Is there human or clinical evidence for CBDV?
Yes, more than for most minor cannabinoids, and none of it shows a benefit. grade: Not supported
Most minor cannabinoids reach the shelf without ever meeting a clinical trial. CBDV, the propyl homolog of CBD (the same cannabidiol scaffold, with a three-carbon side chain where CBD has five), is the exception. It has been through a real clinical programme, in seizures and in nerve pain, and its primary endpoints were missed. Here is that record in full, failed trials included. For anyone putting CBDV on a label, that record takes efficacy claims off the table for every indication.
Strip carbon dioxide from CBGVA and you get CBGV. CBDV sits one enzymatic step further along: CBDA synthase converts the varin mother acid CBGVA into CBDVA, and CBDVA then decarboxylates to neutral CBDV. Of the pathway's four nodes, the third is where the two varin pillars part company.
The branch above rests on one registry-graded record: Taura 1996, the purification and characterization of CBDA synthase. Two limits come with it. It characterizes the pentyl reaction (CBGA → CBDA), so the varin step (CBGVA → CBDVA) is its structural analog, inferred from that enzymology rather than measured. And its job here is biosynthesis only: what CBDV does in the body lies outside it, and it stays with the chemistry.
Six questions to put to a supplier, each followed by the position the registry or this compound's page already holds, in its own words. The questions ask what the supplier states; none asks what anyone should take. Informational only, not medical or legal advice.
Take the answers to the paperwork: Read a COA, then test the label wording. How the site grades what it holds is on How we grade.
With most minor cannabinoids, a gap in the record is a gap in the looking. CBDV's gap is of another kind. Researchers ran controlled trials, and the answer came back negative.
The two columns make sense only side by side. On the left, CBDV has been given to people in registered trials; on the right, none of those trials met its primary endpoint. An absence of evidence and a negative result are different things, and CBDV has the second kind. Anyone weighing a product claim should count a null trial as evidence against it.
Five published studies have given CBDV to people. Ranked by strength of design, the largest and most rigorous comes first, and it happens to be the most negative. With a record like this, start with what was actually tested, and keep the shows / does not show halves together.
Every paper here is published and checkable. What they still lack is a place among the graded entries in the CBG Atlas registry, so the badge beside each names the study's design(“Phase 2 RCT”) rather than a rung on our evidence ladder. Once a paper enters the registry, it takes a grade like any other record.
What was actually tested: Randomised, double-blind, placebo-controlled Phase 2 trial of CBDV as add-on therapy in 162 adults with inadequately controlled focal seizures (81 CBDV, 81 placebo). After a 4-week baseline, participants titrated to 800 mg twice daily over 2 weeks and stayed at that dose for 6 weeks. Registered as NCT02365610. Of the studies on this page, the strongest design.
It missed its primary endpoint. Focal seizure frequency fell by similar amounts in both arms, 40.5% on CBDV and 37.7% on placebo (p = 0.648), the arms matched on every seizure subtype, and the secondary efficacy measures all fell short of a significant treatment difference. The authors note a high placebo response, which “may reflect the participants’ expectations of CBDV”. Treatment-emergent adverse events affected 72.8% of the CBDV group and 48.1% of the placebo group, most often diarrhoea, nausea and somnolence.
What it shows: That CBDV, tested properly in adults with focal seizures, at a substantial dose and for long enough to show an effect, finished level with placebo.
What it does NOT show: Any anticonvulsant benefit, or any reason to change or stop prescribed antiseizure medication. CBD, a different molecule with its own approved medicine, lies outside it entirely.
Caveat: Sponsor study: the authors are affiliated with GW Research Ltd and Greenwich Biosciences, Inc. The trial also produced a liver signal. Serum transaminases rose above three times the upper limit of normal in three participants taking CBDV, two of whom discontinued, and in one taking placebo. All fell short of the criteria for potential Hy’s Law cases.
What was actually tested: Randomised, double-blind, placebo-controlled crossover trial in 32 patients with HIV-associated neuropathic pain. Each participant took CBDV 400 mg per day for 4 weeks and placebo for 4 weeks, in random order, with a 3-week washout between them. The primary endpoint was diary-recorded pain intensity on an 11-point numeric rating scale.
Pain scores moved the wrong way. Mean pain intensity was 0.62 points higher on CBDV than on placebo (P = 0.16; 95% CI −0.27 to 1.51). The difference fell short of statistical significance, but the point estimate sat on placebo's side. Use of additional pain medication, the character of the pain and quality of life all stayed where they were, and adverse-event incidence was similar on both treatments. The authors state they “would currently not consider CBDV as a clinically meaningful treatment option for neuropathic pain”. A larger trial, they add, would be unlikely to change that conclusion, because the observed differences are far from significance.
What it shows: That CBDV was tolerated in this population and failed to reduce HIV-associated neuropathic pain.
What it does NOT show: Any analgesic effect, in this pain condition or any other. The authors offer one possible explanation and hedge it: the failure “may be explained by a lack of CB receptor activation, as indicated by preclinical experiments”.
Caveat: Investigator-led, at Charité Universitätsmedizin Berlin; one author declares an affiliation with SteriPharm Pharmazeutische Produkte. The result appears in the authors’ terms, because calling it merely non-significant would drop the direction of the point estimate, and the direction is part of the finding.
What was actually tested: Five girls with a pathogenic MECP2 variant and drug-resistant epilepsy received CBDV oral solution titrated to 10 mg/kg/day, without a control arm, blinding or randomisation. The study was built to measure safety, tolerability and the pharmacokinetics of CBDV and its 7-OH and 7-COOH metabolites; efficacy sat outside its design.
All five children reached the target dose, which was reported as safe and well tolerated; hypersomnolence and drooling were judged related to CBDV. The paper gives two seizure figures. Its abstract reports a median 79% reduction in monthly seizure frequency, while the Results and Table 3 report 82%. We cite neither as a result, since picking one would hide a discrepancy readers deserve to see. And whichever figure is right, an uncontrolled reduction in five children is indistinguishable from the high placebo response that the controlled trial of the same compound documented.
