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Cannabidiol

PubChem CID
644019
Structure
Cannabidiol_small.png
Cannabidiol_3D_Structure.png
Molecular Formula
Synonyms
  • cannabidiol
  • 13956-29-1
  • (-)-Cannabidiol
  • (-)-trans-Cannabidiol
  • Epidiolex
Molecular Weight
314.5 g/mol
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Dates
  • Create:
    2005-06-08
  • Modify:
    2025-01-18
Description
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 a plant metabolite and an antimicrobial agent. It is a member of resorcinols, an olefinic compound and a phytocannabinoid.
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 practice is still currently hotly debated, however as the body of evidence grows and legislation changes to reflect its wide-spread use, public and medical opinion have changed significantly with regards to its usefulness in a number of medical conditions ranging from anxiety to epilepsy. From a pharmacological perspective, Cannabis' (and CBD's) diverse receptor profile explains its potential application for such a wide variety of medical conditions. Cannabis contains more than 400 different chemical compounds, of which 61 are considered cannabinoids, a class of compounds that act upon endogenous cannabinoid receptors of the body. Cannabinoid receptors are utilized endogenously by the body through the endocannabinoid system, which includes a group of lipid proteins, enzymes, and receptors that are involved in many physiological processes. Through its modulation of neurotransmitter release, the endocannabinoid system regulates cognition, pain sensation, appetite, memory, sleep, immune function, and mood among many other bodily systems. These effects are largely mediated through two members of the G-protein coupled receptor family, cannabinoid receptors 1 and 2 (CB1 and CB2). CB1 receptors are found in both the central and peripheral nervous systems, with the majority of receptors localized to the hippocampus and amygdala of the brain. Physiological effects of using cannabis make sense in the context of its receptor activity as the hippocampus and amygdala are primarily involved with regulation of memory, fear, and emotion. In contrast, CB2 receptors are mainly found peripherally in immune cells, lymphoid tissue, and peripheral nerve terminals. Tetrahydrocannabinol (THC) and cannabidiol (CBD) are two types of cannabinoids found naturally in the resin of the marijuana plant, both of which interact with the cannabinoid receptors that are found throughout the body. Although THC and CBD have been the most studied cannabinoids, there are many others identified to date including cannabinol (CBN), cannabigerol (CBG), [DB14050] (CBDV), and [DB11755] (THCV) that can be found within the medical cannabis. While both CBD and THC are used for medicinal purposes, they have different receptor activity, function, and physiological effects. If not provided in their activated form (such as through synthetic forms of THC like [DB00470] or [DB00486]), THC and CBD are obtained through conversion from their precursors, tetrahydrocannabinolic acid-A (THCA-A) and cannabidiolic acid (CBDA), through decarboxylation reactions. This can be achieved through heating, smoking, vaporization, or baking of dried unfertilized female cannabis flowers. The primary psychoactive component of Cannabis, delta 9-tetrahydrocannabinol (Δ9-THC), demonstrates its effects through weak partial agonist activity at Cannabinoid-1 (CB1R) and Cannabinoid-2 (CB2R) receptors. This activity results in the well-known effects of smoking cannabis such as increased appetite, reduced pain, and changes in emotional and cognitive processes. In contrast to THC's weak agonist activity, CBD has been shown to act as a negative allosteric modulator of the cannabinoid CB1 receptor, the most abundant G-Protein Coupled Receptor (GPCR) in the body. Allosteric regulation is achieved through the modulation of receptor activity on a functionally distinct site from the agonist or antagonist binding site which is clinically significant as direct agonists (such as THC) are limited by their psychomimetic effects such as changes to mood, memory, and anxiety. In addition to the well-known activity on CB1 and CB2 receptors, there is further evidence that CBD also activates 5-HT1A/2A/3A serotonergic and TRPV1–2 vanilloid receptors, antagonizes alpha-1 adrenergic and µ-opioid receptors, inhibits synaptosomal uptake of noradrenaline, dopamine, serotonin and gamma-aminobutyric acid (GABA), and cellular uptake of anandamide, acts on mitochondria Ca2+ stores, blocks low-voltage-activated (T-type) Ca2+ channels, stimulates activity of the inhibitory glycine-receptor, and inhibits activity of fatty amide hydrolase (FAAH). CBD is currently available in Canada within a 1:1 formulation with tetrahydrocannbinol (THC) (as the formulation known as "nabiximols") as the brand name product Sativex. It is approved for use as adjunctive treatment for symptomatic relief of spasticity in adult patients with multiple sclerosis (MS). Sativex was also given a conditional Notice of Compliance (NOC/c) for use as adjunctive treatment for the symptomatic relief of neuropathic pain in adult patients with multiple sclerosis and as adjunctive analgesic treatment for moderate to severe pain in adult patients with advanced cancer. In April 2018, a Food and Drug Administration advisory panel unanimously recommended approval of Epidiolex (cannabidiol oral solution) for the treatment of two rare forms of epilepsy - Lennox-Gastaut syndrome and Dravet syndrome, which are among the two most difficult types of epilepsy to treat. Epidiolex was granted Orphan Drug designation as well as Fast Track Approval from the FDA for further study in these hard to treat conditions. Notably, phase 3 clinical trials of Epidiolex have demonstrated clinically significant improvement in Lennox-Gastaut syndrome and Dravet syndrome. On June 25th, 2018, Epidiolex was approved by the FDA to be the first CBD-based product available on the US market.
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.

