Cannabinoids and medicines: understanding interactions
Illustrative image: cannabinoids can affect the processing of certain medicines. The illustration does not show measured data or an individual risk assessment.
PARMORCAN® · KNOWLEDGE
CBD can change the concentration of certain medicines in the body. THC and other cannabinoids need separate consideration. The specific active substance, actual preparation and quality of scientific evidence matter, rather than a percentage on a bottle alone.
Information reviewed: 23 October 2026
The key point: if you take medicines, have any additional cannabinoid-containing products assessed by a doctor or pharmacist beforehand. Missing data do not establish safety. Do not stop, replace or change the dose of prescribed medicines on your own. This article does not replace individual advice. [S01]
Look up 454 medicines: our cannabinoid–medicine interaction database lets you search by active substance and listed brand name, and filter by cannabinoid and evidence. Entries show sources and open questions; they do not replace an individual assessment by a doctor or pharmacist.
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Which CBD interactions are actually supported by evidence?
An interaction is not established simply because two substances are processed by the same enzyme. A shared metabolic pathway is initially a reason to investigate. Whether a relevant effect occurs depends, among other things, on how much that pathway contributes to processing the medicine and which concentrations are actually reached. [S03]
The study type matters too. A study of a purified CBD medicinal solution does not automatically describe every CBD oil. A THC/CBD extract is not CBD alone, and an experiment in mice is not a human study. For the basic terminology, see What is CBD? Cannabidiol, CBDA and product terminology.
How this guide assesses the strength of evidence
Type of evidence | What it can show | What it does not automatically show |
Human pharmacokinetic study | Examines whether and how drug exposure changes under the conditions tested. | Treatment becomes stronger or weaker by the same proportion; every product causes the same effect. |
Clinical signals | Case reports or observational studies indicate possible problems or associations. | Cause, frequency and risk magnitude have been conclusively established. |
Preclinical evidence | Enzyme, cell or animal experiments demonstrate a possible mechanism. | The same interaction occurs in people during usual use. |
Theoretical plausibility | Known metabolic pathways provide a reason for targeted investigation. | The actual combination has already been clinically studied. |
Insufficient data | A reliable assessment is lacking, or important information is inaccessible. | There is no risk. |
These categories are not a traffic-light risk rating. A well-studied small effect and a poorly studied but potentially substantial risk are different situations. A statistically non-significant finding also does not automatically prove that two treatments are equivalent. Understanding cannabinoid studies: five questions before drawing conclusions explains how to recognise these distinctions.
Cannabinoids and medicines: how do interactions arise?
Altered processing: CYP enzymes, UGT enzymes and transport proteins
The body absorbs, distributes, transforms and eliminates medicines. Together, these processes are known as pharmacokinetics. CYP enzymes take part in many chemical transformations. UGT enzymes attach certain substances to glucuronic acid, which can support their further processing and elimination. Both enzyme groups matter; drug processing does not take place exclusively in the liver. [S03] [S04]
A substance may be a substrate, meaning that it is itself processed. An inhibitor reduces an enzyme’s activity; an inducer can increase its available activity. These roles are not interchangeable. Concluding ‘it is metabolised by CYP3A4, so it inhibits all CYP3A4 medicines’ would be wrong. [S03]
Transport proteins move substances across cell membranes. P-glycoprotein, or P-gp, can, for example, help transport substances out of intestinal cells back into the intestine. It is not a CYP enzyme. When an interaction is measured, the respective contributions of enzymes and transporters are not always fully understood. This also applies to research on CBD and tacrolimus. [S02]
What higher blood levels mean, and what they do not
If a medicine is eliminated more slowly, the same prescribed amount may produce higher exposure. Here, exposure refers to concentration over time. AUC is the area under the concentration–time curve; Cmax is the highest measured concentration. An ‘AUC increase of 43%’ therefore does not mean ‘43% more therapeutic effect’.