What it shows: That 10 mg/kg/day was tolerated in a very small paediatric cohort, and how CBDV and its metabolites behave pharmacokinetically in children.
What it does NOT show: Anticonvulsant efficacy. With five participants and no comparison arm, no change in seizure frequency here can be pinned on the drug.
Caveat: Two findings cut against the headline. The EEG worsened in two of the five children: spike-wave activity doubled in one and rose more than 500-fold in another, with a rhythm considered likely ictal, although the abstract’s summary sentence records no significant EEG change. A transient rise in liver transaminases also led to a dose reduction, matching the Phase 2 signal above. The paper declares its conflicts of interest as “none”, yet GW supplied the study drug and set the dose ceiling, a relationship worth naming.
What was actually tested: Resting-state functional MRI in 28 men, 15 neurotypical and 13 autistic, each scanned twice in a repeated-measures, double-blind, placebo-controlled design: once after 600 mg CBDV and once after placebo, at least 13 days apart. With men only in the sample, the results describe men rather than “adults” in general, a limit on generalisability the authors name themselves. Registered retrospectively as NCT03537950.
Compared with neurotypical participants, autistic participants had lower connectivity between the ventral striatum and frontal and pericentral regions, and higher connectivity within the striatum and between the putamen and temporal regions. CBDV brought the HYPERconnectivity down toward the neurotypical range and left the ventral-striatal HYPOconnectivity where it was, so half of the group difference went untouched. The authors describe the result as “preliminary proof of concept” from a “small pilot study”.
What it shows: That one dose of CBDV can shift one measurable brain-connectivity difference in a small group of autistic men, in a scanner.
What it does NOT show: Any change in autism symptoms, behaviour or function. Connectivity is an imaging biomarker, and whether shifting it shifts symptoms remains, in the authors’ words, an open question.
Caveat: Registered retrospectively (May 2018), which weakens assurance that the analysis was pre-specified. Read it with Pretzsch 2019 below: same group, same one-dose design, and partial nulls that belong next to the positives.
What was actually tested: Magnetic resonance spectroscopy in 34 men (17 autistic, 17 neurotypical) in a repeated-measures, double-blind crossover with randomised order, comparing placebo with 600 mg CBDV. Two brain regions were measured: the dorsomedial prefrontal cortex and the left basal ganglia. One dose per session, with sessions at least 13 days apart.
Read past the headline and the paper is mostly null. CBDV significantly raised Glx (glutamate + glutamine) in the basal ganglia of both groups. Glx in the dorsomedial prefrontal cortex and GABA+ in both regions showed nothing significant: of the four region-by-metabolite comparisons, one moved and three stayed flat. In the autistic group, the size of the basal-ganglia shift correlated negatively with each person’s starting level, so the response varied between individuals.
What it shows: That one dose of CBDV measurably shifts one excitatory metabolite in one brain region, and that the size of the shift depends on a person’s starting level.
What it does NOT show: A GABA effect, a prefrontal effect, or any behavioural or clinical effect. The readings are scanner measurements of brain chemistry taken two hours after a dose, and the authors call for studies of whether the change corresponds to anything a person experiences.
Caveat: Most summaries of this study quote the basal-ganglia increase alone, which is selective reporting. The three null comparisons sit beside it for that reason.
Summaries of the autism-related CBDV work tend to quote the positive half of each paper. Most of what the two papers measured came back null, so here they sit side by side, the nulls in a row of their own.
| Property | Pretzsch 2019 — brain chemistry (MRS) | Pretzsch 2021 — brain connectivity (fMRI) |
|---|---|---|
| What was measured | Brain chemistry: glutamate (Glx) and GABA+ measured by magnetic resonance spectroscopy in two regions | Brain wiring: resting-state functional connectivity of the striatum |
| Who was studied | 34 men (17 autistic, 17 neurotypical), one dose of 600 mg vs placebo, crossover | 28 men (13 autistic, 15 neurotypical), one dose of 600 mg vs placebo, repeated measures |
| What moved | Glx rose in the basal ganglia in both groups | In the autistic group, striatal HYPERconnectivity fell toward the neurotypical range |
| What stayed flat | Glx in the dorsomedial prefrontal cortex, and GABA+ in both regions, all nonsignificant. Three of four comparisons were null. | Ventral-striatal HYPOconnectivity, the other half of the group difference, stayed where it was. |
| What neither is | A clinical result. Symptoms, behaviour and outcomes went unmeasured; the reading is a metabolite level in a scanner two hours after one dose. | A clinical result. Symptoms, behaviour and outcomes went unmeasured, and the authors call the connectivity result preliminary proof of concept from a small pilot. |
| Generalisability | Men only. The authors keep the result to men, leaving women and children outside it. | Men only, and registered retrospectively. The authors list the restricted sample as a limit. |
Both columns describe imaging biomarkers: a metabolite concentration and a connectivity measure, recorded in men in a scanner a couple of hours after one dose. Neither includes a symptom, a behaviour or an outcome, and the authors of both papers describe the work as “preliminary proof of concept” from a “small pilot study”. A biomarker that moves is a reason to run a trial. It is not a trial result. CBG Atlas asserts no effect of CBDV on autism or any of its features, and neither paper supports a product claim about autism. This is educational information, not medical advice.
From the clinic to the bench, where the explanation for how CBDV might act looks shakier still. Switch to Researcher depth for the cited record.
In cell culture, CBDV switches on a family of sensory ion channels and then quietens them. It also damps abnormal electrical bursting in slices of rat brain. Then the same researchers ran the control experiment that would have pinned the effect on the channel, and it came back negative. So the most-cited explanation of how CBDV might work is argued against by its own source paper. The full account sits behind Researcher depth.
What was actually tested: Patch-clamp recordings in transfected HEK293 cells, plus multielectrode-array recordings from rat hippocampal brain slices bathed in magnesium-free solution to provoke epileptiform activity. All of it was bench work, in cells and rodent tissue.