1 Structures

1.1 2D Structure

Chemical Structure Depiction
Cannabidiol.png

1.2 3D Conformer

1.3 Crystal Structures

COD records with this CID as component

2 Names and Identifiers

2.1 Computed Descriptors

2.1.1 IUPAC Name

2-[(1R,6R)-3-methyl-6-prop-1-en-2-ylcyclohex-2-en-1-yl]-5-pentylbenzene-1,3-diol
Computed by Lexichem TK 2.7.0 (PubChem release 2021.10.14)

2.1.2 InChI

InChI=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
Computed by InChI 1.0.6 (PubChem release 2021.10.14)

2.1.3 InChIKey

QHMBSVQNZZTUGM-ZWKOTPCHSA-N
Computed by InChI 1.0.6 (PubChem release 2021.10.14)

2.1.4 SMILES

CCCCCC1=CC(=C(C(=C1)O)[C@@H]2C=C(CC[C@H]2C(=C)C)C)O
Computed by OEChem 2.3.0 (PubChem release 2024.12.12)

2.2 Molecular Formula

C21H30O2
Computed by PubChem 2.2 (PubChem release 2021.10.14)

2.3 Other Identifiers

2.3.1 CAS

3556-78-3

2.3.2 Deprecated CAS

35542-48-4
18436-46-9, 20547-66-4, 521-37-9

2.3.3 European Community (EC) Number

2.3.4 UNII

2.3.5 ChEBI ID

2.3.6 ChEMBL ID

2.3.7 DrugBank ID

2.3.8 DSSTox Substance ID

2.3.9 KEGG ID

2.3.10 Lipid Maps ID (LM_ID)

2.3.11 Metabolomics Workbench ID

2.3.12 NCI Thesaurus Code

2.3.13 Nikkaji Number

2.3.14 PharmGKB ID

2.3.15 Pharos Ligand ID

2.3.16 RXCUI

2.3.17 Wikidata

2.3.18 Wikipedia

2.4 Synonyms

2.4.1 MeSH Entry Terms

  • 1,3-Benzenediol, 2-(3-methyl-6-(1-methylethenyl)-2-cyclohexen-1-yl)-5-pentyl-, (1R-trans)-
  • Cannabidiol
  • Epidiolex

2.4.2 Depositor-Supplied Synonyms

3 Chemical and Physical Properties

3.1 Computed Properties

Property Name
Molecular Weight
Property Value
314.5 g/mol
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
XLogP3-AA
Property Value
6.5
Reference
Computed by XLogP3 3.0 (PubChem release 2021.10.14)
Property Name
Hydrogen Bond Donor Count
Property Value
2
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Hydrogen Bond Acceptor Count
Property Value
2
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Rotatable Bond Count
Property Value
6
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Exact Mass
Property Value
314.224580195 Da
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Monoisotopic Mass
Property Value
314.224580195 Da
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Topological Polar Surface Area
Property Value
40.5 Ų
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Heavy Atom Count
Property Value
23
Reference
Computed by PubChem
Property Name
Formal Charge
Property Value
0
Reference
Computed by PubChem
Property Name
Complexity
Property Value
414
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Isotope Atom Count
Property Value
0
Reference
Computed by PubChem
Property Name
Defined Atom Stereocenter Count
Property Value
2
Reference
Computed by PubChem
Property Name
Undefined Atom Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Defined Bond Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Undefined Bond Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Covalently-Bonded Unit Count
Property Value
1
Reference
Computed by PubChem
Property Name
Compound Is Canonicalized
Property Value
Yes
Reference
Computed by PubChem (release 2021.10.14)

3.2 Experimental Properties

3.2.1 Kovats Retention Index

Standard non-polar
2392 , 2383 , 2365 , 2385 , 2383 , 2366
Semi-standard non-polar
2441.3 , 2368.7

