Cannabidiol (CBD)

2-[(1R,6R)3-Methyl-6-(1-methylethenyl)-2-cyclohexen-1-yl]-5-pentyl-1,3-benzenediol

Overview

Cannabidiol (CBD) belongs to Cannabinoids.

Key safety note: Generally well tolerated and non-intoxicating.[5][3]
Effects
Subjective effects vary. What a substance feels like depends on dose, individual physiology, mindset, and setting. The points below describe commonly reported effects, not guaranteed, uniform, or desirable outcomes.
  • Non-intoxicating: CBD does not cause the euphoria, impairment or perceptual changes of THC, and can even reduce some of THC's effects.
  • At medicinal doses (as Epidiolex) it reduces seizure frequency in specific epilepsies. Commonly reported effects include somnolence, decreased appetite and diarrhoea.
  • Anxiolytic, anti-nausea and possible antipsychotic effects are reported and under study, largely linked to 5-HT1A agonism, though consumer-product doses are far lower than the doses used in trials.
Dosing & duration
Harm-reduction note: These are commonly cited reference ranges, not a recommendation or a “safe” dose. Potency, purity, body chemistry, tolerance, and drug combinations vary widely. Start low, go slow, wait for full effects before redosing, and never assume an unknown product matches these figures. Missing data is not evidence of safety.

Not reported

Dose ranges

Duration

Chemical & Physical Properties
FormulaC21H30O2
Molar mass314.46 g/mol
StateNot reported
Melting pointNot reported
Boiling pointNot reported
DensityNot reported
Vapor pressureNot reported
pKaNot reported
LogP6.5 (predicted, XLogP3)
SolubilityNot reported
Refractive indexNot reported
Identifiers & Synonyms
CAS13956-29-1
CAS (enantiomer)
PubChem CID644019
InChIKeyQHMBSVQNZZTUGM-ZWKOTPCHSA-N
InChIInChI=1S/C21H30O2/c1-5-6-7-8-16-12-19(22)21(20(23)13-16)18-11-15(4)9-10-17(18)14(2)3/h11-13,17-18,22-23H,2,5-10H2,1,3-4H3/t17-,18+/m0/s1
SMILESCCCCCC1=CC(=C(C(=C1)O)[C@@H]2C=C(CC[C@H]2C(=C)C)C)O

Synonyms

  • Cannabidiol
  • CBD
  • Epidiolex (active)
  • (−)-CBD
Pharmacodynamics & Biochemistry

Cannabidiol (CBD) is the major non-intoxicating cannabinoid of cannabis. Unlike THC it produces no 'high' because it has only low direct affinity for the CB1 and CB2 receptors. At CB1 it instead acts as a negative allosteric modulator, reshaping how the receptor responds to THC and the body's own endocannabinoids rather than activating it. This is one reason CBD can blunt some of THC's effects. CBD's pharmacology is unusually broad. Better-supported actions include agonism at the serotonin 5-HT1A receptor (linked to anxiolytic, anti-nausea and neuroprotective effects), agonism and desensitisation of TRPV1 and related TRP channels, antagonism of the orphan receptor GPR55, and enhancement of endocannabinoid tone by inhibiting anandamide breakdown/reuptake. It also blocks a range of voltage-gated sodium channels (Nav1.1–1.7). No single target fully explains its anticonvulsant effect: the antiseizure action of CBD (as Epidiolex) is thought to combine GPR55 antagonism, TRPV1 desensitisation and modulation of adenosine signalling and intracellular calcium. Many of these targets are engaged only at relatively high (micromolar) concentrations. CBD is highly lipophilic, with poor and variable oral bioavailability (extensive first-pass metabolism, increased by fatty food), and is metabolised by CYP2C19, CYP3A4 and UGT enzymes to 7-hydroxy-CBD and other metabolites: the basis of its clinically important drug interactions.

Biological targets

  • CB1
  • CB2
  • 5-HT1A
  • TRPV1

Binding & functional measurements

TargetMeasurementSpecies
TRPA1pEC50 6.3Rat
TRPV2pEC50 5.4Rat
TRPV3pEC50 5.4Rat
CB1 receptorEC50 1,469 nMHuman
CB1 receptorKi 4,330 nMHuman
CB2 receptorEC50 58 nM
Emax 23 ± 2.8%		Human
CB2 receptorKi 2,370 nMHuman
Pharmacokinetics
BioavailabilityOral ≈6–19% (high first-pass, increased with fatty food)
Tmax≈2.5–5 h
Half-life≈18–32 h
VdNot reported
Protein bindingNot reported
MetabolismCYP2C19/CYP3A4 and UGT to 7-OH-CBD
ExcretionMainly faecal. Some renal
Toxicology & Safety
Harm-reduction note: Toxicity and risk depend on dose, route, purity, combinations, setting, and individual health factors. Missing harms should never be interpreted as evidence of safety.