CBD and CBDV activated and then rapidly desensitised TRPV1, TRPV2 and TRPA1. In the brain-slice model, CBDV reduced the amplitude and duration of epileptiform bursts. The paper then tested its own hypothesis. The selective TRPV1 antagonist IRTX reversed capsaicin's effect on burst amplitude and left CBDV's intact. The authors conclude that CBDV's antiepileptiform effect in this model is “not uniquely mediated via activation of TRPV1”.
What it shows: That CBDV interacts with TRPV1, TRPV2 and TRPA1 in cultured cells and damps epileptiform bursting in rodent brain slices.
What it does NOT show: That TRPV1 is the mechanism, since the paper's own antagonist experiment argues against it. Seizures in people are a separate question, and the controlled trial that asked it, Brodie 2021, was null.
Caveat: The De Petrocellis papers do not support a longer target list. In PMID 21175579, CBDV is named for DAGLα inhibition and TRPV2 by inclusion, and is explicitly absent from that paper's TRPV1, TRPA1 and TRPM8 lists. PMID 21726418 is a TRPV3/TRPV4 paper in which CBDV stimulated TRPV4 only. Citing either paper for TRPV1, TRPA1 or TRPM8 activity would be a miscitation.
A summary table doing the rounds credits CBDV with TRPV1, TRPA1 and TRPM8 activity, citing De Petrocellis 2011 (PMID 21175579). Open that paper and CBDV appears for DAGLα inhibition and for TRPV2 by inclusion, and is explicitly absent from its TRPV1, TRPA1 and TRPM8 lists. A second 2011 paper (PMID 21726418) covers TRPV3 and TRPV4; there, CBDV stimulated TRPV4 only. The TRPV1 / TRPV2 / TRPA1 observation comes from Iannotti 2014, refutation and all. The error is worth spelling out because a real PMID attached to the wrong finding sails through any check that the paper exists.
In the Phase 2 seizure trial, CBDV finished level with placebo on efficacy yet produced substantially more adverse events. Each signal below is tied to the study it came from.
The liver signal is the one that recurs. In the Phase 2 focal-seizure trial, serum transaminases rose above three times the upper limit of normal in three participants taking CBDV, two of whom discontinued, and in one on placebo; all fell short of the criteria for potential Hy's Law cases (Brodie 2021, PMID 33998885). Then, in a separate study of girls with Rett syndrome, a transient transaminase rise led to a dose reduction (Hurley 2022, PMID 35364618).
In the Phase 2 trial, 72.8% of the CBDV group reported at least one treatment-emergent adverse event, against 48.1% on placebo. The most common were diarrhoea, nausea and somnolence. Serious adverse events were uncommon in both arms (Brodie 2021, PMID 33998885).
Spike-wave activity doubled in one child and rose more than 500-fold in another, with a rhythm considered likely ictal (Hurley 2022, PMID 35364618). Those readings come from an open-label study of five children whose summary led with a seizure reduction, which is why we do not treat that uncontrolled headline figure as evidence.
In laboratory enzyme assays, CBDV inhibited CYP2C19 (Jiang 2013, PMID 23318708) and CYP1A1 (Yamaori 2013, PMID 23811569), in both cases somewhat less potently than CBD (the enzyme is CYP1A1, a different one from CYP1A2). For CYP1A2, CYP2B6 and CYP2C9 no CBDV data has been published, and no interaction study in people has been published. If you take prescription medicines, particularly ones metabolised by CYP2C19, discuss any cannabinoid product with your prescriber or pharmacist.
In the trial, CBDV was added on top of existing antiseizure medication, and it did not beat placebo. Nothing on this page supports replacing, reducing or stopping a prescribed antiseizure medicine; changes to epilepsy treatment belong with a treating clinician. This is educational information, not medical advice.
The World Anti-Doping Agency exempts CBD and prohibits CBDV, and an athlete can take in the second while buying the first. After 10 weeks of daily use of a broad-spectrum CBD product, CBDV turned up in 68% of pre-exercise and 84% of post-exercise urine samples (Gillham 2025, PMID 40920736). The source leaves that product's CBDV content unreported. Regulatory and testing status, then, rather than a health claim.
Two registered CBDV trials get cited as if they had produced results. Both were terminated, with a handful of participants between them and nothing to say about effect: NCT03848481 (CBDV in Prader-Willi syndrome) — Terminated with 6 participants enrolled, before completion. It supports no efficacy statement. NCT03849456 (CBDV in autism spectrum disorder (paediatric)) — Terminated with 1 participant enrolled; the reason is unverified, so we leave it unstated. It supports no efficacy statement. Where a termination reason cannot be verified, we give none: a plausible cause attached to an unverified record would be an invented fact.
What was actually tested: Human liver microsomes and recombinant CYP2C19, in vitro. The study is about CBD. CBDV is one of several structurally related comparators used to work out which part of the CBD molecule does the inhibiting.
CBDV inhibited CYP2C19 in this assay, slightly less potently than CBD; the potency values stay in the paper.
What it shows: That CBDV can inhibit a major drug-metabolising enzyme in the laboratory.
What it does NOT show: A measured interaction in a person. No CBDV drug-interaction study in people has been published, so the practical size of the effect is unknown.
What was actually tested: Recombinant human CYP1A1, a different enzyme from CYP1A2. Another CBD structure-activity study, with CBDV as one of several comparators.
CBDV inhibited CYP1A1 activity, less potently than CBD. The paper has the potency values.
What it shows: That CBDV inhibits CYP1A1 in a recombinant enzyme preparation.
What it does NOT show: Anything about CYP1A2, CYP2B6 or CYP2C9, for which no CBDV data has been published, or about what happens in a person.
What was actually tested: Thirty-six healthy adults took a broad-spectrum CBD product or a matched placebo every day for 10 weeks, then did a 90-minute session of moderate-intensity exercise. Blood and urine were sampled before supplementation and before and after exercise.
Urine was clean of CBDV at baseline. After supplementation it turned up in 68% of pre-exercise urine samples and 84% of post-exercise samples, and urinary concentrations rose with exercise. The authors conclude that athletes should avoid broad-spectrum CBD products because of the anti-doping risk. The product itself is harder to pin down: the abstract describes the 150 mg/day product as carrying trace concentrations of CBG and is silent on CBDV, so its CBDV content awaits the full text. Product content and urinary detection are separate facts, and the paper reports the second.