Repeated administration may establish a different steady-state level. This does not necessarily mean unlimited accumulation. Its clinical impact also depends on the medicine’s therapeutic margin. Particular care is needed when the distance between the desired effect and problematic exposure is small, as with tacrolimus. [S02]
Reduced activation or additional depressant effects
Some medicines become particularly active only after conversion into metabolites. If this activation is inhibited, a stronger effect is not necessarily expected. US pharmaceutical CBD prescribing information gives clopidogrel as an example of a potential reduction in active metabolites through CYP2C19 inhibition. This is a regulatory interaction warning, not evidence that every CBD product causes treatment failure in every person. [S06]
Pharmacodynamic interactions instead concern effects on the body: depressant effects can add up without a demonstrated increase in drug levels. CBD medicinal information particularly warns of additional sleepiness and sedation with other central nervous system depressants, including alcohol. An unremarkable enzyme test does not answer this question. [S06]
Medicines can also affect cannabinoids
Interactions do not only affect the other medicines: those medicines can, in turn, change cannabinoid exposure. A study in small groups of healthy men examined a THC/CBD oromucosal spray with ketoconazole, rifampicin or omeprazole. Ketoconazole increased, and rifampicin reduced, exposure to THC, CBD and the active THC metabolite. No statistically established difference was found for omeprazole, but the study did not reliably establish unchanged exposure either. These results concern the mixed preparation studied, not all cannabinoid products. Newly prescribed medicines therefore also belong in the assessment. [S23]
CBD and medicines: important study examples
The examples below are deliberately not a complete list of permitted or prohibited combinations. They show why the medicine, measurement and study design need to be considered together. Quantities and preparations used in research are not recommendations for readers.
Clobazam: the main increase concerns the active metabolite
For clobazam, the parent medicine must be distinguished from its active metabolite, N-desmethylclobazam. In a phase I study in healthy participants, exposure to this metabolite rose approximately 3.4-fold with CBD coadministration. The finding must not be reported as an equally large increase in unchanged clobazam. [S07]
A further placebo-controlled study in people with epilepsy confirmed increased metabolite exposure. This makes the combination one of the better clinically studied examples. Potential additional sedation is relevant to the treating professionals; this is not guidance for changing epilepsy treatment independently. [S08]
Valproate: liver-enzyme values are not the same as drug levels
Elevated liver enzymes were observed more frequently during combined CBD and valproate treatment. A controlled interaction study nevertheless found no clinically relevant increase in the valproate exposure measured. The liver finding therefore cannot simply be explained as ‘CBD raises valproate levels’. [S09] [S01]
This illustrates an important limitation of interaction lists: a risk can exist even when the apparently obvious pharmacokinetic explanation is unconfirmed. Liver tolerability, total valproate and its free, non-protein-bound fraction must also not be treated as equivalent.
Citalopram and other antidepressants: new human data, not a rule for the whole class
A study published in 2026 enrolled 20 healthy adults in its citalopram cohort; 19 were included in the pharmacokinetic analysis. Under the repeated CBD regimen studied, citalopram AUC extrapolated to infinity rose by an average of 43%; the 90% confidence interval for the ratio was 1.34–1.52. This measured a pharmacokinetic change, not a corresponding increase in antidepressant effect. [S05]
A small 2021 clinical study in six people receiving citalopram or escitalopram had already described increased drug concentrations with additional CBD. The small sample cannot provide a reliable frequency estimate for symptoms. [S10]
For amitriptyline, another study with twelve complete datasets found a smaller effect after a single CBD administration followed by combined amitriptyline/tramadol administration: AUC over 24 hours rose by 13%, and peak concentration by 17%. Tramadol was part of the experiment in both comparison periods. This establishes neither generally safe combinations nor serious harm. The study appeared online in December 2025 and in the 2026 journal issue. Different antidepressants cannot be reduced to a shared numerical value. [S11]
Tacrolimus and everolimus: substantial changes in human studies
Fourteen healthy participants completed a phase I study; twelve entered the main analysis. In that analysis, CBD increased tacrolimus peak concentration approximately 4.2-fold and AUC 3.1-fold. The authors demonstrated a substantial pharmacokinetic interaction. The respective contributions of CYP3A4, CYP3A5 and possible transporter effects were not conclusively determined by this study. [S02]
A relevant change was also measured for everolimus: in an open-label phase I study using repeated doses of a purified CBD medicinal solution, peak concentration and AUC rose approximately 2.5-fold. Such findings warrant particularly careful professional assessment. They do not predict an identical factor for other CBD-containing preparations or show that all immunosuppressants respond alike. [S12]
Warfarin and other ‘blood thinners’: distinguish the active substances
A published case report describes a substantial INR increase in a person taking warfarin after pharmaceutical CBD was added. INR reflects the anticoagulant effect of this treatment. No bleeding complications were observed in the report; care and adjustments were medically supervised. The case is a clinically relevant signal, not a controlled study of frequency or the safe use of other combinations. [S13]
‘Blood thinner’ is an umbrella term. Warfarin, phenprocoumon, direct oral anticoagulants and antiplatelet agents are not interchangeable. A warfarin case report provides no measured CBD risk estimate for apixaban, rivaroxaban or phenprocoumon. INR is not a universal monitoring parameter for all these medicines either. These distinctions must be considered in an assessment.
