Cannabidiol (CBD) Research Dashboard
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As a subscriber, you will be able to access dashboard insights including chemotype overviews and dosing summaries for medical conditions and organ system and receptor breakdowns for cannabinoid and terpene searches. Study lists present important guidance including dosing and chemotype information with the ability to drill down to the published material. And all outputs are fully filterable, to help find just the information you need. Stay up-to-date with the science of cannabis and the endocannabinoid system with CannaKeys.
CannaKeys has 1553 studies associated with Cannabidiol (CBD).
Here is a small sampling of Cannabidiol (CBD) studies by title:
- New Drugs for Managing Acne
- THC and CBD: Similarities and differences between siblings
- Inhibition of Nicotine Metabolism by Cannabidiol (CBD) and 7-Hydroxycannabidiol (7-OH-CBD)
- Efficacy and safety of topical 0.1% cannabidiol for managing recurrent aphthous ulcers: a randomized controlled trial
- Oral THC: CBD cannabis extract in main symptoms of Alzheimer disease: agitation and weight loss
Components of the Cannabidiol (CBD) Research Dashboard
- Top medical conditions associated with Cannabidiol (CBD)
- Proven effects in clinical trials for Cannabidiol (CBD)
- Receptors associated with Cannabidiol (CBD)
- Individual study details for Cannabidiol (CBD)
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Overview - Cannabidiol (CBD)
Description of Cannabidiol (CBD)
Cannabidiol (CBD) was discovered in 1940. By 2021 there were 14 proposed members in the CBD family (i.e., CBD, CBDA-C5, CBDV, CBDM-C5, CBD-C1, CBD-C4, CBDVA-C3, CMPD1, CMPD5, CMPD6, CMPD16, CMPD18, CBDH, CBDB). CBD is a significant cannabinoid that occurs naturally in cannabis in amounts large enough to produce various and substantial changes in the human body, mind, and emotions.
Unlike its psychoactive sister, compound THC, CBD does not induce changes in cognition but is quite capable of generating a gentle uplift in affect (or mood), which is why the growing body of clinical trials indicates its therapeutic potential in several mood disorders or psychiatric conditions such as:
- Alcohol Dependence, Withdrawal, and Intoxication
- Anorexia Nervosa
- Anxiety and Panic Disorders
- Attention Deficit and Hyperkinetic Disorders
- Autism and Pervasive Developmental Disorders
- Behavioral Disorders
- Benzodiazepine Use Disorder
- Bipolar Affective Disorder
- Cannabis Adverse Effects
- Cannabis Use Disorder
- Cocaine Dependence
- Depression
- Domestic Abuse
- Grief, Bereavement, and Adjustment Disorders
- Intermittent Explosive Disorder
- Loss of Appetite
- Nicotine Dependence and Withdrawal
- Obsessive Compulsive Disorder
- Opioid Dependency and Overdose
- Post-Traumatic Stress Disorder
- Psychosis
- Schizophrenia
- Stress and Life Management Difficulty
- Suicide Attempt
- Stimulant Dependence and Psychosis
- Stuttering
Other Names:
Cannabidiol(-)-Cannabidiol, (-)-trans-Cannabidiol, Epidiolex and other supplier-based synonyms.
IUPAC Name: 2-[(1R,6R)-3-methyl-6-prop-1-en-2-ylcyclohex-2-en-1-yl]-5-pentylbenzene-1,3-diol
Molecular Formula: C21H30O2
Source–PubChem
Cannabidiol (CBD) Properties and Effects
FDA approved (June 25, 2018) in the form of Epidiolex, a pharmaceutical version of CBD, for the treatment of rare pediatric seizure disorders that do not respond to orthodox anti-epileptics:
- Lennox-Gastaut syndrome
- Dravet syndrome
CBD is a multi-target molecule that binds with numerous cell receptors throughout the body; thus, it, directly and indirectly initiates complex biological changes to the body, mind, and emotion.