What it shows: That CBDV from a broad-spectrum consumer CBD product becomes detectable in urine with daily use, and that exercise raises the measured concentration.
What it does NOT show: Anything about effects, benefit or harm; the finding concerns detection and regulatory status. Check the current WADA Prohibited List and the product's certificate of analysis.
CBDV has no approved use in any jurisdiction and is no substitute for prescribed antiseizure medication. In the seizure trial it went on top of existing medication, and it finished level with placebo. Nothing here diagnoses, treats, cures or prevents any disease. If you take prescription medicines, discuss any cannabinoid product with your prescriber or pharmacist. See the safety page and how we grade.
Close names and a near-identical scaffold tempt people to hand CBDV its famous parent's standing. The trial record says otherwise. CBD and CBGV sit in the table as reference chemistry, and each compound keeps a column of its own.
| Property | CBD (pentyl parent) | CBDV (this page) | CBGV (the other varin) |
|---|---|---|---|
| Side chain | Pentyl — five carbons | Propyl — three carbons (the varin form) | Propyl — three carbons (the varin form) |
| Precursor acid | CBDA, made from CBGA by CBDA synthase | CBDVA, made from CBGVA on the varin branch | CBGVA, the varin mother acid itself, decarboxylated |
| Randomised controlled trials in people | Many, including the programme behind an approved medicine | Four published: a Phase 2 in focal epilepsy, a crossover trial in HIV-associated neuropathic pain, and two one-dose imaging trials. Both efficacy trials missed their primary endpoints, and the imaging trials measured biomarkers rather than clinical outcomes. (A fifth study, in Rett syndrome, was open-label and uncontrolled.) | None published, for effects or exposure |
| Approved medicine | Yes. A prescription medicine containing purified plant-derived CBD is approved in the US and EU for specific rare seizure disorders | None in any jurisdiction, for any indication | None |
| Strongest class of evidence held | Human randomised controlled trials supporting a licensed indication | A completed Phase 2 randomised controlled trial, with a null primary endpoint | Cell assays and mice only |
| Does the neighbouring column transfer? | — | No. CBDV is a different molecule with a clinical record of its own; the two were tested separately and produced different results. | No. The shared varin side chain is structural; each compound's evidence stands alone. |
CBD's clinical record stays with CBD. A prescription medicine containing purified CBD is approved for specific rare seizure disorders; no CBDV medicine is approved anywhere, and when CBDV was tested for seizures, it finished level with placebo. Two molecules, tested separately, with different results, and a CBDV product has to stand on CBDV's own record.
Which leaves the practical questions: legality, product labelling, drug testing, and what exactly CBDV is.
Of the 44 answers, 22 carry a verified grade on the six-rung evidence ladder. 7 carry an evidence state instead of a rung, most often no primary evidence, meaning our registry holds nothing on that question, a different claim from not supported. The remaining 15 carry an author qualifier still outside the controlled vocabulary, so they appear without a grade chip rather than with a guessed one. Catalogue in progress.
CBDV (cannabidivarin) is a minor cannabinoid in cannabis and hemp that doesn't intoxicate. Chemically it is CBD with a shorter tail: a three-carbon (propyl) side chain where CBD carries five. Chemists first isolated it in 1969, early enough to make it one of the first "varin" cannabinoids anyone characterised.
CBDV is short for cannabidivarin, a name built entirely from chemistry. "Cannabidi-" ties it to cannabidiol (CBD), and "-varin" marks the three-carbon (propyl) side chain standing in for CBD's five-carbon (pentyl) one. Formula C₁₉H₂₆O₂, molecular weight 286.41, CAS number 24274-48-4, and all of it Established. The name describes a molecule. What that molecule does in a person is a question for the clinical trials.
The cannabis plant makes it, mostly in low-THC chemotypes rich in propyl ("varin") cannabinoids, among them some hemp and indica landraces. It sits on the varin branch of cannabinoid biosynthesis: the plant builds the acid, CBDVA, first, and heat converts that acid to CBDV, the propyl homolog of CBD.
Natural. Cannabis produces CBDV, and it was first isolated from the plant in 1969. Labs can make it for research or manufacturing, but the CBDV in a hemp product is usually plant-derived, and plant-made or lab-made, it doesn't intoxicate.
No. CBDV doesn't intoxicate or produce the high people associate with THC. That high comes from switching on the CB₁ receptor, which CBDV is not known to do; the activity laboratories have confirmed for CBDV sits at other targets.
CBDV doesn't intoxicate or impair anyone the way THC does. "Psychoactive" is a wider word, covering anything that acts on the brain, and on that wider question the human record goes quiet. No controlled human study has shown CBDV shifting mood or perception, and its effects in people are not established.
There is no primary evidence, because nobody has measured it. People have taken CBDV in trials, but none of those trials recorded subjective experience as an outcome. As a non-intoxicating compound it shouldn't produce a high; beyond that, user reports are anecdote that no clinical study has confirmed. Not medical advice.
Its effect profile is not established, because nobody has measured it. Somnolence was one of the three most common adverse events in the Phase 2 trial (Brodie 2021), which sounds like an answer until you remember what an adverse-event tally is: a safety record, kept to catch harm. Turning it into an effect profile would take a study designed to ask whether CBDV sedates, energises or does neither, and no such study has been run. Without it, a label promising either sleep or pep is claiming more than the evidence holds. Not medical advice.
It depends on where you are, the product class (food, supplement, cosmetic), where the CBDV came from and how much THC the product carries. Many jurisdictions put hemp-derived CBDV under novel-food or cannabis rules that are still moving, so the answer changes with the border and with the calendar. Check the law where you live; this is informational, not legal advice.
Generally yes, within one limit. Under the 2018 Farm Bill, US cannabinoids derived from hemp with ≤0.3% Δ⁹-THC (dry weight) are federally legal as hemp, and CBDV can fall inside that. The limit is the FDA, which has not approved CBDV as a food or supplement, so a lawful hemp derivative can still be an unlawful food ingredient. State laws add their own layer. Not legal advice; verify current rules.
