The propyl homolog of CBD — the same cannabidiol scaffold with a shorter three-carbon side chain. CBDV is the rare minor cannabinoid that has been through a real clinical programme. Its primary endpoints were not met. This page publishes that record in full, because a reference that only carries the studies that worked is not a reference.
CBDV does not come from CBGVA by simply losing carbon dioxide — that route gives CBGV. CBDV sits one enzymatic step further along: CBDA synthase converts the varin mother acid CBGVA into CBDVA, and it is CBDVA that decarboxylates to neutral CBDV. Four nodes, not three, and the third one is where the two varin pillars part company.
One registry-graded record underwrites the branch above: Taura 1996, the purification and characterization of CBDA synthase. ⚠ Two limits travel with it. First, that record characterizes the pentyl reaction (CBGA → CBDA); the varin step (CBGVA → CBDVA) is its structural analog, which is an inference from that enzymology and not a measurement of it. Second, it may be cited for biosynthesis only — it says nothing whatever about what CBDV does in a body, and it is never used on this page for pharmacology.
A first-class reference is as clear about its limits as its knowledge. For most minor cannabinoids the limit is that nobody has looked. For CBDV it is the opposite — people looked, carefully, and the answer came back negative.
Read those two columns together. The left column says CBDV has been given to people in registered trials; the right column says none of those trials met its primary endpoint. Both are true, and collapsing either into the other is the mistake this page exists to prevent. An absence of evidence and a negative result are not the same thing — and on this page you are looking at the second one. We do not write a null as “mixed”, as “promising”, or as a call for more research; we write it as what it is.
Five published studies in which CBDV was given to human participants. They are ordered by weight of design, not by how encouraging they sound: the largest and most rigorous is first, and it is the most negative. Each entry leads with what was actually tested, and each carries a paired shows / does not show that cannot be separated from it.
These papers are real, checkable, and not graded entries in the CBG Atlas registry — the gated pipeline has not ingested them, so none carries a rung on our evidence ladder and nothing here is asserted on their authority. The badges below name each study's design (“Phase 2 RCT”), which is not a grade and is deliberately rendered in the neutral chip. If and when these enter the registry through the gated pipeline, they will appear graded and cited like every other record.
What was actually tested: A randomised, double-blind, placebo-controlled Phase 2 trial of CBDV as add-on therapy in 162 adults (81 CBDV, 81 placebo) with inadequately controlled focal seizures. After a 4-week baseline, participants titrated to 800 mg twice daily over 2 weeks, then held that dose for 6 weeks. Registered as NCT02365610. This is a real clinical trial in people — the strongest study design on this page.
The primary endpoint was not met. Focal seizure frequency fell by a similar amount in both arms — 40.5% on CBDV and 37.7% on placebo (p = 0.648). There were no differences between the arms for any seizure subtype, and no significant treatment difference on any secondary efficacy measure. The authors note the placebo response was high, which “may reflect the participants’ expectations of CBDV”. Treatment-emergent adverse events affected 72.8% of the CBDV group against 48.1% of the placebo group; the three most common were diarrhoea, nausea and somnolence.
What it shows: That CBDV was tested properly in adults with focal seizures, at a substantial dose, for long enough to show an effect — and did not separate from placebo.
What it does NOT show: Any anticonvulsant benefit. It is also not a reason to change or stop prescribed antiseizure medication, and it says nothing about CBD, which is a different molecule with its own approved medicine.
Read it with this: Sponsor study: authors are affiliated with GW Research Ltd and Greenwich Biosciences, Inc. ⚠ Safety signal, reported here because it is a safety signal and not a footnote: serum transaminase elevations above three times the upper limit of normal occurred in three participants taking CBDV — two of whom discontinued — and in one taking placebo. None met the criteria for potential Hy’s Law cases.
What was actually tested: A randomised, double-blind, placebo-controlled crossover trial in 32 patients with HIV-associated neuropathic pain. Each participant took CBDV 400 mg per day and placebo for 4 weeks each, in randomised order, separated by a 3-week washout. The primary endpoint was pain intensity on an 11-point numeric rating scale, recorded in a diary.
This is not merely a null. Mean pain intensity was 0.62 points HIGHER on CBDV than on placebo (P = 0.16; 95% CI −0.27 to 1.51) — the point estimate ran in the wrong direction, without reaching statistical significance. CBDV did not change the amount of additional pain medication taken, the character of the pain, or quality of life. 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”, and note that a larger trial would not be expected to change the conclusion because the differences observed are far from significance.