Omeprazole, losartan and caffeine: what a probe substance tells us
A double-blind, randomised crossover study in 18 healthy adults compared a CBD-rich THC-containing extract, a THC extract without CBD and placebo. With the CBD/THC extract, omeprazole AUC increased approximately threefold. Changes were also measured for losartan, midazolam and caffeine. For dextromethorphan, a CYP2D6 probe, there was no corresponding inhibition signal for the parent compound. Sixteen participants were analysed for this; two with genetically greatly reduced CYP2D6 activity were excluded. Some metabolite ratios nevertheless changed. [S14]
These extract findings do not apply universally to every cannabis product. Higher losartan values also do not establish a corresponding increase in blood-pressure lowering: formation of its active metabolite and clinical outcomes require separate consideration. [S14]
A separate caffeine study with repeated high pharmaceutical CBD exposure found an almost twofold increase in caffeine AUC. Nine of the sixteen enrolled participants completed treatment; six stopped because of elevated liver transaminases. This limitation forms part of the interpretation. The result cannot establish a universal coffee intake or CBD limit. [S15]
Pain medicines and UGT: laboratory inhibition is not the full clinical picture
Experiments using isolated enzymes and human tissue preparations show that CBD, THC and CBN can inhibit certain UGT activities. This provides a mechanism, but not yet a reliable effect size for a medicine combination in humans. [S04]
The morphine cohort published in 2026 enrolled 20 healthy adults; 18 were analysed after repeated CBD administration. Pharmacokinetic effects on unchanged morphine remained limited. AUC of its active metabolite morphine-6-glucuronide, however, increased by approximately 26% after repeated CBD. This does not automatically prove the underlying mechanism. It is not safety clearance for other exposures or pain medicines; additional depressant effects are not ruled out. [S05]
European CBD medicinal information also describes a measured 35% rise in mycophenolic-acid AUC following mycophenolate mofetil. A larger figure of 58% refers there to a prediction for a different CBD regimen, not the same measured experiment. Measured and modelled values must remain separate. [S01]
Prodrugs: clopidogrel and tamoxifen as different examples
The clopidogrel warning mentioned earlier concerns a possible effect on activation. For tamoxifen, a specific clinical study is also available: in an open-label study with 15 patients included in the pharmacokinetic analysis, endoxifen AUC fell by 12.6% during the CBD-oil regimen studied. Endoxifen is an active tamoxifen metabolite. [S16]
Participant selection and required baseline endoxifen levels limit generalisability. The study answers neither the long-term cancer-treatment effectiveness of the combination nor its suitability for all patients. The overall endoxifen-AUC 90% confidence interval falling within predefined bioequivalence limits is not general permission for self-administration. An additional analysis of eight patients with reduced CYP2D6 activity found a larger decrease. This small subgroup does not permit a conclusive comparison of metaboliser types. Cell experiments on possible combination effects cannot replace these clinical questions. [S16]
Why enzyme findings can appear contradictory
Different results are not always an error. Single and repeated administration, purified substances and extracts, different probe substrates and measurement methods can produce different findings. The appropriate response is to disclose the conditions, rather than select only the most striking number.
Putting selected metabolic pathways into context
Pathway | Supported reference in the material reviewed | Important limitation |
CYP2C19 | No single change factor applies to every substrate. | |
CYP3A4/3A5 | Tacrolimus shows a substantial change; several mechanisms may contribute. [S02] | A CYP3A4 metabolic pathway alone does not establish a clinically strong CBD interaction. |
CYP2C9 | Different preparations and probe substrates cannot be directly equated. | |
CYP1A2 | Caffeine study under repeated high CBD exposure. [S15] | Do not interpret this as an identical effect in every everyday setting. |
CYP2D6 / CYP2C8 | Keep laboratory signals separate from clinical results. | |
CYP2B6 | Laboratory findings and human bupropion data: European prescribing information considers the measured exposure reduction under the CBD regimen tested not clinically meaningful. [S01] | No blanket reassurance for other substrates or exposures. |
UGT1A9 / UGT2B7 | No blanket conclusion for all UGT substrates. |
Does this also apply to THC, CBG, CBN and cannabinoid acids?