Not necessarily. Federal legality for hemp cannabinoids leaves each state free to write its own rules, and some restrict or ban particular hemp cannabinoids, novel forms or intoxicating derivatives. CBDV's status can differ from one state to the next and shift over time, so check your state's current law. Not legal advice.
Not as a freely sold supplement. The UK and EU treat extracted cannabinoids such as CBDV as novel foods, which generally need authorisation before they reach a shelf as food, while Canada regulates phytocannabinoids under the Cannabis Act. Each market sets its own rules, and all of them keep changing. Not legal advice; check with the regulator.
None has been shown in people, and for CBDV that is a result rather than a gap: it went to randomised controlled trials and came back flat. A Phase 2 trial in adults with inadequately controlled focal seizures failed to separate from placebo, and in a crossover trial in HIV-associated neuropathic pain, pain scores ran numerically higher on CBDV (Brodie 2021; Eibach 2021). What survives is cell work. In vitro, CBDV inhibits the enzyme DAGLα and activates and desensitises the TRPV2 ion channel (De Petrocellis 2011), a mechanism in a dish, not a benefit anyone can feel, and no marketed benefit has been confirmed. Not medical advice.
Mostly research. CBDV has been through registered clinical trials for focal seizures and for HIV-associated neuropathic pain, and both missed their primary efficacy endpoints (Brodie 2021; Eibach 2021). The rest of the human record is small: an open-label study in five girls with Rett syndrome, and two single-dose brain-imaging studies in men. No therapeutic use is established, no jurisdiction has approved one, and on the shelf CBDV sells simply as a minor cannabinoid. Not medical advice.
No, and this is one question that was properly tested. In a Phase 2 randomised controlled trial, 162 adults with inadequately controlled focal seizures took CBDV on top of their existing medication, titrated to 800 mg twice daily. Seizures fell in both arms, by 40.5% on CBDV and 37.7% on placebo, with no significant difference on any seizure subtype or secondary measure (Brodie 2021). Earlier animal work had reported anticonvulsant activity (Hill et al. 2012); the human trial failed to reproduce it. CBDV is no substitute for prescribed antiseizure medication. Not medical advice.
Not established, because autism has never been tested as a clinical question for CBDV. Both published human studies of CBDV in autism gave a single dose and scanned the brain (Pretzsch 2019; Pretzsch 2021). They measured scanner signals, and no trial has asked the question a family would ask, whether anything changes at home. That makes autism the opposite case to seizures: untested where seizures were tested and null, with no primary evidence pointing either way. CBDV is no autism therapy. Not medical advice.
Yes, more than for most minor cannabinoids, and none of it shows a benefit. A Phase 2 randomised controlled trial in 162 adults with inadequately controlled focal seizures missed its primary endpoint: 40.5% on CBDV against 37.7% on placebo (Brodie 2021). A randomised crossover trial in 32 people with HIV-associated neuropathic pain found pain numerically higher on CBDV, and its investigators wrote that they would not consider CBDV a clinically meaningful treatment option (Eibach 2021). The trials exist; the efficacy doesn't. CBD's clinical record belongs to a different molecule and stays with it. Not medical advice.
Yes, once, and the study leaves more questions than it settles. Five girls with Rett syndrome took CBDV in an open-label study with no control group. The paper gives two different seizure-reduction figures for the same cohort, and the EEG got worse in two of the five children (Hurley 2022). Add the two single-dose brain-imaging studies in men, which measured scanner signals rather than symptoms (Pretzsch 2019; Pretzsch 2021), and the controlled efficacy evidence still comes to zero. For Rett syndrome, CBDV has no primary evidence pointing either way. Not medical advice.
Untested. Our registry holds no CBDV study of relaxation, stress or calm in any model, and the human trials measured seizures, neuropathic pain and neurodevelopmental outcomes, a different set of questions from the one a relaxation claim asks. Untested is its own state, distinct from tested-and-failed, and both differ from supported.
All three are untested. CBDV's human record, a Phase 2 in focal seizures, a neuropathic-pain crossover and imaging pilots, stops short of inflammation, autoimmune conditions and skin, and our file on CBDV for all three is empty. An untested claim counts neither for nor against CBDV; for now it simply stands on air.
Not fully established, and the trial data argue for caution. In the Phase 2 focal-seizure trial, 72.8% of people on CBDV reported at least one treatment-emergent adverse event, against 48.1% on placebo, most often diarrhoea, nausea and somnolence. Serum transaminases rose above three times the upper limit of normal in three people on CBDV, and two of them stopped treatment (Brodie 2021). A transient transaminase rise also prompted a dose reduction in the Rett syndrome study (Hurley 2022): two studies, one liver signal. Long-term and general consumer safety are catalogue in progress here. If you take medications or have a health condition, talk to a clinician. Not medical advice.
Diarrhoea, nausea and somnolence were the commonest in trials. In the Phase 2 focal-seizure trial, 72.8% of people on CBDV reported at least one treatment-emergent adverse event, against 48.1% on placebo, and three participants had liver transaminase elevations, two of whom discontinued (Brodie 2021). A small open-label study recorded a transient transaminase rise and EEG worsening in two of five children (Hurley 2022). Nobody has measured the side effects of consumer products at consumer amounts, and that gap is catalogue in progress, an absence of testing rather than a clean result. Ask a clinician about your own situation. Not medical advice.
Nobody can say, because CBDV has no established safe or maximum dose, and no standard consumer dosing guidelines either. With any cannabinoid, more isn't automatically better, and effects and safety vary by person and product. Consult a clinician. Not medical or dosing advice.
How CBDV behaves alongside medicines in people is unknown, because no human drug-interaction study exists; the evidence so far is laboratory enzyme work. In vitro, CBDV inhibited the drug-metabolising enzymes CYP2C19 (Jiang et al. 2013) and CYP1A1 (Yamaori et al. 2013), both times as a comparator in studies of CBD, and less potently than CBD. For CYP1A2, CYP2B6 and CYP2C9 the published CBDV record is empty, so we make no claim about those three. Anyone on other medicines should check with a clinician or pharmacist first. Not medical advice.
