database named after each passage, never summarized.
The exact mechanism of action of CBD and THC is not currently fully understood. However, it is known that CBD acts on cannabinoid (CB) receptors of the endocannabinoid system, which are found in numerous areas of the body, including the peripheral and central nervous systems, including the brain. The endocannabinoid system regulates many…
DrugBank Although the exact mechanism and magnitude of effects of THC and CBD are not fully understood, CBD has been shown to have analgesic, anticonvulsant, muscle relaxant, anxiolytic, neuroprotective, anti-oxidant, and anti-psychotic activity. This wide variety of effects is likely due to it's complex pharmacological mechanisms. In addition to…
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.
- Mood 2
- matched on “anxiolytic”, “mood” · in Pharmacology: Mechanism of Action; Pharmacology: Pharmacodynamics
- Cognition 1
- matched on “memory” · in Pharmacology: Mechanism of Action
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 411.4, midbrain 149.5, spinal cord 115.7, pituitary gland 91.0.
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.
retina
411.4 nTPMcerebral cortex
201.5 nTPMhypothalamus
168.6 nTPMmidbrain
149.5 nTPMbasal ganglia
148.1 nTPMamygdala
124.7 nTPMcerebellum
122.7 nTPMhippocampal formation
120.5 nTPMspinal cord
115.7 nTPMpituitary gland
91.0 nTPM
Peripheral & autonomic
Tissues outside the CNS expressing the same targets — where a compound's bodily effects become possible.
skeletal muscle
845.9 nTPMliver
658.2 nTPMkidney
355.4 nTPMadrenal gland
323.8 nTPMheart muscle
321.8 nTPMsmall intestine
273.2 nTPMcolon
262.4 nTPMsalivary gland
242.3 nTPMlung
232.6 nTPMurinary bladder
210.6 nTPMspleen
176.6 nTPMthyroid gland
172.7 nTPMstomach 1
170.7 nTPMduodenum
148.7 nTPMpancreas
140.2 nTPMsmooth muscle
116.0 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.
6 of this compound’s targets could not be resolved to a gene and are absent from both columns: Cholinesterase, Fatty-acid amide hydrolase 1, Gamma-aminobutyric acid receptor subunit beta-2, High affinity cGMP-specific 3',5'-cyclic phosphodiesterase 9A, Sigma 2, Transient receptor potential cation channel subfamily M member 8.
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 23 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 4
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 1A1Ki160nMCHEMBL4687717
- Cytochrome P450 2C19Ki790nMCHEMBL4687732
- Cytochrome P450 1A2Ki2,690nMCHEMBL4687718
- Cytochrome P450 1B1Ki3,630nMCHEMBL4687719
As published
Quoted verbatim from the database named after each passage, never summarized — a summary of a toxicology statement is a new claim.
Hepatotoxicity
In prelicensure studies, serum aminotransferase elevations arose during cannabidiol therapy for epilepsy in 34% to 47% of patients compared to 18% of controls who were receiving other anticonvulsant medications. Elevations above 3 times ULN occurred in 13% of cannabidiol treated compared to 1% on placebo. ALT and AST elevations were more frequent with higher doses and were particularly common (and sometimes delayed)…
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 24
Ki and Kd — a concentration at equilibrium. Directly comparable across rows at the same target.