3.3 Chemical Classes

Stimulant
S120 | DUSTCT2024 | Substances from Second NORMAN Collaborative Dust Trial | DOI:10.5281/zenodo.13835254

3.3.1 Drugs

3.3.1.1 Human Drugs
Breast feeding; Lactation; Milk, Human; Anticonvulsants; Cannabinoids
Human drug -> Prescription
Human drug -> Active ingredient (CANNABIDIOL)
Human drugs -> Orphan -> Antiepileptics -> Human pharmacotherapeutic group -> EMA Drug Category
Paediatric drug
Pharmaceuticals
S72 | NTUPHTW | Pharmaceutically Active Substances from National Taiwan University | DOI:10.5281/zenodo.3955664

3.3.2 Endocrine Disruptors

Potential endocrine disrupting compound
S109 | PARCEDC | List of 7074 potential endocrine disrupting compounds (EDCs) by PARC T4.2 | DOI:10.5281/zenodo.10944198

3.3.3 Lipids

Polyketides [PK] -> Aromatic polyketides [PK13] -> Other aromatic polyketides [PK1312]

4 Spectral Information

4.1 1D NMR Spectra

4.1.1 1H NMR Spectra

Instrument Name
Varian CFT-20
Copyright
Copyright © 2009-2024 John Wiley & Sons, Inc. All Rights Reserved.
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4.2 Mass Spectrometry

4.2.1 GC-MS

1 of 2
Source of Spectrum
Mass Spectrometry Committee of the Toxicology Section of the American Academy of Forensic Sciences
Copyright
Copyright © 2012-2024 John Wiley & Sons, Inc. Portions provided by AAFS, Toxicology Section. All Rights Reserved.
Thumbnail
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2 of 2
Source of Spectrum
HE-1986-1547-0
Copyright
Copyright © 2020-2024 John Wiley & Sons, Inc. All Rights Reserved.
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4.3 IR Spectra

4.3.1 ATR-IR Spectra

1 of 2
Instrument Name
Bio-Rad FTS
Technique
ATR-Film (MeCl2) (DuraSamplIR II)
Source of Spectrum
Forensic Spectral Research
Source of Sample
Lipomed AG
Catalog Number
THC-303-1LM
Lot Number
303.1B19.1L6
Copyright
Copyright © 2014-2024 John Wiley & Sons, Inc. All Rights Reserved.
Thumbnail
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2 of 2
Instrument Name
Bio-Rad FTS
Technique
ATR-Neat
Source of Spectrum
Forensic Spectral Research
Source of Sample
Cayman Chemical Company
Catalog Number
<a href=https://www.caymanchem.com/product/90080>90080</a>
Lot Number
0592969-52
Copyright
Copyright © 2019-2024 John Wiley & Sons, Inc. All Rights Reserved.
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4.4 Raman Spectra

Technique
FT-Raman
Source of Spectrum
Forensic Spectral Research
Source of Sample
Cayman Chemical Company
Catalog Number
<a href=https://www.caymanchem.com/product/90080>90080</a>
Copyright
Copyright © 2015-2024 John Wiley & Sons, Inc. All Rights Reserved.
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6 Chemical Vendors

7 Drug and Medication Information

7.1 Drug Indication

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 following indications: 1) as adjunctive treatment for the symptomatic relief of neuropathic pain in adult patients with multiple sclerosis; 2) as adjunctive analgesic treatment in adult patients with advanced cancer who experience moderate to severe pain during the highest tolerated dose of strong opioid therapy for persistent background pain.
Epidyolex is indicated for use as adjunctive therapy of seizures associated with Lennox Gastaut syndrome (LGS) or Dravet syndrome (DS), in conjunction with clobazam, for patients 2 years of age and older.
Epilepsy with myoclonic atonic seizures

7.2 LiverTox Summary

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 cannabidiol found typically in over-the-counter CBD products are generally well tolerated without evidence of liver injury.