What it shows: That CBDV was tolerated in this population, and that it did not reduce HIV-associated neuropathic pain.
What it does NOT show: Any analgesic effect — and nothing here supports use for any other pain condition either. The authors offer a possible explanation rather than a conclusion: the failure “may be explained by a lack of CB receptor activation, as indicated by preclinical experiments”. That is their hedge, and it is kept as they wrote it.
Read it with this: Investigator-led (Charité Universitätsmedizin Berlin); one author declares an affiliation with SteriPharm Pharmazeutische Produkte. This result is stated here in the authors’ own terms rather than softened into “no significant difference”, because the direction of the point estimate is part of the finding.
What was actually tested: Five girls with a pathogenic MECP2 variant and drug-resistant epilepsy, given CBDV oral solution titrated to 10 mg/kg/day. ⚠ This design carries no control arm, no blinding and no randomisation, and the cohort is five children. It was built to measure safety, tolerability and the pharmacokinetics of CBDV and its 7-OH and 7-COOH metabolites — not to establish efficacy.
The dose was reached by all five children and was reported as safe and well tolerated; hypersomnolence and drooling were judged related to CBDV. ⚠ THE PAPER DISAGREES WITH ITSELF ON THE SEIZURE FIGURE: the abstract reports a median 79% reduction in monthly seizure frequency, while the Results and Table 3 report 82%. CBG Atlas therefore does not carry either number as a citable result — printing one silently would hide a discrepancy the reader is entitled to see. In any case, an uncontrolled reduction in five children cannot be separated from the high placebo response the same compound’s controlled trial documented.
What it shows: That 10 mg/kg/day was tolerated in a very small paediatric cohort, and what CBDV and its metabolites do pharmacokinetically in children.
What it does NOT show: Anticonvulsant efficacy. With no control arm and five participants, no seizure-frequency change from this study can be attributed to the drug.
Read it with this: ⚠ TWO SIGNALS RUN AGAINST THE HEADLINE. First, 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 — even though the abstract’s summary sentence records no significant EEG change. Second, a transient rise in liver transaminases prompted a dose reduction, echoing the Phase 2 signal above. On funding: the declared conflicts of interest are “none”, but GW supplied the study drug and set the dose ceiling, which is a relationship worth naming.
What was actually tested: Resting-state functional MRI in 28 MEN — 15 neurotypical, 13 autistic — 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. ⚠ Men only: this is not a study of “adults”, and the authors name the restriction as a limit on generalisability. Registered as NCT03537950, retrospectively.
Compared with the neurotypical participants, the 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 reduced the HYPERconnectivity toward the neurotypical range. It did not change the ventral-striatal HYPOconnectivity — that half of the difference was untouched, and reporting the reduction without it would overstate what the drug did. 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. A connectivity measure is an imaging biomarker, not a clinical endpoint, and the authors say explicitly that whether modulating it changes symptoms is still an open question.
Read it with this: Registered retrospectively (May 2018), which weakens the guarantee that the analysis was pre-specified. Read alongside Pretzsch 2019 below — the same group, the same one-dose paradigm, and a set of partial nulls that must travel with the positives.
What was actually tested: Magnetic resonance spectroscopy in 34 men (17 autistic, 17 not), in a repeated-measures, double-blind, randomised-order crossover design, comparing placebo with 600 mg CBDV. Two brain regions were measured: the dorsomedial prefrontal cortex and the left basal ganglia. Men only, one dose, sessions at least 13 days apart.
⚠ THE NULLS ARE MOST OF THIS RESULT AND SHIP WITH IT. CBDV significantly raised Glx (glutamate + glutamine) in the basal ganglia of both groups. It had NO significant effect on Glx in the dorsomedial prefrontal cortex, and NO significant effect on GABA+ in EITHER region. So of the four region-by-metabolite comparisons the study made, one moved and three did not. Within the autistic group, the size of the basal-ganglia shift correlated negatively with each individual’s starting level — the response was not uniform across people.
What it shows: That one dose of CBDV measurably shifts one excitatory metabolite in one brain region, and that the size of that shift depends on where a person starts.
What it does NOT show: A GABA effect, a prefrontal effect, or any behavioural or clinical effect. This is brain chemistry measured in a scanner two hours after a dose; the authors call for studies of whether it corresponds to anything a person experiences.
Read it with this: Reporting only the basal-ganglia increase — the way this study is usually summarised — is selective reporting. The three null comparisons are printed above for that reason.