Not on a standard workplace test, which looks for THC and its metabolite. Sport is another matter. The World Anti-Doping Agency prohibits CBDV: CBD is the exempt cannabinoid, and CBDV sits on the wrong side of that line. After ten weeks on a broad-spectrum CBD product, CBDV turned up in 68% of pre-exercise and 84% of post-exercise urine samples (Gillham et al. 2025), a finding any brand selling broad-spectrum CBD to athletes should read twice. Full- and broad-spectrum hemp products can also carry enough trace THC to trigger a positive on a standard test. Only the product's lab test (COA) shows what it contains. Not legal or medical advice.
No. CBDV is a separate, non-intoxicating compound. The product is where THC can creep in: depending on source and formulation, full-spectrum hemp products carry small amounts, and isolates should carry none. Check the certificate of analysis (COA). Not legal advice.
Pure CBDV should pass a standard workplace test, because that test looks for THC; the workplace risk is trace THC in some full- or broad-spectrum hemp products. Sport turns this around. CBDV itself is on the prohibited list and has been found in athletes' urine (Gillham et al. 2025), so a competing athlete should treat it as a risk in its own right. If the result matters to you, choose a product whose COA confirms what it contains. Not legal or medical advice.
In the same formats as other cannabinoids: oils or tinctures held under the tongue, capsules, or as part of full-spectrum hemp extracts. CBDV lacks established dosing guidelines or a verified protocol for human use, so the formats are as far as we go. Not medical or dosing advice.
Mostly oils and tinctures, capsules, and full- or broad-spectrum hemp extracts, with isolate turning up now and then. CBDV sells as a minor or "specialty" cannabinoid and is far rarer than CBD. Actual CBDV content varies from one bottle to the next, which makes the certificate of analysis (COA) the document to read.
CBDV has no established dose. The amounts given in clinical trials were research protocols, and we keep them out of consumer advice; beyond them, there are no verified consumer dosing guidelines. Effects and safety vary by person and product, so talk to a qualified clinician before use. Not medical or dosing advice.
Consumer onset and duration are not established, and we publish no figures we cannot confirm. CBDV's pharmacokinetics have been tracked in people once: an open-label study in five girls with Rett syndrome followed blood levels of CBDV and two of its breakdown products, 7-OH-CBDV and 7-COOH-CBDV (Hurley 2022), with no control group and at a clinical rather than a consumer dose. As a general rule, sublingual and inhaled routes tend to act sooner than swallowed ones. "Work" is the harder half of the question, since the randomised trials that went looking for a benefit came back without one. Consumer onset and duration remain catalogue in progress. Not medical advice.
The side chain. CBDV is CBD's propyl homolog, identical except for a side chain two carbons shorter (three-carbon propyl against CBD's five-carbon pentyl), which gives it the formula C₁₉H₂₆O₂ to CBD's C₂₁H₃₀O₂. Neither intoxicates. CBD has far more research behind it, while most of CBDV's effects are not established. Not medical advice.
Intoxication, above all. THC activates the CB₁ receptor and produces a high; CBDV does neither. Structurally CBDV belongs to CBD's family, as its propyl homolog, rather than to THC's. THC has been studied extensively, while CBDV's effects in people are largely not established. Not medical advice.
Lineage. CBDV is the propyl homolog of CBD, while CBG, the "mother cannabinoid", derives from CBGA and has a receptor profile of its own. Neither intoxicates. Their verified activities differ, and neither has an established benefit in people. Not medical advice.
Neither can be called better, because no trial has compared them directly. CBD has much more research behind it, and a purified-CBD medicine is approved for specific rare seizure disorders, a regulatory fact that belongs to that molecule alone. CBDV's own randomised trials missed their primary endpoints. Without comparative human data or a defined goal, "better" has no answer. Not medical advice.
CBDV is C₁₉H₂₆O₂, with a molecular weight of 286.41 g/mol and CAS number 24274-48-4. Structurally it is cannabidiol (CBD) carrying a three-carbon propyl side chain where CBD has a five-carbon pentyl chain, which accounts both for the two missing carbons and for the "varin" in its name.
CBDV is extracted from cannabis and hemp, especially propyl-rich ("varin") chemotypes, with standard cannabinoid methods such as CO₂ or solvent extraction, then purified. Heating its acid, CBDVA, also forms CBDV (decarboxylation). Plants usually hold little of it, which keeps CBDV comparatively hard and costly to produce.
CBDV is the varin (propyl) homolog of CBD: a sibling, and neither a precursor of CBD nor a breakdown product of it. It has its own biosynthetic branch, where the plant makes the acid CBDVA and heat decarboxylates it to CBDV. The two molecules are built by parallel pathways, and neither is made from the other.
Yes. In the living plant CBDV sits mostly as its acid, CBDVA (cannabidivarinic acid, C₂₀H₂₆O₄, CAS 31932-13-5). Heat strips off carbon dioxide (decarboxylation) and turns CBDVA into CBDV, with conversion reported as near-complete at about 130 °C for 30 minutes, so a raw product and a heated one carry different chemistry.
From a few specialty hemp and cannabinoid retailers, mostly online, as oils, isolates or part of broad- or full-spectrum extracts. It is much rarer on the shelf than CBD, and whether you can buy it at all depends on your jurisdiction and the product class. Buy from sellers who publish third-party lab results (a COA). Not legal or purchasing advice.
Because most cannabis makes very little of it. CBDV concentrates in specific propyl-rich ("varin") chemotypes, so producing it takes selected plants and extra purification, and small-scale production and limited demand push the cost up further. That same scarcity is why a certificate of analysis (COA) confirming the real content matters.
Ask for a current certificate of analysis (COA) from an accredited third-party lab. It should show the actual CBDV content, matching the label, confirm THC is within legal limits, and screen for contaminants such as pesticides, solvents and heavy metals. A missing or mismatched COA is a red flag. Not purchasing advice.