| Target | Class | Type | Value (nM) | pX | Organism | Assay |
|---|---|---|---|---|---|---|
| D2 | Dopamine receptors | Ki | 0.066 | 10.18 | Homo sapiens | CHEMBL6080643 |
| Caspase-1 | Unclassified | Kd | 18.80 | 7.73 | Homo sapiens | CHEMBL4840409 |
| CB1 | Cannabinoid receptors | Ki | 151 | 6.82 | Homo sapiens | CHEMBL5527146 |
| Cytochrome P450 1A1 | Enzymes | Ki | 160 | 6.80 | Homo sapiens | CHEMBL4687717 |
| Equilibrative nucleoside transporter 1 | Unclassified | Ki | 250 | 6.60 | Homo sapiens | CHEMBL6080641 |
| Cytochrome P450 2C19 | Enzymes | Ki | 790 | 6.10 | Homo sapiens | CHEMBL4687732 |
| 5-HT2C | Serotonin receptors | Ki | 1,100 | 5.96 | Homo sapiens | CHEMBL4687691 |
| MOR | Opioid receptors | Ki | 1,300 | 5.89 | Homo sapiens | CHEMBL4687692 |
| KOR | Opioid receptors | Ki | 2,300 | 5.64 | Homo sapiens | CHEMBL4687693 |
| Cytochrome P450 1A2 | Enzymes | Ki | 2,690 | 5.57 | Homo sapiens | CHEMBL4687718 |
| D1 | Dopamine receptors | Ki | 2,700 | 5.57 | Homo sapiens | CHEMBL4687694 |
| D2 | Dopamine receptors | Ki | 2,800 | 5.55 | Homo sapiens | CHEMBL6080644 |
| CB2 | Cannabinoid receptors | Ki | 2,860 | 5.54 | Homo sapiens | CHEMBL3239823 |
| CB2 | Cannabinoid receptors | Ki | 2,900 | 5.54 | Homo sapiens | CHEMBL6083333 |
| H3 | Unclassified | Ki | 3,100 | 5.51 | Homo sapiens | CHEMBL4687695 |
| Alpha2B | Adrenergic receptors | Ki | 3,200 | 5.49 | Homo sapiens | CHEMBL4687696 |
| Sigma 2 | Sigma receptors | Ki | 3,400 | 5.47 | Homo sapiens | CHEMBL4687697 |
| Cytochrome P450 1B1 | Enzymes | Ki | 3,630 | 5.44 | Homo sapiens | CHEMBL4687719 |
| Alpha2C | Adrenergic receptors | Ki | 3,700 | 5.43 | Homo sapiens | CHEMBL4687698 |
| CB1 | Cannabinoid receptors | Ki | 4,350 | 5.36 | Homo sapiens | CHEMBL3239822 |
| CB1 | Cannabinoid receptors | Ki | 4,400 | 5.36 | Mus musculus | CHEMBL6083331 |
| CB2 | Cannabinoid receptors | Ki | 4,582 | 5.34 | Homo sapiens | CHEMBL5527148 |
| DOR | Opioid receptors | Ki | 6,400 | 5.19 | Homo sapiens | CHEMBL4687699 |
| L-lactate dehydrogenase A chain | Enzymes | Ki | 24,000 | 4.62 | Homo sapiens | CHEMBL4842434 |
Functional readouts 11
IC₅₀, EC₅₀, AC₅₀ and potency. Assay-dependent, and not interchangeable with a binding constant.
| Target | Class | Type | Value (nM) | pX | Organism | Assay |
|---|---|---|---|---|---|---|
| Transient receptor potential cation channel subfamily M member 8 | Ion channels | IC50 | 60.00 | 7.22 | Homo sapiens | CHEMBL5253448 |
| High affinity cGMP-specific 3',5'-cyclic phosphodiesterase 9A | Enzymes | IC50 | 110 | 6.96 | Homo sapiens | CHEMBL5634669 |
| Gamma-aminobutyric acid receptor subunit beta-2 | GABA receptors | IC50 | 130 | 6.89 | Homo sapiens | CHEMBL5531590 |
| G-protein coupled receptor 55 | Other named receptors | EC50 | 445 | 6.35 | Homo sapiens | CHEMBL1117885 |
| G-protein coupled receptor 55 | Other named receptors | IC50 | 445 | 6.35 | Homo sapiens | CHEMBL6080640 |
| Cholinesterase | Enzymes | IC50 | 670 | 6.17 | Equus caballus | CHEMBL4832641 |
| Acetylcholinesterase | Enzymes | IC50 | 17,070 | 4.77 | Electrophorus electricus | CHEMBL4832643 |
| Fatty-acid amide hydrolase 1 | Enzymes | IC50 | 27,500 | 4.56 | Mus musculus | CHEMBL6080635 |
| MOR | Opioid receptors | EC50 | 41,700 | 4.38 | Homo sapiens | CHEMBL5335496 |
| Hemozoin | Unclassified | IC50 | 51,100 | 4.29 | Plasmodium falciparum | CHEMBL5054968 |
| Fatty-acid amide hydrolase 1 | Enzymes | IC50 | 53,200 | 4.27 | Rattus norvegicus | CHEMBL4424979 |
- 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.