7.3 Drug Classes

Breast feeding; Lactation; Milk, Human; Anticonvulsants; Cannabinoids
Anticonvulsants

7.4 FDA Medication Guides

Drug
Active Ingredient
CANNABIDIOL
Form;Route
SOLUTION;ORAL
Company
GW RES LTD
Date
03/04/2024

7.5 FDA Approved Drugs

7.6 FDA Orange Book

7.7 FDA National Drug Code Directory

7.8 Drug Labels

Drug and label
Active ingredient and drug

7.9 Clinical Trials

7.9.1 ClinicalTrials.gov

7.9.2 EU Clinical Trials Register

7.10 EMA Drug Information

1 of 4
View All
Medicine
Category
Human drugs -> Orphan
Therapeutic area
Lennox Gastaut Syndrome; Epilepsies, Myoclonic
Active Substance
Cannabidiol
INN/Common name
cannabidiol
Pharmacotherapeutic Classes
Antiepileptics
Status
This medicine is authorized for use in the European Union
Company
Jazz Pharmaceuticals Ireland Limited
Market Date
2019-09-19
2 of 4
View All
Type
Paediatric investigation
Active Substance
Therapeutic Area
Neurology
Drug Form
Oral solution
Administration Route
Oral use
Decision Type
P: decision agreeing on a investigation plan, with or without partial waiver(s) and or deferral(s)
Decision Date
2022-07-08

8 Pharmacology and Biochemistry

8.1 Pharmacodynamics

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 stores, blocks low-voltage-activated (T-type) Ca2 channels, stimulates activity of the inhibitory glycine-receptor, and inhibits activity of fatty amide hydrolase (FAAH).

8.2 MeSH Pharmacological Classification

Anticonvulsants
Drugs used to prevent SEIZURES or reduce their severity. (See all compounds classified as Anticonvulsants.)

8.3 FDA Pharmacological Classification

1 of 2
FDA UNII
19GBJ60SN5
Active Moiety
CANNABIDIOL
Pharmacological Classes
Chemical Structure [CS] - Cannabinoids
Pharmacological Classes
Mechanisms of Action [MoA] - Cytochrome P450 2C8 Inhibitors
Pharmacological Classes
Mechanisms of Action [MoA] - Cytochrome P450 2C9 Inhibitors
Pharmacological Classes
Mechanisms of Action [MoA] - Cytochrome P450 2C19 Inhibitors
Pharmacological Classes
Mechanisms of Action [MoA] - UGT1A9 Inhibitors
Pharmacological Classes
Mechanisms of Action [MoA] - UGT2B7 Inhibitors
Pharmacological Classes
Mechanisms of Action [MoA] - Cytochrome P450 1A2 Inhibitors
Pharmacological Classes
Mechanisms of Action [MoA] - Cytochrome P450 2B6 Inhibitors
Pharmacological Classes
Mechanisms of Action [MoA] - Cytochrome P450 2B6 Inducers
FDA Pharmacology Summary
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.
2 of 2
Non-Proprietary Name
CANNABIDIOL
Pharmacological Classes
UGT2B7 Inhibitors [MoA]; Cannabinoids [CS]; Cytochrome P450 2B6 Inducers [MoA]; UGT1A9 Inhibitors [MoA]; Cytochrome P450 2C19 Inhibitors [MoA]; Cytochrome P450 2B6 Inhibitors [MoA]; Cytochrome P450 1A2 Inhibitors [MoA]; Cytochrome P450 2C9 Inhibitors [MoA]; Cytochrome P450 2C8 Inhibitors [MoA]

8.4 ATC Code

N03AX

N - Nervous system

N03 - Antiepileptics

N03A - Antiepileptics

N03AX - Other antiepileptics

N03AX24 - Cannabidiol

8.5 Absorption, Distribution and Excretion

Absorption
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 2.80hr and a Cmax of 3.02ng/mL.
Route of Elimination
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.
Volume of Distribution
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.

8.6 Metabolism / Metabolites

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.

8.7 Biological Half-Life

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.

8.8 Mechanism of Action

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 has been shown to act as a negative allosteric modulator of the cannabinoid CB1 receptor, the most abundant G-Protein Coupled Receptor (GPCR) in the body. Allosteric regulation of a receptor is achieved through the modulation of the activity of a receptor on a functionally distinct site from the agonist or antagonist binding site. The negative allosteric modulatory effects of CBD are therapeutically important as direct agonists are limited by their psychomimetic effects while direct antagonists are limited by their depressant effects.

8.9 Biochemical Reactions

9 Use and Manufacturing

9.1 Uses

EPA CPDat Chemical and Product Categories
The Chemical and Products Database, a resource for exposure-relevant data on chemicals in consumer products, Scientific Data, volume 5, Article number: 180125 (2018), DOI:10.1038/sdata.2018.125

9.1.1 Use Classification

Human drugs -> Orphan -> Antiepileptics -> Human pharmacotherapeutic group -> EMA Drug Category
Human Drugs -> EU pediatric investigation plans
Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients
Pharmaceuticals
S72 | NTUPHTW | Pharmaceutically Active Substances from National Taiwan University | DOI:10.5281/zenodo.3955664

10 Safety and Hazards

10.1 Hazards Identification

10.1.1 GHS Classification

Pictogram(s)
Irritant
Health Hazard
Signal
Warning
GHS Hazard Statements

H302 (41.2%): Harmful if swallowed [Warning Acute toxicity, oral]

H332 (11.8%): Harmful if inhaled [Warning Acute toxicity, inhalation]

H361 (79.4%): Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]

Precautionary Statement Codes

P203, P261, P264, P270, P271, P280, P301+P317, P304+P340, P317, P318, P330, P405, and P501

(The corresponding statement to each P-code can be found at the GHS Classification page.)