The autism-related CBDV work is usually summarised by its positive halves. Both papers are mostly nulls. Here they are side by side, with the partial nulls in their own row so they cannot be dropped from a summary.
| Property | Pretzsch 2019 — brain chemistry (MRS) | Pretzsch 2021 — brain connectivity (fMRI) |
|---|---|---|
| What was measured | Brain chemistry — glutamate (Glx) and GABA+ by magnetic resonance spectroscopy, in two regions | Brain wiring — resting-state functional connectivity of the striatum |
| Who was studied | 34 men (17 autistic, 17 not), one dose of 600 mg vs placebo, crossover | 28 men (13 autistic, 15 not), one dose of 600 mg vs placebo, repeated measures |
| What moved | Glx rose in the basal ganglia, in both groups | Striatal HYPERconnectivity in the autistic group came down toward the neurotypical range |
| What did NOT move | No significant Glx effect in the dorsomedial prefrontal cortex. No significant GABA+ effect in either region. Three of four comparisons were null. | Ventral-striatal HYPOconnectivity — the other half of the group difference — was unchanged. |
| What neither is | Not a symptom, not a behaviour, not an outcome. A metabolite level in a scanner two hours after one dose. | Not a symptom, not a behaviour, not an outcome. A connectivity measure the authors call preliminary proof of concept from a small pilot. |
| Generalisability | Men only. The authors do not extend the result to women or to children. | Men only, and registered retrospectively. The authors name the restricted sample as a limit. |
Both columns describe imaging biomarkers: a metabolite concentration and a connectivity measure, recorded in a scanner a couple of hours after one dose, in men. Neither column contains a symptom, a behaviour or an outcome, and the authors of both papers say so themselves — “preliminary proof of concept” from a “small pilot study”. A biomarker that moves is a reason to run a trial, not a result from one. CBG Atlas asserts no effect of CBDV on autism or on any of its features. This is educational information, not medical advice.
Laboratory work on how CBDV might act. Mechanism detail is researcher-tier on this platform; switch to Researcher depth for the cited record.
In plain terms: in a dish, CBDV switches on and then quietens a family of sensory ion channels, and it damps abnormal electrical bursting in slices of rat brain. Then the same researchers ran the control that would prove the channel was responsible — and it came back negative. So the most-cited explanation of how CBDV might work is one its own source paper argues against. Switch to Researcher depth for the cited detail.
What was actually tested: Patch-clamp recordings in transfected HEK293 cells, plus multielectrode-array recordings from rat hippocampal brain slices bathed in a magnesium-free solution to provoke epileptiform activity. Cells and rodent tissue — no animals dosed, and no people.
CBD and CBDV activated and then rapidly desensitised TRPV1, and also TRPV2 and TRPA1. In the brain-slice model CBDV reduced the amplitude and duration of epileptiform bursts. ⚠ AND THEN THE PAPER UNDERCUT ITS OWN HYPOTHESIS: the selective TRPV1 antagonist IRTX reversed capsaicin's effect on burst amplitude but did NOT reverse CBDV's. The authors' own conclusion is 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 a dish, and that it damps epileptiform bursting in rodent brain slices.
What it does NOT show: That TRPV1 is the mechanism — the paper's own antagonist experiment argues against it. And it does not show anything about seizures in a person: the controlled trial that asked that question in people is Brodie 2021, and it was null.
Read it with this: ⚠ DO NOT EXTEND THIS TARGET LIST FROM THE DE PETROCELLIS PAPERS. 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. Attributing TRPV1, TRPA1 or TRPM8 to CBDV from either would be a miscitation.
A circulating summary table credits CBDV with TRPV1, TRPA1 and TRPM8 activity on the authority of De Petrocellis 2011 (PMID 21175579). That paper names CBDV for DAGLα inhibition and for TRPV2 by inclusion, and CBDV is explicitly absent from its TRPV1, TRPA1 and TRPM8 lists. A second 2011 paper (PMID 21726418) covers TRPV3 and TRPV4, where CBDV stimulated TRPV4 only. The TRPV1 / TRPV2 / TRPA1 observation on this page rests on Iannotti 2014 and travels with that paper's own refutation. A real identifier attached to the wrong finding passes every existence check — which is exactly why it is named here.
A compound that did not beat placebo on efficacy still produced more adverse events than placebo. Every signal below is tied to the study it came from.
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 — against one on placebo; none met the criteria for potential Hy's Law cases (Brodie 2021, PMID 33998885). In the Rett syndrome study, a transient transaminase rise prompted a dose reduction (Hurley 2022, PMID 35364618). Two studies, the same signal.