278T
Registered studies
87T
Open or ongoing
264T
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.
- Early phase 125
- Phase 165
- Phase 2141
- Phase 339
- Phase 415
- Not applicable23
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.
- Completed113
- Recruiting57
- Unknown status32
- Withdrawn20
- Terminated19
- Not yet recruiting17
- Active, not recruiting12
- No longer available4
- Available2
- Enrolling by invitation1
- Approved for marketing1
The 25 most recently started, of 278
Newest first by start date. Each identifier opens the registry record it came from; the title is the sponsor’s own, quoted.
- NCT03883360Withdrawn · Phase 2
Effects of Cannabidiol on Psychiatric Symptoms, Cognition, and Cannabis Consumption in Cannabis Users With Recent-Onset Psychosis
- Enrollment
- 0Tactual
- Started
- 2050-01
- Sponsor
- University of Maryland, Baltimore
Conditions Schizophrenia Spectrum Disorders · Cannabis Use
Matched “Cannabidiol” in the study’s intervention “Cannabidiol (CBD)”
- NCT06924827Not yet recruiting · Phase 4
A Study to Investigate the Transition of Children From 'Artisanal" Cannabidiol (CBD) to Epidiolex
- Enrollment
- 25Testimated
- Started
- 2027-01-01
- Sponsor
- Elizabeth Donner
Conditions Dravet Syndrome (DS) · Lennox-Gastaut Syndrome (LGS)
Matched “Epidiolex” in the study’s intervention “Epidiolex 100 mg/mL Oral Solution”
- NCT07728097Not yet recruiting · Phase 4
A Study to Investigate the Effect of Gradual Titration to Optimize Cannabidiol Treatment in Adults With LGS
- Enrollment
- 40Testimated
- Started
- 2026-11-18
- Sponsor
- Jazz Pharmaceuticals
Conditions Lennox-Gastaut Syndrome
Matched “Cannabidiol” in the study’s intervention “Cannabidiol Oral Solution”
- NCT07148843Not yet recruiting · Phase 2 / Phase 3
Cannabidiol as an Adjunct Treatment for Alcohol Withdrawal and Craving
- Enrollment
- 105Testimated
- Started
- 2026-10-01
- Sponsor
- Johns Hopkins University
Conditions Alcohol Use Disorder (AUD) · Withdrawal From Addictive Substance; Detoxification · Craving
Matched “Cannabidiol” in the study’s intervention “Cannabidiol (CBD)”
- NCT07148206Not yet recruiting · Phase 3
Dronabinol and Epidiolex to Manage Uncontrolled Residual Symptoms of Buprenorphine Initiation Trial
- Enrollment
- 40Testimated
- Started
- 2026-10
- Sponsor
- Montefiore Medical Center
Conditions Opioid Use Disorder
Matched “Epidiolex” in the study’s intervention “Epidiolex 100 mg/mL Oral Solution”
- NCT06222268Not yet recruiting · Phase 1 / Phase 2
Wayne State Warriors Marijuana Clinical Research Program: Cannabinoid Adjunct to Prolonged Exposure & Recovery
- Enrollment
- 280Testimated
- Started
- 2026-09
- Sponsor
- Leslie Lundahl
Conditions PTSD · Post Traumatic Stress Disorder · Suicide · Cannabis Use
Matched “Cannabidiol” in the study’s intervention “Cannabidiol (CBD) only”
- NCT07778810Recruiting · Phase 2
Epidiolex Trial for Presymptomatic Treatment of Sturge-Weber Syndrome
- Enrollment