Not reported

Generally well tolerated and non-intoxicating. The main concerns are drug interactions (CYP inhibition), dose-related liver-enzyme elevations, diarrhoea, somnolence and decreased appetite. Purified CBD is approved as Epidiolex/Epidyolex for Lennox-Gastaut syndrome, Dravet syndrome and tuberous-sclerosis-complex seizures. Most consumer 'CBD' products are unregulated supplements of variable content and are not approved medicines.[5][3]

Legal Status
Legal note: Legal status can change over time and may vary by country, region, formulation, analogue status, prescription context, and enforcement practice. Always confirm with current official sources before relying on this section.
Interactions & Contraindications

Drug interactions

Drugs cleared by shared CYP enzymes (e.g. CYP2C9, CYP3A4) Inhibits CYP2C19/CYP3A4, raising levels of clobazam, valproate (hepatotoxicity), warfarin and other antiepileptics.[5][3]
Alcohol, Benzodiazepines Additive sedation with CNS depressants.[5]

Contraindications

Kidney or liver impairment severe hepatic impairment (dose adjustment needed), and caution with hepatotoxic co-medication such as valproate.[5]
Known hypersensitivity to the drug[3]
Usage & Context
  • Therapeutic (epilepsy).
  • Wellness/consumer products.
  • Research.
Sources & Evidence
  1. PubChem: Cannabidiol (CID 644019) — identifiers & computed properties
  2. FDA / DailyMed: Cannabidiol (Epidiolex) prescribing information — pharmacokinetics & metabolism
  3. Millar SA, Stone NL, Yates AS, et al. (2018). A Systematic Review on the Pharmacokinetics of Cannabidiol in Humans. Front Pharmacol 9:1365.

    PMID 30534073 · doi:10.3389/fphar.2018.01365

  4. Ibeas Bih C, Chen T, Nunn AV, et al. (2015). Molecular Targets of Cannabidiol in Neurological Disorders. Neurotherapeutics 12:699-730.

    PMID 26264914 · doi:10.1007/s13311-015-0377-3

  5. Britch SC, Babalonis S, Walsh SL (2021). Cannabidiol: pharmacology and therapeutic targets. Psychopharmacology (Berl) 238:9-28.

    PMID 33221931 · doi:10.1007/s00213-020-05712-8

  6. Laprairie RB, Bagher AM, Kelly ME, et al. (2015). Cannabidiol is a negative allosteric modulator of the cannabinoid CB1 receptor. Br J Pharmacol 172:4790-805.

    PMID 26218440 · doi:10.1111/bph.13250

  7. IUPHAR/BPS Guide to PHARMACOLOGY: cannabidiol (ligand 4150) — GPR55/TRP/Nav binding data CC BY-SA 4.0
  8. U.S. FDA: Regulation of cannabis and cannabidiol (CBD) products
  9. Chianese G, Lopatriello A, Schiano-Moriello A, et al. (2020). Cannabitwinol, a Dimeric Phytocannabinoid from Hemp, Cannabis sativa L., Is a Selective Thermo-TRP Modulator. J Nat Prod 83:2727-2736.

    PMID 32880179 · doi:10.1021/acs.jnatprod.0c00668

  10. Qin N, Neeper MP, Liu Y, et al. (2008). TRPV2 is activated by cannabidiol and mediates CGRP release in cultured rat dorsal root ganglion neurons. J Neurosci 28:6231-8.

    PMID 18550765 · doi:10.1523/JNEUROSCI.0504-08.2008

  11. De Petrocellis L, Orlando P, Moriello AS, et al. (2012). Cannabinoid actions at TRPV channels: effects on TRPV3 and TRPV4 and their potential relevance to gastrointestinal inflammation. Acta Physiol (Oxf) 204:255-66.

    PMID 21726418 · doi:10.1111/j.1748-1716.2011.02338.x

  12. PubChem computed properties (CID 644019)

Further Information