CBD Drug Interaction Potential: The latest review published in the Journal Seizure (March 2021) suggests that CBD interacts with anti-epileptic drugs through both pharmacodynamic (what the drug does to the body) and pharmacokinetics (what the body does to the drug) means primarily (but not exclusively) via the cytochrome p450 system.
Pharmacodynamic interactions with CBD:
- Clobazam
- Valproate
- Levetiracetam
Pharmacokinetic interactions between CBD (frequently associated with CYP2C19 and CYP3A4):
- Brivaracetam
- Clobazam
- Eslicarbazepine
- Lacosamide
- Gabapentin
- Oxcarbazepine
- Phenobarbital
- Potassium bromide
- Pregabalin
- Rufinamide
- Sirolimus/everolimus
- Stiripentol
- Tiagabine
- Topiramate
- Zonisamide
Cannabidiol (CBD) Receptor Binding
Endocannabinoid system (ECS) and CBD:
- CB1 very weak agonist with a mean Ki = 3245 ± 803 nM using data from 15 trials (J. McPartland et al., 2015)
- CB2 very weak agonist with a mean Ki = 3612 ± 1382 nM using data from 6 trials (J. McPartland et al., 2015)
Numerous studies have posited complex and sometimes contradictory results in their findings and attempted to understand better the specific ways CBD may interact with CB1 and CB2. For instance, a review published in 2020 posits that CBD is an antagonist at CB1 and CB2 based on previous trial data (2007) that discovered that CBD decreased the potencies of the CB1 agonists THC and the power of the synthetic cannabinoid WIN55212 at CB2.
CBD inhibits the enzyme fatty acid amide hydroxylase (FAAH), which breaks down the body’s endocannabinoid anandamide (AEA), increasing its bioavailability and agonistic binding at CB1 and CB2 and their associated effects. Other researchers have resolved these contradictory interpretations by introducing the concept of CBD being an antagonist of CB1 and CB2 agonists. Other mechanisms by which CBD modulates the classical endocannabinoid receptors CB1 and CB2 are posited to include negative allosteric modulation at CB1.
Endocannabinoidome (eCBome) and CBD:
- TRPA1
- TRPV1 agonist with a Ki of 3600 ± 200nM (J. McPartland et al., 2015)
- TRPV2
- TRPM8 antagonist with a mean EC50 = 70.0 ± 14.1nM using data from 2 trials (J. McPartland et al., 2015)
- Dopamine 2 (D2) receptor sites (via partial agonism)
- GPR3 (via inverse agonism)
- GPR6 (via inverse agonism)
- GPR12 (via inverse agonism)
- GPR55 (via antagonism)
- PPAR-gamma (via agonism)
- Ca2+ channels (as an inhibitor)
- Na+ channels (as an inhibitor)
- Adenosine 1 channel (via agonism)
- Adenosine 2 channel (via agonism)
- Serotonin 5‐HT1A receptor (via agonist activity)
- Modulation of mu-opioid receptor sites (MOR) (via negative allosteric modulation)
- Modulation of delta-opioid receptor sites and (DOR) (via negative allosteric modulation)
Ki legend:
- Full/strong agonist Ki ~1-9nM
- Moderate agonist Ki ~10-99nM
- Weak agonist Ki ~100-999nM
- Very weak agonist Ki ~1,000-up nM
(The reader is reminded that a smaller Ki is associated with the most potent effects.)
Disclaimers: Information on this site is provided for informational purposes only and is not meant to substitute for the advice provided by your own physician or other medical professional. You should not use the information contained herein for diagnosing a health problem or disease. If using a product, you should read carefully all product packaging. If you have or suspect that you have a medical problem, promptly contact your health care provider.
Information on this site is based on scientific studies (human, animal, or in vitro), clinical experience, or traditional usage as cited in each article. The results reported may not necessarily occur in all individuals. For many of the conditions discussed, treatment with prescription or over-the-counter medication is also available. Consult your physician, nutritionally oriented health care practitioner, and/or pharmacist for any health problem and before using any supplements or before making any changes in prescribed medications.