Your call, but the record is unusually clear: CBDV has been tested and did not work, which is why it carries Not-supported rather than an open verdict. Two randomised controlled trials measured benefit, one in focal seizures and one in HIV-associated neuropathic pain, and both missed their primary endpoints (Brodie 2021; Eibach 2021). Adverse events were also more common on CBDV than on placebo. Buying it means accepting that record, and a brand claiming efficacy would be arguing with it. If you go ahead, choose lab-tested products and consult a clinician. Not medical or purchasing advice.
Start with a current third-party COA confirming the CBDV content and a legal THC level. After that: contaminant screening (pesticides, heavy metals, solvents), a label that matches the COA, transparent hemp sourcing, and no disease or "cure" claims, which are a legal red flag. Confirm legality where you live. Not medical, legal, or purchasing advice.
Each of the three below needs a new study. Any one of them, once published, would go into our registry and onto the page, graded and cited.
The Phase 2 seizure trial and the pain trial both asked whether CBDV works, and both came back empty, the pain trial's point estimate on placebo's side. Moving it off a null would take a controlled trial in a defined population that beats placebo on a pre-specified clinical endpoint. Until one does, efficacy claims for any indication stay off the table.
One dose of CBDV can shift brain chemistry and brain connectivity in men, in a scanner. Whether either shift corresponds to a change in symptoms is still unknown, as the authors acknowledge, and the missing step is work that ties the biomarker to a clinical outcome.
Transaminase elevations appeared in two independent studies, and the interaction evidence comes from laboratory enzyme work in which CBDV was a comparator. Dedicated safety and interaction studies in people, extending to CYP1A2, CYP2B6 and CYP2C9, where no CBDV data exists, would replace “uncharacterized” with something firmer.
The sources come in two lists, kept apart. First, the single registry-graded record behind the biosynthesis, which covers the pathway rather than CBDV itself. Then every CBDV-specific paper cited above: published, checkable, and ungraded.
Phase 2 RCT · in people · primary endpoint missed
Randomised crossover trial · in people · endpoint missed
Phase 1 · open-label, non-randomised, uncontrolled · n = 5
Imaging biomarker only · pilot
Imaging biomarker only · partial nulls
In vitro · transfected cells + rat brain slices
In vitro enzyme assay · CBDV as comparator
In vitro enzyme assay · CBDV as comparator
Regulatory & testing status · not an evidence claim
NCT03848481 — CBDV in Prader-Willi syndrome: Terminated with 6 participants enrolled, before completion. It supports no efficacy statement. NCT03849456 — CBDV in autism spectrum disorder (paediatric): Terminated with 1 participant enrolled; the reason is unverified, so we leave it unstated. It supports no efficacy statement.
For the other varin pillar, see CBGV; for the varin family, see the varin cannabinoids; and for the platform's most fully graded record, see the CBG monograph.
The subject here is CBDV (cannabidivarin), a compound with a human record of its own, and a much larger one than most minor cannabinoids carry. Nothing in this section describes CBG, and the CBG cautions on the safety page do not transfer to it.
CBDV is the propyl homolog of CBD: the same cannabidiol scaffold, two carbons shorter. Three things follow from that, and all three are easy to get wrong.
CBD's record does not transfer. CBD has an approved prescription medicine. CBDV has no approved use in any jurisdiction, for any indication. The two were tested separately and got different results. A shared scaffold means shared chemistry, not shared evidence.
CBG's record does not transfer either, in either direction. The α2-adrenoceptor blood-pressure note on the safety page is a CBG finding and says nothing about CBDV. The food-effect finding on the safety page comes from a CBG pharmacokinetic study and does not extend to CBDV. Equally, none of the CBDV signals below tells you anything about CBG.
CBDV has been given to people repeatedly, in registered trials. Few minor cannabinoids can say as much, and that record gives this section something to report. The main findings follow; the full account is on the CBDV pillar.
In a randomised, double-blind, placebo-controlled Phase 2 trial (Brodie et al., 2021), 162 adults with inadequately controlled focal seizures took CBDV or placebo as add-on therapy, titrated to 800 mg twice daily. CBDV did not outperform placebo. Seizure frequency fell 40.5% on CBDV and 37.7% on placebo (p = 0.648), and the primary efficacy endpoint was not met.
CBDV also produced substantially more adverse effects than placebo. Treatment-emergent adverse events were reported by 72.8% of the CBDV group against 48.1% on placebo. The three most common were diarrhoea, nausea and somnolence. Serious adverse events were uncommon in both arms: 3.7% on CBDV against 1.2% on placebo. The trial reported little or no effect on vital signs, physical examination or ECG. (Brodie et al., 2021, Cannabis Cannabinoid Res 6(6):528-536, PMID 33998885, trial registration NCT02365610.)
Read the two halves as one finding; we never print either alone. An adverse-event profile on its own invites the obvious assumption: this is what a working drug costs. In fact it is what CBDV cost the people who took it while not separating from placebo. Put together, the strongest evidence anyone has produced shows a cost with no measured benefit to set against it.
Verified against its PubMed record and cited in prose. The paper has yet to become a graded entry in the CBG Atlas registry, so it stays ungraded here. Disclosed interest: this is a sponsor study. The authors are affiliated with GW Research Ltd and Greenwich Biosciences, Inc.
If one CBDV finding sticks, make it this one. In the Phase 2 trial, alanine or aspartate aminotransferase rose above three times the upper limit of normal in three participants taking CBDV, two of whom discontinued as a result, against one participant on placebo. None met the criteria for a potential Hy's Law case, the pattern regulators treat as a marker of serious drug-induced liver injury. (Brodie et al., 2021, PMID 33998885.)
A second, entirely separate study saw the same organ system respond. In an open-label Phase 1 study in five girls with Rett syndrome and drug-resistant epilepsy, a transient transaminase rise, smaller and staying below one and a half times the upper limit of normal, prompted a dose reduction. (Hurley et al., 2022, Epilepsia 63(7):1736-1747, PMID 35364618.)
Two independent research groups, working with different populations and designs, saw the same signal. None of it amounts to a diagnosis or shows that CBDV damages livers: the numbers are small, most participants were unaffected, and nobody has characterised any of it over the long term. What it does justify is treating CBDV as a research-stage compound and not a benign ingredient. Anyone with liver disease, or taking a medicine that is watched for liver effects, should raise a CBDV product with a clinician before taking it, not after.