72.8% of the CBDV group reported at least one treatment-emergent adverse event, against 48.1% on placebo; the three most common were diarrhoea, nausea and somnolence. Serious adverse events were uncommon in both arms (Brodie 2021, PMID 33998885). A compound that did not beat placebo on efficacy did produce more side effects than placebo.
Spike-wave activity doubled in one child and rose more than 500-fold in another, with a rhythm considered likely ictal — in an open-label study of five children whose summary reported a seizure reduction (Hurley 2022, PMID 35364618). This is why an uncontrolled headline figure is not treated as evidence here.
CBDV inhibited CYP2C19 (Jiang 2013, PMID 23318708) and CYP1A1 (Yamaori 2013, PMID 23811569) in laboratory enzyme assays, in both cases somewhat less potently than CBD. ⚠ CYP1A1, not CYP1A2 — and there is no published CBDV data for CYP1A2, CYP2B6 or CYP2C9, so nothing is claimed about them. 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.
CBDV was tested as ADD-ON therapy 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.
CBDV is prohibited by the World Anti-Doping Agency — CBD is the exempt cannabinoid, and CBDV is not exempt. After 10 weeks of daily use of a broad-spectrum CBD product, CBDV was detected in 68% of pre-exercise and 84% of post-exercise urine samples (Gillham 2025, PMID 40920736). How much CBDV that product contained is not reported in the source and is not stated here. Regulatory and testing status, not a health claim.
Two registered CBDV trials are routinely cited as though they had produced results. They did not — both were terminated, with a handful of participants between them, and neither supports any statement about effect: NCT03848481 (CBDV in Prader-Willi syndrome) — TERMINATED, with 6 participants enrolled. Not completed, and it supports no efficacy statement. NCT03849456 (CBDV in autism spectrum disorder (paediatric)) — TERMINATED, with 1 participant enrolled. The reason for termination is unverified and is deliberately not stated here. It supports no efficacy statement. Where a termination reason is not verifiable, none is stated: a plausible-sounding cause attached to an unverified record is a fabricated fact, not a helpful gloss.
What was actually tested: Human liver microsomes and recombinant CYP2C19 in the test tube. The study is about CBD; CBDV appears as one of several structurally related comparator compounds used to work out which part of the CBD molecule does the inhibiting.
CBDV inhibited CYP2C19 in this assay, slightly less potently than CBD. Potency values are not reproduced on this page — they are researcher-tier figures and this is a consumer surface.
What it shows: That CBDV can inhibit a major drug-metabolising enzyme in a laboratory preparation.
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 this is unknown.
What was actually tested: Recombinant human CYP1A1 — ⚠ CYP1A1, not CYP1A2. Again a CBD structure-activity study, with CBDV as one comparator among several.
CBDV inhibited CYP1A1 activity, less potently than CBD. Potency values are not reproduced here.
What it shows: That CBDV inhibits CYP1A1 in a recombinant enzyme preparation.
What it does NOT show: Anything about CYP1A2, CYP2B6 or CYP2C9 — no published CBDV data exists for those enzymes — and nothing about what happens in a person.
What was actually tested: Thirty-six healthy adults took a broad-spectrum CBD product or a matched placebo daily for 10 weeks, then completed a 90-minute bout of moderate-intensity exercise. Blood and urine were sampled before supplementation and before and after exercise.
CBDV was detected in 68% of pre-exercise urine samples and 84% of post-exercise samples. Urinary concentrations rose from before to after exercise. Nothing was detectable at baseline. The authors conclude that athletes should avoid broad-spectrum CBD products because of the anti-doping risk. ⚠ HOW MUCH CBDV THE PRODUCT CONTAINED IS NOT IN THE SOURCE — needs full text. The abstract describes the 150 mg/day product as containing trace concentrations of CBG, and says nothing about its CBDV content. What a product holds and what appears in urine are two separate facts; only the second one is published here.
What it shows: That CBDV from a broad-spectrum consumer CBD product becomes detectable in urine with repeated daily use, and that exercise raises the measured concentration.
What it does NOT show: Anything about effects, benefit or harm. This is detection and regulatory status. Check the current WADA Prohibited List and your product's certificate of analysis.
CBDV has no approved use in any jurisdiction and is not a substitute for prescribed antiseizure medication — in the trial that tested it for seizures it was given on top of existing medication, and it did not beat 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.