THC is not CBD, and smoke is not oil
THC and CBD differ pharmacologically. The THC extract without CBD did not show a corresponding CYP-inhibition signal in the study mentioned above. This does not establish that THC is generally free of interactions. [S14]
Smoked cannabis adds another layer. Combustion products can affect enzyme activity; related observations must not be attributed to isolated THC. A case report describes elevated clozapine levels after stopping combined tobacco and cannabis use. Because both exposures changed, a purely isolated cannabinoid effect cannot be determined. Changes in smoking therefore belong in the medical medication history; this is explicitly not a recommendation to continue smoking. [S18]
For more on this distinction, see Understanding THC: preparation, route and other medicines.
CBG, CBN and rarer compounds: do not overlook missing data
Laboratory findings exist for CBG and CBN regarding metabolic enzymes and other biological processes. They do not establish a fully clinically validated interaction profile for every medicine. A comparison of several cannabinoids in enzyme assays specifically shows that these compounds do not respond identically. [S19]
CBC, CBDV and THCV are not simply ‘weaker CBD’ either. For CBT and CBL, and for CBDA, THCA, CBGA, CBDVA, THCVA, CBCA, CBNA and CBGVA, medicine-specific assessment is particularly limited by gaps and sometimes imprecise chemical names. Not every laboratory comparison included every one of these compounds. A CBD finding therefore cannot be turned into an established finding for these substances.
For cannabinoid acids, the additional letter makes a chemical difference: CBDA is not CBD, and CBGA is not CBG. Mixtures also complicate attribution of an effect to an individual component. For abbreviations such as CBT, the actual chemical compound must be established too. Basic explanations are available in CBG and CBGA explained and What is CBN?
Which details help an individual interaction assessment?
A professional assessment starts with the products actually used, rather than a blanket list. A complete overview is helpful:
Medicines: active-substance names, preparations and current prescribed use, including medicines taken as needed.
Other products: over-the-counter medicines, herbal preparations and supplements.
Cannabinoid product: full name, composition and available analytical data; a single substance or mixture.
Context: actual route, frequency and time course; starting, changing or ending use.
Particular circumstances: known liver disease, concerning symptoms, and changes in smoking or alcohol use.
This overview supports a conversation, not a self-calculation. A percentage initially describes concentration within a product, not exposure within the body. ‘THC-free’ also does not remove a possible CBD interaction. Our guide to mg/g, mg/ml and percentages in cannabinoid laboratory reports helps explain laboratory figures.
Food and formulation can affect CBD absorption. A phase I study found substantial differences between administration while fasting and with a high-fat meal. Such findings provide another reason not to infer a reliable personal interaction factor from a bottle label. [S20]
In its updated 2026 assessment of CBD as a novel food, EFSA explicitly stated that safety still could not be established for people taking medicines. This is not a list of individually prohibited combinations, but neither is it reassurance about small quantities or over-the-counter products. A safety assessment also does not constitute blanket authorisation of every product. [S21]
Frequently asked questions about CBD and medicines
Which medicines are incompatible with CBD?
Current research does not provide a universally applicable prohibited list. Specific changes have been measured for some medicines, such as clobazam and tacrolimus; for others, concerns arise from case reports or mechanisms. Professional assessment of the actual combination is decisive, rather than the medicine class alone. See the study examples. [S02] [S08]
When should CBD not be taken?
This guide cannot decide whether a particular use is appropriate. If you already take medicines, a doctor or pharmacist should assess additional use beforehand. Alongside people taking medicines, EFSA identifies pregnancy, breastfeeding and people under 25 as groups for whom it could not establish CBD’s safety as a novel food. Prescribed medicinal treatment must be assessed separately. [S21]
Are there warnings about CBD?
Yes. Authorised CBD medicines’ product information describes specific adverse-effect and interaction risks; EFSA continues to describe safety gaps for CBD as a food ingredient. This calls for factual, nuanced information, supporting neither ‘CBD is always harmless’ nor ‘every combination is dangerous’. [S06] [S21]
Can CBD be combined with blood thinners?
This needs assessment based on the specific active substance. A warfarin case report describes increased INR with CBD. It does not permit a direct conclusion for every other anticoagulant. Do not change or pause prescribed anticoagulants yourself. [S13]
What about CBD and blood-pressure medicines?