Verified against their PubMed records and cited in prose. Neither paper is yet a graded entry in the CBG Atlas registry, so neither carries an evidence grade here.
In that same open-label study (five participants, no control arm, no blinding, no randomisation, doses up to 10 mg/kg/day), the EEG worsened in two of the five. Spike-wave activity doubled in one participant and rose more than 500-fold in another, with a rhythm the investigators considered likely ictal.
The paper reports this inconsistently, and we cannot resolve it for you. Its abstract summary line records no significant change in EEG; its Results section reports the worsening described above. Both readings stand, and neither wins. The published record leaves the authors' intent unclear, and quietly picking one, especially the reassuring one, would hide a discrepancy readers are entitled to see. If this matters to a decision you are making, read the paper itself. (Hurley et al., 2022, PMID 35364618.)
The design cuts both ways. With five participants and no control arm, the study cannot attribute any change to the drug: not the worsening, nor the seizure reduction it also reported. It was built as a tolerability and pharmacokinetic study, and attribution lies beyond its design.
Verified against its PubMed record and cited in prose. The paper has yet to become a graded entry in the CBG Atlas registry, so it stays ungraded here. Disclosed interest: the declared conflicts of interest are “none”, but GW Pharmaceuticals supplied the study drug and set the dose ceiling. That relationship is worth naming even though the declaration does not.
In laboratory assays, CBDV inhibited CYP2C19 and CYP1A1, two of the enzyme systems the liver uses to clear many medicines. Know what those studies were before you weigh the finding. Both are papers about cannabidiol, in which CBDV is one of several structurally related comparator compounds used to work out which part of the CBD molecule does the inhibiting. In the CYP2C19 work CBDV was slightly less potent than CBD. Beyond that qualitative comparison, the potency figures stay in the papers. (Jiang et al., 2013, PMID 23318708; Yamaori et al., 2013, PMID 23811569.)
CYP1A1, not CYP1A2. They are different enzymes, and mixing them up is a real error that circulates in secondary write-ups. No published CBDV data exists for CYP1A2, CYP2B6 or CYP2C9, so those three stay blank, and a blank is no reassurance. They sit in the same “no primary evidence” state as the gaps set out on the safety page under what we don't know.
Both halves of this matter, and the second matters more. An enzyme inhibited in a test tube is a signal worth acting on cautiously, and not a demonstrated interaction in a person. No CBDV drug-interaction study in people has been published, so the practical size of the effect, including whether it moves the blood level of anything you actually take, is unknown. The stakes run highest for anyone on antiseizure polypharmacy, or on any medicine with a narrow safe range. A pharmacist can check your specific list against CYP2C19. We cannot, and a reference page should not try.
Verified against their PubMed records and cited in prose. Neither paper is yet a graded entry in the CBG Atlas registry, so neither carries an evidence grade here. Both are in vitro enzyme studies in which CBDV was a comparator, not the subject. Read them as a reason for caution, not as a measured interaction.
Nothing on this page supports stopping, reducing or replacing a prescribed antiseizure medicine, or any other prescribed medicine, with CBDV. CBDV is not an approved medicine in any jurisdiction, for any indication, and in the trial that tested it for seizures it went on top of existing antiseizure medication as an add-on, where it did not beat placebo. Changes to epilepsy treatment belong with the clinician managing it; stopping an antiseizure medicine without one is dangerous in its own right. This is educational information, not medical advice.
A CBDV food-effect figure. A widely repeated claim says a high-fat meal multiplies CBDV exposure several times over. No published paper reports it; it traces to a trial document, and a number without a published source to check it against stays off this site. The food-effect section of the safety page is about CBG (Story 2024) and does not extend to CBDV, which has no published food-effect study of its own.
Two registered trials, cited as though they produced results. They did not. Both were terminated with a handful of participants between them, which leaves nothing to say about safety or effect. Where the reason for stopping can't be verified, it goes unstated: a plausible cause pinned to an unverified record would be a fabricated fact. Their status is set out on the CBDV pillar.
Phase 2 RCT · in people · primary endpoint missed
Phase 1 · open-label, non-randomised, uncontrolled · n = 5
In vitro enzyme assay · CBDV as comparator
In vitro enzyme assay · CBDV as comparator
Regulatory & testing status · not an evidence claim
The four sources from this section, plus the paper behind the anti-doping section, which measured CBG and CBDV in the same study. All are real, published and checkable, and all sit outside the CBG Atlas registry, so they are cited in prose and kept out of the study feeds. Under each title sits its study design, the thing that limits it, and never an evidence grade; every grade on this site comes from our evidence registry.
Informational only, not medical advice. CBG Atlas is a scientific reference. Nothing here diagnoses, treats, cures or prevents any disease. Every claim on the page carries the grade of the evidence behind it, and the grade sets the words the claim may use. How we grade evidence.
Cardiovascular note. CBG is a potent α2-adrenoceptor agonist in vitro, and α2 agonism can lower blood pressure. Anyone taking blood-pressure or other cardiovascular medication should consult a clinician before use. This is educational information, not medical advice.
Funding and independence. Peregrine Biopharma funds the platform and holds no editorial authority.
Report a safety event →Seven compounds, each with its own monograph. The line under each one is what the verified registry actually holds for it — including where that is nothing yet.
The mother cannabinoid. CBGa decarboxylates to CBG, and both occur in the plant. The three synthases act on CBGa, the acid, branching it into THC, CBD and CBC. CBG carries more evidence than any other compound on the platform.
The acid CBG comes from, and the shared substrate the three branch synthases compete for. Heat decarboxylates it to CBG.
The propyl (varin) analogue of CBG, with a three-carbon side chain in place of five.
One of the three branches off the shared CBGA substrate, and a non-intoxicating one.
Forms as THC ages and oxidises, so it builds up in stored material rather than being made by the plant directly.
THC's propyl analogue, which in laboratory work behaves differently from THC at its receptors.
Its acid or neutral form
Its varin or pentyl analogue