ECHA C&L Notifications Summary

Aggregated GHS information provided per 34 reports by companies from 13 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown.

10.1.2 Hazard Classes and Categories

Acute Tox. 4 (41.2%)

Acute Tox. 4 (11.8%)

Repr. 2 (79.4%)

10.2 Regulatory Information

New Zealand EPA Inventory of Chemical Status
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.

11 Toxicity

11.1 Toxicological Information

11.1.1 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) in patients who were receiving valproate and clobazam. The aminotransferase elevations typically arose within the first two months of treatment and were transient, mild-to-moderate in severity, and not associated with symptoms or jaundice. There have been no convincing reports of clinically apparent liver injury with jaundice attributable to prescription forms of cannabidiol, but it has had very limited general use.

There have been few studies of liver test abnormalities during therapy with lower doses of CBD or with commercially available, over-the-counter CBD products. In doses between 200 and 400 mg daily, mild-to-moderate serum aminotransferase elevations have occasionally been reported, but there have been no reports of clinically apparent liver injury. Furthermore, liver injury arising in persons taking supplements with CBD must also consider the possibility of contaminants in the products or other herbal and dietary supplement use.

Likelihood score: E* (unproven but suspected rare cause of clinically apparent liver injury, particularly with high doses).

11.1.2 Effects During Pregnancy and Lactation

◉ Summary of Use during Lactation

Cannabidiol is a component of cannabis. Cannabidiol has not been studied in nursing women taking the pharmaceutical product, but it has been detected in the breastmilk of some mothers who used cannabis products. Because no published information is available with cannabidiol use as an antiepileptic during breastfeeding, an alternate drug may be preferred, especially while nursing a newborn or preterm infant.

◉ Effects in Breastfed Infants

Relevant published information was not found as of the revision date.

◉ Effects on Lactation and Breastmilk

Relevant published information was not found as of the revision date.

11.1.3 Acute Effects

12 Associated Disorders and Diseases

13 Literature

13.1 Consolidated References

13.2 NLM Curated PubMed Citations

13.3 Springer Nature References

13.4 Thieme References

13.5 Nature Journal References

13.6 Chemical Co-Occurrences in Literature

13.7 Chemical-Gene Co-Occurrences in Literature

13.8 Chemical-Disease Co-Occurrences in Literature

14 Patents

14.1 Depositor-Supplied Patent Identifiers

14.2 WIPO PATENTSCOPE

14.3 FDA Orange Book Patents

14.4 Chemical Co-Occurrences in Patents

14.5 Chemical-Disease Co-Occurrences in Patents

14.6 Chemical-Gene Co-Occurrences in Patents

15 Interactions and Pathways

15.1 Protein Bound 3D Structures

15.1.1 Ligands from Protein Bound 3D Structures

PDBe Ligand Code
PDBe Structure Code
PDBe Conformer

15.2 Chemical-Target Interactions

15.3 Drug-Drug Interactions

15.4 Drug-Food Interactions

  • Avoid excessive or chronic alcohol consumption. Ingesting alcohol may increase the risk of sedation.
  • Avoid grapefruit products. Grapefruit inhibits the CYP3A metabolism of cannabidiol, which may increase its serum concentration. Cannabidiol dose reduction may be necessary if used together.
  • Avoid St. John's Wort. This herb induces the CYP3A metabolism of cannabidiol and may reduce its serum concentration. The dose of cannabidiol may need to be increased if used together.
  • Take with food. Taking cannabidiol with food (particularly high-fat food) increases its bioavailability. The absorption of cannabidiol is more consistent when meal macronutrients remain the same.