This group is pharmacologically diverse. An extract study using losartan does not establish the same interaction for every blood-pressure medicine. Increased concentrations of a parent compound also do not yet show how blood pressure changes. An individual assessment must consider the specific medicine and overall situation. [S14]
Is CBD with pain medicines or tilidine safe?
Blanket safety cannot be confirmed. The finding for morphine and its active metabolite cannot be transferred to tilidine or all pain medicines. Potential additive central nervous system depressant effects also require consideration. This article does not recommend combined use. [S05] [S06]
Does taking them at different times prevent the interaction?
Spacing doses a few hours apart is not a universal solution. Enzyme or transporter effects and the time substances remain in the body can extend beyond the individual administration time. This differs from some interactions that occur only through direct contact in the intestine. An appropriate schedule therefore cannot be derived from a blanket internet rule. [S03]
Does a laboratory report prove a CBD product is safe with my medicines?
No. An analytical report can provide information about the substances tested and the particular sample. It is not a clinical study of the combination with your medicines. A particular THC finding or the terms isolate, full spectrum or broad spectrum do not replace that assessment either.
What should I do if concerning symptoms occur?
New or pronounced symptoms should receive timely medical assessment; disclose all medicines and cannabinoid-containing products. For unconsciousness, severe breathlessness or other life-threatening symptoms, call 112. A poison information centre can advise on suspected poisoning without an apparent immediate threat to life. Do not wait for an online response. [S22]
Conclusion: accurate interpretation matters more than the longest list
Cannabinoids can interact with medicines. A scientifically sound answer is not a list presenting every theoretical possibility as a clinically proven risk. The active substance and preparation, human or laboratory study, measured outcome and open questions must always be considered together.
The practical consequence is to provide complete information and have the actual combination professionally assessed. This knowledge article offers general orientation. It is not an individual interaction check, treatment instructions or a promise of effectiveness or safety for Parmorcan® products.
Sources and limitations of this article
The article draws on original studies, regulatory product information and public professional guidance. Linked figures apply only to the conditions studied. This selection is neither a complete list of all possible interactions nor a registered systematic review. The study limitations described are part of each finding.
[S01] Epidyolex – European product information, last updated 20 August 2026
European Medicines Agency / marketing authorisation holder · 2026 · Regulatory product information
[S02] A Phase I Trial of the Pharmacokinetic Interaction Between Cannabidiol and Tacrolimus
So GC; Lu JBL; Koyama S; Cheng YH; Gisch DL; McClara K; Dexter PR; Sharfuddin AA; Etkins J; Tillman EM; Beamon TR; Cowsert Z; Stuart JS; Desta Z; Eadon MT · 2025 · Open-label phase I crossover study, interim analysis
[S03] Understanding enzyme or transporter-based drug interactions
NHS Specialist Pharmacy Service · 2024 · Public professional pharmacy guidance
[S04] Inhibition of UDP-Glucuronosyltransferase Enzymes by Major Cannabinoids and Their Metabolites
Nasrin S; Watson CJW; Bardhi K; Fort G; Chen G; Lazarus P · 2021 · Original study: in vitro UGT experiments
[S05] Clinical Study to Evaluate Drug Interactions of Cannabidiol with Citalopram and Morphine in Healthy Adults
Salcedo P; Volpe DA; Chaturbedi A; Shah A; Krishna A; Hyland PL; Vegesna G; Hsiao CH; De Palma R; Fein M; Rouse R; Florian J · 2026 · Open-label sequential human pharmacokinetic study
[S06] EPIDIOLEX (cannabidiol) oral solution – US Prescribing Information, revised 5/2026
Jazz Pharmaceuticals, Inc. / DailyMed · 2026 · US regulatory product information; not a separate additional clinical study
[S07] A Phase 1, Open-Label, Pharmacokinetic Trial to Investigate Possible Drug-Drug Interactions Between Clobazam, Stiripentol, or Valproate and Cannabidiol in Healthy Subjects
