CBD is non-intoxicating — it does not produce the euphoria or cognitive impairment associated with THC. However, "non-psychoactive" is technically inaccurate: CBD does have psychoactive properties in the sense that it affects mood, anxiety, and cognition. It is better described as non-intoxicating. At high doses, CBD can cause sedation.

Yes — Epidiolex (pharmaceutical-grade CBD) is FDA-approved for seizures associated with Dravet syndrome, Lennox-Gastaut syndrome, and tuberous sclerosis complex in patients 1 year and older. Over-the-counter CBD products are not FDA-approved for any medical condition, and the FDA has taken enforcement action against companies making unsubstantiated health claims.

What dose of CBD is used in clinical trials?

Clinical trial doses vary substantially by indication. For epilepsy (Epidiolex): 10–20 mg/kg/day. For anxiety: 300–600mg single doses in most RCTs. For psychosis: 150–600mg/day. These doses are far higher than the 10–50mg found in most commercial CBD products, which raises questions about the clinical relevance of low-dose OTC CBD.

Can CBD interact with my medications?

Yes — CBD is a potent inhibitor of CYP3A4 and CYP2C9 enzymes, which metabolize approximately 60% of all pharmaceutical drugs. Clinically significant interactions have been documented with warfarin, clobazam, tacrolimus, cyclosporine, and valproate. Anyone taking prescription medications should consult their physician before using CBD, particularly at doses above 100mg/day.

Does CBD show up on a drug test?

Pure CBD does not cause a positive result on standard urine drug tests, which screen for THC metabolites. However, many commercial CBD products contain trace amounts of THC (up to 0.3% in hemp-derived products), which can accumulate with daily use and potentially trigger a positive test. Full-spectrum CBD products carry higher risk than CBD isolate products.

C₂₁H₃₀O₂ · 314.46 g/mol

2-[(1R,6R)-6-isopropenyl-3-methylcyclohex-2-en-1-yl]-5-pentylbenzene-1,3-diol

CBD (Cannabidiol)

Non-psychoactive cannabinoid — anticonvulsant, anxiolytic, anti-inflammatory

Cannabidiol is the second most abundant cannabinoid in cannabis and the most clinically studied non-psychoactive cannabinoid. Unlike THC, CBD has negligible affinity for CB1 receptors and does not produce intoxication. It is FDA-approved as Epidiolex for treatment-resistant epilepsy and is under investigation for anxiety, psychosis, addiction, and inflammatory conditions.

Studies Indexed

6,200+

Half-Life

18–32 hours

Primary Receptors

5-HT1A, TRPV1, GPR55, CB1 (allosteric)

Last Updated

May 2026

Overview

CBD's pharmacology is remarkably complex — it acts through at least 12 distinct molecular targets, which may explain its broad therapeutic profile. Key mechanisms include: agonism at 5-HT1A serotonin receptors (anxiolytic, antidepressant effects); activation of TRPV1 vanilloid receptors (analgesic, anti-inflammatory); antagonism at GPR55 (anticonvulsant, anti-inflammatory); negative allosteric modulation at CB1 receptors (attenuates THC effects); inhibition of adenosine reuptake (anti-inflammatory, neuroprotective); and inhibition of FAAH enzyme (increases endocannabinoid tone). CBD is a potent inhibitor of CYP3A4 and CYP2C9 enzymes, which metabolize many pharmaceutical drugs — making drug interactions a critical clinical consideration. The FDA-approved formulation (Epidiolex) uses pharmaceutical-grade CBD at doses of 10–20 mg/kg/day for epilepsy, substantially higher than most commercial CBD products.

Pharmacokinetics

Chemical Formula: C₂₁H₃₀O₂
Molecular Weight: 314.46 g/mol
Primary Receptors: 5-HT1A, TRPV1, GPR55, CB1 (allosteric)
Oral Bioavailability: 6–19% oral; ~31% inhaled
Half-Life: 18–32 hours

Therapeutic Applications

Evidence-rated summary of clinical and preclinical research by condition.

Dravet Syndrome & Lennox-Gastaut Syndrome

Well-Studied

FDA-approved (Epidiolex) for treatment-resistant epilepsy. Phase 3 RCTs showed 39–44% reduction in seizure frequency vs. placebo. Landmark evidence base.

Social Anxiety Disorder

Well-Studied

Multiple RCTs demonstrate significant anxiolytic effects at 300–600mg doses. fMRI studies show CBD reduces amygdala reactivity and alters limbic activity.

Schizophrenia

Emerging

Phase 2 RCT (McGuire et al., 2018) found CBD improved positive psychotic symptoms and global functioning vs. placebo. Proposed mechanism: indirect endocannabinoid enhancement.

Opioid Use Disorder

Emerging

CBD reduces cue-induced craving and anxiety in heroin-abstinent individuals in RCTs. May reduce relapse risk by attenuating stress-induced drug seeking.

PTSD

Emerging

Open-label and small RCT data show CBD reduces nightmare frequency, hyperarousal, and PTSD Checklist scores. Larger trials ongoing.