- 10Testimated
- Started
- 2026-09
- Sponsor
- Johns Hopkins University
Conditions Sturge - Weber Syndrome (SWS)
Matched “Epidiolex” in the study’s intervention “Epidiolex 100 mg/mL Oral Solution”
- NCT05650697Not yet recruiting · Early phase 1
Topical CBD Scar Outcomes Study
- Enrollment
- 22Testimated
- Started
- 2026-09
- Sponsor
- University of Oklahoma
Conditions Forehead; Wound
Matched “Cannabidiol” in the study’s intervention “Group 1 cannabidiol (CBD) with silicone ointment”
- NCT07434895Recruiting · Early phase 1
Repeated CBD Administration and Cannabis Outcomes
- Enrollment
- 23Testimated
- Started
- 2026-08-05
- Sponsor
- Hannah Harris
Conditions Cannabis · Abuse Liability · Experimental Pain in Healthy Human Participants
Matched “Cannabidiol” in the study’s intervention “Cannabidiol, Medium Dose”
- NCT07527338Not yet recruiting · Phase 2
Mechanisms of Cannabidiol and Sleep in the Context of Alcohol Use
- Enrollment
- 58Testimated
- Started
- 2026-07-01
- Sponsor
- University of Colorado, Boulder
Conditions Sleep · Alcohol Misuse
Matched “Cannabidiol” in the study’s intervention “Cannabidiol”
- NCT07638189Not yet recruiting · Phase 2
CBD Knee Osteoarthritis Study
- Enrollment
- 30Testimated
- Started
- 2026-07-01
- Sponsor
- University of Tennessee
Conditions Osteoarthitis
Matched “Cannabidiol” in the study’s intervention “Cannabidiol (CBD)”
- NCT07549256Recruiting · Phase 2
Cannabidiol for Pain Relief of Patients With End-stage mCRPC
- Enrollment
- 58Testimated
- Started
- 2026-06-12
- Sponsor
- Regionshospital Nordjylland
Conditions Metastatic Castration Resistant Prostate Cancer (mCRPC)
Matched “Cannabidiol” in the study’s intervention “Cannabidiol”
- NCT07624279Not yet recruiting · Phase 2
nVNS, CBD, and SoC for Persistent Post-Traumatic Headache
- Enrollment
- 80Testimated
- Started
- 2026-06-01
- Sponsor
- American Society of Pain and Neuroscience, Inc.
Conditions Persistent Post Traumatic Headache
Matched “Cannabidiol” in the study’s intervention “Cannabidiol”
- NCT07696871Recruiting · Phase 1 / Phase 2
Cannabidiol Oil for Treatment-Resistant Major Depression
- Enrollment
- 120Testimated
- Started
- 2026-06-01
- Sponsor
- Universidade do Sul de Santa Catarina
Conditions Major Depressive Disorder (MDD) · Treatment-resistant Depression (TRD)
Matched “CBD Oil” in the study’s intervention “Full-spectrum CBD oil 100 mg/mL”
- NCT07434973Not yet recruiting · Phase 3
Stratification and Treatment in Early Psychosis Study - PROMOTE
- Enrollment
- 586Testimated
- Started
- 2026-05-01
- Sponsor
- University of Oxford
Conditions Clinical High Risk for Psychosis (CHR) · Clinical High Risk for Psychosis · Clinical High Risk for Developing Psychosis
Matched “Cannabidiol” in the study’s intervention “Cannabidiol (CBD)”
- NCT07564245Not yet recruiting · Phase 2
Efficacy of Cannabidiol in the Management of Self-injuries in Children and Adolescents With Severe Neurodevelopmental Disorders.