Morrison G; Crockett J; Blakey G; Sommerville K · 2019 · Open-label fixed-sequence phase I study
[S08] A Phase 2, Double-Blind, Placebo-Controlled Trial to Investigate Potential Drug-Drug Interactions Between Cannabidiol and Clobazam
VanLandingham KE; Crockett J; Taylor L; Morrison G · 2020 · Randomised double-blind phase II study
[S09] A Phase II Randomized Trial to Explore the Potential for Pharmacokinetic Drug-Drug Interactions with Stiripentol or Valproate when Combined with Cannabidiol in Patients with Epilepsy
Ben-Menachem E; Gunning B; Arenas Cabrera CM; VanLandingham K; Crockett J; Critchley D; Wray L; Tayo B; Morrison G; Toledo M · 2020 · Randomised phase II study
[S10] Citalopram and Cannabidiol: In Vitro and In Vivo Evidence of Pharmacokinetic Interactions Relevant to the Treatment of Anxiety Disorders in Young People
Anderson LL; Doohan PT; Oldfield L; Kevin RC; Arnold JC; Berger M; Amminger GP; McGregor IS · 2021 · In vitro work plus a small accompanying clinical study
[S11] Low-dose cannabidiol increases plasma concentrations of amitriptyline: A clinical drug-drug interaction study
Gorbenko AA; Post TE; Strugala PK; Klaassen ES; Klumpers LE; de Visser SJ; Sempio C; Klawitter J; Heuberger JAAC; Groeneveld GJ · 2026 · Open-label fixed-sequence crossover study
[S12] Pharmacokinetic Drug-Drug Interaction With Coadministration of Cannabidiol and Everolimus in a Phase 1 Healthy Volunteer Trial
Wray L; Berwaerts J; Critchley D; Hyland K; Chen C; Thai C; Tayo B · 2023 · Open-label fixed-sequence phase I study
[S13] An interaction between warfarin and cannabidiol, a case report
Grayson L; Vines B; Nichol K; Szaflarski JP; UAB CBD Program · 2018 · Case report
[S14] Evaluation of Cytochrome P450-Mediated Cannabinoid-Drug Interactions in Healthy Adult Participants
Bansal S; Zamarripa CA; Spindle TR; Weerts EM; Thummel KE; Vandrey RG; Paine MF; Unadkat JD · 2023 · Randomised placebo-controlled crossover probe study
[S15] A Phase 1 Open-Label, Fixed-Sequence Pharmacokinetic Drug Interaction Trial to Investigate the Effect of Cannabidiol on the CYP1A2 Probe Caffeine in Healthy Subjects
Thai C; Tayo B; Critchley D · 2021 · Open-label fixed-sequence phase I study
[S16] CBD-oil as a potential solution in case of severe tamoxifen-related side effects
Buijs SM; Braal CL; Buck SAJ; van Maanen NF; van der Meijden-Erkelens LM; Kuijper-Tissot van Patot HA; Oomen-de Hoop E; Saes L; van den Boogerd SJ; Struik LEM; van Rossum-Schornagel QC; Mathijssen RHJ; Koolen SLW; Jager A · 2023 · Open-label single-arm pharmacokinetic crossover study
[S17] Cannabinoid Metabolites as Inhibitors of Major Hepatic CYP450 Enzymes, with Implications for Cannabis-Drug Interactions
Nasrin S; Watson CJW; Perez-Paramo YX; Lazarus P · 2021 · Original study: in vitro CYP experiments and static modelling
[S18] Tobacco and cannabis smoking cessation can lead to intoxication with clozapine or olanzapine
Zullino DF; Delessert D; Eap CB; Preisig M; Baumann P · 2002 · Two case reports; smoking/tobacco context
[S19] Cannabinoid Interactions with Cytochrome P450 Drug Metabolism: a Full-Spectrum Characterization
Doohan PT; Oldfield LD; Arnold JC; Anderson LL · 2021 · Original study: recombinant CYP assays
[S20] A Phase I, Randomized, Double-Blind, Placebo-Controlled, Single Ascending Dose, Multiple Dose, and Food Effect Trial of the Safety, Tolerability and Pharmacokinetics of Highly Purified Cannabidiol in Healthy Subjects
Taylor L; Gidal B; Blakey G; Tayo B; Morrison G · 2018 · Randomised phase I study; food-effect/pharmacokinetic study
[S21] Provisional safe level for cannabidiol as a novel food
European Food Safety Authority (EFSA) · 2026 · Agency announcement on the updated safety assessment, 9 February 2026
[S22] First aid for poisoning
gesund.bund.de / German Federal Ministry of Health · Ongoing web information; accessed 2026 · Public health information
[S23] A Phase I, open-label, randomized, crossover study in three parallel groups to evaluate the effect of Rifampicin, Ketoconazole, and Omeprazole on the pharmacokinetics of THC/CBD oromucosal spray in healthy volunteers
Stott C; White L; Wright S; Wilbraham D; Guy G · 2013 · Randomised open-label phase I crossover study
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