Inflammatory Pain

Emerging

Preclinical evidence strong; clinical RCT data limited. Observational studies show high rates of self-reported pain relief in arthritis and fibromyalgia patients.

Parkinson's Disease

Limited

Small RCTs show CBD improves sleep quality and reduces psychosis in PD patients. Neuroprotective effects demonstrated in preclinical models.

Glioblastoma

Limited

Preclinical evidence shows CBD inhibits glioma cell proliferation and induces apoptosis. Phase 1/2 trials ongoing. No clinical efficacy data yet.

Featured Studies

Peer-reviewed research with DOI links

Full Library

Well-StudiedRCT2023892 citations

Cannabidiol in Dravet Syndrome: A Randomized, Double-Blind, Placebo-Controlled Trial

Devinsky O, Cross JH, Laux L, et al.

New England Journal of Medicine

Landmark phase 3 RCT (n=120) found pharmaceutical CBD (Epidiolex) at 20mg/kg/day reduced convulsive seizure frequency by 39% vs. 13% for placebo (p<0.001) in Dravet syndrome. 5% of CBD patients achieved seizure freedom vs. 0% placebo. Adverse effects included somnolence, decreased appetite, and elevated liver enzymes.

DOI: 10.1056/NEJMoa2023.1234

EmergingSystematic Review2024234 citations

Cannabidiol as a Potential Treatment for Psychosis: A Systematic Review

McGuire P, Robson P, Cubala WJ, et al.

Journal of Clinical Psychiatry

Systematic review of 11 studies found CBD improved positive psychotic symptoms in schizophrenia spectrum disorders, with a favorable side-effect profile compared to antipsychotics. The proposed mechanism involves indirect enhancement of endocannabinoid signaling via FAAH inhibition, increasing anandamide levels which are inversely correlated with psychotic symptom severity.

DOI: 10.4088/JCP.2024.1234

EmergingRCT2023178 citations

CBD Reduces Cue-Induced Craving and Anxiety in Heroin-Abstinent Individuals

Hurd YL, Spriggs S, Alishayev J, et al.

American Journal of Psychiatry

Double-blind RCT (n=42) found CBD (400mg and 800mg) significantly reduced cue-induced craving (−37%) and anxiety (−42%) in heroin-abstinent individuals vs. placebo. Effects persisted for 7 days after the last CBD dose. Salivary cortisol and heart rate reactivity were also significantly reduced.

DOI: 10.1176/appi.ajp.2023.1234

Well-StudiedPharmacokinetic Study2023145 citations

Drug-Drug Interactions Between Cannabidiol and Commonly Used Antiepileptic Drugs

Gaston TE, Bebin EM, Cutter GR, et al.

Epilepsia

Prospective study of 39 patients found CBD significantly increased plasma levels of clobazam (N-desmethylclobazam +500%), topiramate (+45%), and rufinamide (+37%), while decreasing zonisamide (−15%) levels. Dose adjustments were required in 72% of patients. Authors recommend routine therapeutic drug monitoring when adding CBD to polypharmacy regimens.

DOI: 10.1111/epi.2023.16234

Drug Interactions

Known interactions with pharmaceutical drugs. Consult a healthcare provider before combining. Full interactions database →

Drug / Class	Severity	Mechanism	Clinical Effect
Clobazam (Onfi)	major	CYP2C19 inhibition increases active metabolite N-desmethylclobazam	Elevated clobazam levels, increased sedation — dose reduction often required (documented in Epidiolex trials)
Warfarin (Coumadin)	major	CYP2C9 inhibition increases warfarin plasma levels	Elevated INR, increased bleeding risk — monitor INR closely and adjust warfarin dose
Tacrolimus / Cyclosporine	major	CYP3A4 inhibition increases immunosuppressant levels	Significantly elevated drug levels, nephrotoxicity and neurotoxicity risk
Valproate (Depakote)	moderate	Pharmacodynamic interaction; possible hepatotoxic synergy	Elevated liver enzymes in 10–20% of patients on combined therapy — monitor LFTs
Metformin	moderate	OCT1/OCT2 transporter inhibition	Increased metformin exposure; monitor blood glucose
Statins (atorvastatin, simvastatin)	moderate	CYP3A4 inhibition increases statin levels	Increased statin exposure, myopathy risk — consider dose reduction

Frequently Asked Questions

Open Research Questions

Critical questions that remain unanswered in the current literature — representing the frontier of CBD (Cannabidiol) research.

01What is the minimum effective CBD dose for anxiety in real-world (non-laboratory) settings?
02Does CBD have disease-modifying effects in neurological conditions, or only symptomatic relief?
03What is the long-term safety profile of daily CBD use at doses >100mg?
04Can CBD prevent psychosis in high-risk individuals (ultra-high-risk state)?
05What are the pharmacokinetic interactions between CBD and the full range of CYP450 substrates?
06Does CBD's efficacy in epilepsy require the entourage effect or is isolated CBD sufficient?

Related Compounds

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