15.5 Pathways

16 Biological Test Results

16.1 BioAssay Results

17 Taxonomy

The LOTUS Initiative for Open Natural Products Research: frozen dataset union wikidata (with metadata) | DOI:10.5281/zenodo.5794106
S29 | PHYTOTOXINS | Toxic Plant Phytotoxin (TPPT) Database | DOI:10.5281/zenodo.2652993

18 Classification

18.1 MeSH Tree

18.2 NCI Thesaurus Tree

18.3 ChEBI Ontology

18.4 LIPID MAPS Classification

18.5 KEGG: Lipid

18.6 KEGG: Phytochemical Compounds

18.7 KEGG: USP

18.8 KEGG: ATC

18.9 KEGG: Target-based Classification of Drugs

18.10 KEGG: Drug Groups

18.11 WHO ATC Classification System

18.12 ChemIDplus

18.13 IUPHAR / BPS Guide to PHARMACOLOGY Target Classification

18.14 ChEMBL Target Tree

18.15 UN GHS Classification

18.16 EPA CPDat Classification

18.17 NORMAN Suspect List Exchange Classification

18.18 EPA DSSTox Classification

18.19 LOTUS Tree

18.20 FDA Drug Type and Pharmacologic Classification

18.21 MolGenie Organic Chemistry Ontology

19 Information Sources

  1. BindingDB
    LICENSE
    All data curated by BindingDB staff are provided under the Creative Commons Attribution 3.0 License (https://creativecommons.org/licenses/by/3.0/us/).
    https://www.bindingdb.org/rwd/bind/info.jsp
    2-(6-Isopropenyl-3-methyl-cyclohex-2-enyl)-5-pentyl-benzene-1,3-diol
    https://www.bindingdb.org/rwd/bind/chemsearch/marvin/MolStructure.jsp?monomerid=50121429
  2. ChEMBL
    LICENSE
    Access to the web interface of ChEMBL is made under the EBI's Terms of Use (http://www.ebi.ac.uk/Information/termsofuse.html). The ChEMBL data is made available on a Creative Commons Attribution-Share Alike 3.0 Unported License (http://creativecommons.org/licenses/by-sa/3.0/).
    http://www.ebi.ac.uk/Information/termsofuse.html
  3. Comparative Toxicogenomics Database (CTD)
    LICENSE
    It is to be used only for research and educational purposes. Any reproduction or use for commercial purpose is prohibited without the prior express written permission of NC State University.
    http://ctdbase.org/about/legal.jsp
  4. Drug Gene Interaction database (DGIdb)
    LICENSE
    The data used in DGIdb is all open access and where possible made available as raw data dumps in the downloads section.
    http://www.dgidb.org/downloads
  5. DrugBank
    LICENSE
    Creative Common's Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/legalcode)
    https://www.drugbank.ca/legal/terms_of_use
  6. IUPHAR/BPS Guide to PHARMACOLOGY
    LICENSE
    The Guide to PHARMACOLOGY database is licensed under the Open Data Commons Open Database License (ODbL) https://opendatacommons.org/licenses/odbl/. Its contents are licensed under a Creative Commons Attribution-ShareAlike 4.0 International License (http://creativecommons.org/licenses/by-sa/4.0/)
    https://www.guidetopharmacology.org/about.jsp#license
    Guide to Pharmacology Target Classification
    https://www.guidetopharmacology.org/targets.jsp
  7. CAS Common Chemistry
    LICENSE
    The data from CAS Common Chemistry is provided under a CC-BY-NC 4.0 license, unless otherwise stated.
    https://creativecommons.org/licenses/by-nc/4.0/
  8. ChemIDplus
    ChemIDplus Chemical Information Classification
    https://pubchem.ncbi.nlm.nih.gov/source/ChemIDplus
  9. EPA DSSTox
    CompTox Chemicals Dashboard Chemical Lists
    https://comptox.epa.gov/dashboard/chemical-lists/
  10. European Chemicals Agency (ECHA)
    LICENSE
    Use of the information, documents and data from the ECHA website is subject to the terms and conditions of this Legal Notice, and subject to other binding limitations provided for under applicable law, the information, documents and data made available on the ECHA website may be reproduced, distributed and/or used, totally or in part, for non-commercial purposes provided that ECHA is acknowledged as the source: "Source: European Chemicals Agency, http://echa.europa.eu/". Such acknowledgement must be included in each copy of the material. ECHA permits and encourages organisations and individuals to create links to the ECHA website under the following cumulative conditions: Links can only be made to webpages that provide a link to the Legal Notice page.
    https://echa.europa.eu/web/guest/legal-notice
    2-[(1R,6R)-3-methyl-6-prop-1-en-2-ylcyclohex-2-en-1-yl]-5-pentylbenzene-1,3-diol
    https://echa.europa.eu/substance-information/-/substanceinfo/100.215.986
    2-[(1R,6R)-3-methyl-6-prop-1-en-2-ylcyclohex-2-en-1-yl]-5-pentylbenzene-1,3-diol (EC: 689-176-3)