- Enrollment
- 21Testimated
- Started
- 2026-05
- Sponsor
- Assistance Publique - Hôpitaux de Paris
Conditions Neurodevelopmental Disorders With Severe Self-injuries
Matched “Cannabidiol” in the study’s intervention “Cannabidiol”
- NCT07279558Recruiting · Phase 2
Cannabidiol and Alcohol Use Disorder Phenotypes
- Enrollment
- 150Testimated
- Started
- 2026-04-21
- Sponsor
- University of Colorado, Denver
Conditions Alcohol Use Disorder
Matched “Cannabidiol” in the study’s intervention “Full-Spectrum Cannabidiol (CBD)”
- NCT07016971Recruiting · Phase 1
CBG/CBD Oil for Chemotherapy-Induced Peripheral Neuropathy
- Enrollment
- 12Testimated
- Started
- 2026-04-03
- Sponsor
- Milton S. Hershey Medical Center
Conditions Chemotherapy-Induced Peripheral Neuropathy
Matched “CBD Oil” in the study’s intervention “CBG/CBD Oil”
- NCT07298408Recruiting · Phase 1 / Phase 2
Cannabidiol for the Treatment of Diabetic Peripheral Neuropathy: Pilot Study
- Enrollment
- 20Testimated
- Started
- 2026-04-02
- Sponsor
- Florida A&M University
Conditions Diabetic Peripheral Neuropathic Pain (DPN) · Diabetic Neuropathies
Matched “Cannabidiol” in the study’s intervention “Cannabidiol (CBD) oral solution”
- NCT06333041Recruiting · Phase 2 / Phase 3
Study of Cannabidiol in Sanfilippo Syndrome
- Enrollment
- 35Testimated
- Started
- 2026-04-01
- Sponsor
- Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center
Conditions Sanfilippo Syndrome · Mucopolysaccharidosis III
Matched “Epidiolex” in the study’s intervention “Epidiolex”
- NCT07570472Recruiting · Phase 2
The Effect of CBD on Sleep Quality Following Late Evening Exercise
- Enrollment
- 20Testimated
- Started
- 2026-03-19
- Sponsor
- KU Leuven
Conditions Sleep Quality
Matched “Cannabidiol” in the study’s intervention “Cannabidiol or placebo”
- NCT07462559Not yet recruiting · Phase 1
KF2025#1 Trial: Ketamine, Cannabidiol and Cobicistat Interaction Study
- Enrollment
- 12Testimated
- Started
- 2026-03-04
- Sponsor
- Helsinki University Central Hospital
Conditions Drug Drug Interaction
Matched “Cannabidiol” in the study’s intervention “Cannabidiol Epidyolex 100 mg/ml”
- NCT07271030Recruiting · Not applicable
The Use of Cannabidiol Suppositories for Sexual Pain
- Enrollment
- 50Testimated
- Started
- 2026-01-16
- Sponsor
- London Metropolitan University
Conditions Well-Being, Psychological · Quality of Life · Sexual Behavior · Sexual Pain Disorder
Matched “Cannabidiol” in the study’s intervention “Cannabidiol suppository intervention 1”
- NCT06787118Not yet recruiting · Phase 3
Study Assessing the Efficacy and Safety of cANnabidiol Oral Solution for Joint Pain of Adjuvant enDOcrine theRApy in Patients With Early Breast Cancer
- Enrollment
- 130Testimated
- Started
- 2025-12
- Sponsor
- Gustave Roussy, Cancer Campus, Grand Paris
Conditions Breast Cancer Stage I · Breast Cancer Stage II · Breast Cancer Stage III · HR+ Breast Cancer · AI-related Musculoskeletal Pain
Matched “CBD Oil” in the study’s intervention “CBD oil”
- NCT07245238Recruiting · Phase 3
Topical Cannabidiol Lotion for Pruritus Relief in Scleroderma
- Enrollment
- 36Testimated
- Started
- 2025-11-05
- Sponsor
- Khon Kaen University
Conditions Mediciine · Systemic Sclerosis (SSc) · Intervention Study
Matched “Cannabidiol” in the study’s intervention “10% urea lotion plus 1% cannabidiol”
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 Cannabidiol · (-)-Cannabidiol · (-)-trans-Cannabidiol. 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 Cannabidiol 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 Cannabidiol — chemical-safety and national inventories, each naming itself. They are not scheduling decisions.
Cannabidiol: Does not have an individual approval but may be used as a component in a product covered by a group standard. It is not approved for use as a chemical in its own right.
An absent DEA record is not a finding that Cannabidiol 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.