    https://echa.europa.eu/information-on-chemicals/cl-inventory-database/-/discli/details/221242
    2-[(1R,6R)-3-methyl-6-prop-1-en-2-ylcyclohex-2-en-1-yl]-5-pentylbenzene-1,3-diol
    https://echa.europa.eu/substance-information/-/substanceinfo/100.304.438
  11. FDA Global Substance Registration System (GSRS)
    LICENSE
    Unless otherwise noted, the contents of the FDA website (www.fda.gov), both text and graphics, are not copyrighted. They are in the public domain and may be republished, reprinted and otherwise used freely by anyone without the need to obtain permission from FDA. Credit to the U.S. Food and Drug Administration as the source is appreciated but not required.
    https://www.fda.gov/about-fda/about-website/website-policies#linking
  12. New Zealand Environmental Protection Authority (EPA)
    LICENSE
    This work is licensed under the Creative Commons Attribution-ShareAlike 4.0 International licence.
    https://www.epa.govt.nz/about-this-site/general-copyright-statement/
  13. ChEBI
  14. FDA Pharm Classes
    LICENSE
    Unless otherwise noted, the contents of the FDA website (www.fda.gov), both text and graphics, are not copyrighted. They are in the public domain and may be republished, reprinted and otherwise used freely by anyone without the need to obtain permission from FDA. Credit to the U.S. Food and Drug Administration as the source is appreciated but not required.
    https://www.fda.gov/about-fda/about-website/website-policies#linking
  15. LiverTox
  16. LOTUS - the natural products occurrence database
    LICENSE
    The code for LOTUS is released under the GNU General Public License v3.0.
    https://lotus.nprod.net/
  17. NCI Thesaurus (NCIt)
    LICENSE
    Unless otherwise indicated, all text within NCI products is free of copyright and may be reused without our permission. Credit the National Cancer Institute as the source.
    https://www.cancer.gov/policies/copyright-reuse
  18. Open Targets
    LICENSE
    Datasets generated by the Open Targets Platform are freely available for download.
    https://platform-docs.opentargets.org/licence
  19. ClinicalTrials.gov
    LICENSE
    The ClinicalTrials.gov data carry an international copyright outside the United States and its Territories or Possessions. Some ClinicalTrials.gov data may be subject to the copyright of third parties; you should consult these entities for any additional terms of use.
    https://clinicaltrials.gov/ct2/about-site/terms-conditions#Use
  20. Therapeutic Target Database (TTD)
  21. Crystallography Open Database (COD)
    LICENSE
    All data in the COD and the database itself are dedicated to the public domain and licensed under the CC0 License. Users of the data should acknowledge the original authors of the structural data.
    https://creativecommons.org/publicdomain/zero/1.0/
  22. DailyMed
  23. European Medicines Agency (EMA)
    LICENSE
    Information on the European Medicines Agency's (EMA) website is subject to a disclaimer and copyright and limited reproduction notices.
    https://www.ema.europa.eu/en/about-us/legal-notice
  24. Drugs and Lactation Database (LactMed)
  25. Drugs@FDA
    LICENSE
    Unless otherwise noted, the contents of the FDA website (www.fda.gov), both text and graphics, are not copyrighted. They are in the public domain and may be republished, reprinted and otherwise used freely by anyone without the need to obtain permission from FDA. Credit to the U.S. Food and Drug Administration as the source is appreciated but not required.
    https://www.fda.gov/about-fda/about-website/website-policies#linking
  26. NORMAN Suspect List Exchange
    LICENSE
    Data: CC-BY 4.0; Code (hosted by ECI, LCSB): Artistic-2.0
    https://creativecommons.org/licenses/by/4.0/
    Cannabidiol
    NORMAN Suspect List Exchange Classification
    https://www.norman-network.com/nds/SLE/
  27. EPA Chemical and Products Database (CPDat)
  28. EU Clinical Trials Register
  29. FDA Orange Book
    LICENSE
    Unless otherwise noted, the contents of the FDA website (www.fda.gov), both text and graphics, are not copyrighted. They are in the public domain and may be republished, reprinted and otherwise used freely by anyone without the need to obtain permission from FDA. Credit to the U.S. Food and Drug Administration as the source is appreciated but not required.
    https://www.fda.gov/about-fda/about-website/website-policies#linking
  30. WHO Anatomical Therapeutic Chemical (ATC) Classification
    LICENSE
    Use of all or parts of the material requires reference to the WHO Collaborating Centre for Drug Statistics Methodology. Copying and distribution for commercial purposes is not allowed. Changing or manipulating the material is not allowed.
    https://www.whocc.no/copyright_disclaimer/
  31. FDA Medication Guides
    LICENSE
    Unless otherwise noted, the contents of the FDA website (www.fda.gov), both text and graphics, are not copyrighted. They are in the public domain and may be republished, reprinted and otherwise used freely by anyone without the need to obtain permission from FDA. Credit to the U.S. Food and Drug Administration as the source is appreciated but not required.
    https://www.fda.gov/about-fda/about-website/website-policies#linking
  32. National Drug Code (NDC) Directory
    LICENSE
    Unless otherwise noted, the contents of the FDA website (www.fda.gov), both text and graphics, are not copyrighted. They are in the public domain and may be republished, reprinted and otherwise used freely by anyone without the need to obtain permission from FDA. Credit to the U.S. Food and Drug Administration as the source is appreciated but not required.
    https://www.fda.gov/about-fda/about-website/website-policies#linking
  33. Japan Chemical Substance Dictionary (Nikkaji)
  34. KEGG
    LICENSE
    Academic users may freely use the KEGG website. Non-academic use of KEGG generally requires a commercial license
    https://www.kegg.jp/kegg/legal.html
    Anatomical Therapeutic Chemical (ATC) classification
    http://www.genome.jp/kegg-bin/get_htext?br08303.keg
    Target-based classification of drugs
    http://www.genome.jp/kegg-bin/get_htext?br08310.keg
  35. LIPID MAPS
    Lipid Classification
    https://www.lipidmaps.org/
  36. Natural Product Activity and Species Source (NPASS)
  37. Metabolomics Workbench
  38. Nature Chemical Biology
  39. NIST Mass Spectrometry Data Center
    LICENSE
    Data covered by the Standard Reference Data Act of 1968 as amended.
    https://www.nist.gov/srd/public-law
    Resorcinol, 2-p-mentha-1,8-dien-3-yl-5-pentyl-, (-)-(E)-
    http://www.nist.gov/srd/nist1a.cfm
  40. NLM RxNorm Terminology
    LICENSE
    The RxNorm Terminology is created by the National Library of Medicine (NLM) and is in the public domain and may be republished, reprinted and otherwise used freely by anyone without the need to obtain permission from NLM. Credit to the U.S. National Library of Medicine as the source is appreciated but not required. The full RxNorm dataset requires a free license.
    https://www.nlm.nih.gov/research/umls/rxnorm/docs/termsofservice.html
  41. PharmGKB
    LICENSE
    PharmGKB data are subject to the Creative Commons Attribution-ShareALike 4.0 license (https://creativecommons.org/licenses/by-sa/4.0/).
    https://www.pharmgkb.org/page/policies
  42. Pharos
    LICENSE
    Data accessed from Pharos and TCRD is publicly available from the primary sources listed above. Please respect their individual licenses regarding proper use and redistribution.
    https://pharos.nih.gov/about
  43. Protein Data Bank in Europe (PDBe)
  44. RCSB Protein Data Bank (RCSB PDB)
    LICENSE
    Data files contained in the PDB archive (ftp://ftp.wwpdb.org) are free of all copyright restrictions and made fully and freely available for both non-commercial and commercial use. Users of the data should attribute the original authors of that structural data.
    https://www.rcsb.org/pages/policies
  45. SpectraBase
    1,3-Benzenediol, 2-[3-methyl-6-(1-methylethenyl)-2-cyclohexen-1-yl]-5-pentyl-, (1R-trans)-
    https://spectrabase.com/spectrum/39DIszsyULi
    2-(6-isopropenyl-3-methyl-2-cyclohexen-1-yl)-5-pentylresorcinol
    https://spectrabase.com/spectrum/911VVHbOMoD
  46. Springer Nature
  47. Thieme Chemistry
    LICENSE
    The Thieme Chemistry contribution within PubChem is provided under a CC-BY-NC-ND 4.0 license, unless otherwise stated.
    https://creativecommons.org/licenses/by-nc-nd/4.0/
  48. Wikidata
  49. Wikipedia
  50. Medical Subject Headings (MeSH)
    LICENSE
    Works produced by the U.S. government are not subject to copyright protection in the United States. Any such works found on National Library of Medicine (NLM) Web sites may be freely used or reproduced without permission in the U.S.
    https://www.nlm.nih.gov/copyright.html
  51. PubChem
  52. GHS Classification (UNECE)
  53. MolGenie
    MolGenie Organic Chemistry Ontology
    https://github.com/MolGenie/ontology/
  54. PATENTSCOPE (WIPO)
  55. NCBI
CONTENTS