The likeliest misreading of this page is that CBDV inherits CBD's standing because the names and the scaffolds are close. It does not. Three columns, so the difference is structural rather than rhetorical — CBD and CBGV are reference chemistry here, not pillars of this page.
| 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. ⚠ Neither efficacy trial met its primary endpoint, and the two imaging trials had no clinical endpoint at all. (A fifth study, in Rett syndrome, was open-label with no control arm.) | None published, for effects or for 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; nothing in people |
| Does the neighbouring column transfer? | — | NO. CBDV is not CBD and does not inherit CBD's clinical record. They are different molecules, tested separately, with different results. | NO. A varin side chain is a shared structural feature, not shared evidence. |
CBD's clinical record does not transfer to CBDV. There is a prescription medicine containing purified CBD, approved for specific rare seizure disorders. There is no approved CBDV medicine anywhere, and the trial that tested CBDV for seizures did not separate from placebo. Two molecules, tested separately, with different results — and a shared side-chain family is a structural fact, not shared evidence.
The consumer question corpus for CBDV, kept on this page rather than moved elsewhere. It answers the practical questions the evidence sections above do not: legality, product labelling, drug testing, and what CBDV is and is not.
42 questions are answered here. 22 carry a verified grade on the six-rung evidence ladder. 5 are marked with an evidence state rather than a rung — most often no primary evidence, which means our registry holds nothing on that question. That is not the same claim as not supported, and we do not render it as one. The remaining 15 carry an author qualifier that is not yet part of the controlled vocabulary, so they are shown without a grade chip rather than with a guessed one — catalogue in progress.
CBDV (cannabidivarin) is a non-intoxicating minor cannabinoid found in cannabis and hemp — the propyl homolog of CBD, meaning it shares CBD's structure with a shorter three-carbon side chain. First isolated in 1969, it is one of the earliest-characterized "varin" cannabinoids.
CBDV stands for cannabidivarin, and the name is pure chemistry: "cannabidi-" ties it to cannabidiol (CBD), and "-varin" marks the propyl (three-carbon) side chain that replaces CBD's pentyl (five-carbon) chain. Its formula is C₁₉H₂₆O₂ (molecular weight 286.41), CAS number 24274-48-4. That identity is Established; the name says nothing about what CBDV does in a person.
CBDV comes from the cannabis plant, especially low-THC, propyl-rich ("varin") chemotypes such as certain hemp and indica landraces. The plant builds it on the varin branch of cannabinoid biosynthesis: the acid CBDVA forms, then heat converts it to CBDV. It is the propyl homolog of CBD.
CBDV is natural — a phytocannabinoid the cannabis plant produces itself, first isolated from cannabis in 1969. It can also be made in a lab for research or manufacturing, but the CBDV in hemp products is typically plant-derived. It is non-intoxicating in either case.
No. CBDV is non-intoxicating — it does not produce the "high" associated with THC. Unlike THC, which activates the CB₁ receptor to cause intoxication, CBDV is not known to do so. Its verified activity in laboratory studies is at other targets, not CB₁ intoxication.
CBDV is non-intoxicating: it does not cause the intoxication or impairment THC does. "Psychoactive" is broader — any compound affecting the brain — and CBDV has not been shown in controlled human studies to alter mood or perception. Reported effects remain unestablished; it will not get you high.
There is no primary evidence describing what CBDV "feels like." CBDV has been given to people in trials, but subjective experience was never measured as an outcome in any of them, so nobody has actually asked this question. Because it is non-intoxicating, it should not produce a high. Any subjective effects some users report are anecdotal and not confirmed by clinical studies. Not medical advice.
CBDV's effect profile is not established. No study has measured whether CBDV is sedating, energizing, or neutral as an outcome. Somnolence was among the three most common adverse events reported in its Phase 2 trial (Brodie 2021), but an adverse-event count is a safety observation, not a characterised effect. Marketing or anecdotal reports may claim one or another; our evidence supports neither a sedation nor a stimulation claim. Not medical advice.
Legality depends on your jurisdiction, the product class (food, supplement, cosmetic), and its source and THC content — it is not a single global yes/no. In many places hemp-derived CBDV sits under novel-food or cannabis frameworks that are still evolving. Check your local law. This is informational, not legal advice.
Generally yes, with one important limit. In the US, cannabinoids derived from hemp containing ≤0.3% Δ⁹-THC (dry weight) are federally legal as hemp under the 2018 Farm Bill, and that can include CBDV. But the FDA has not approved CBDV as a food or supplement, so a lawful hemp derivative is not automatically a lawful food ingredient, and state laws vary. Not legal advice; verify current rules.
Not necessarily. Even where hemp-derived cannabinoids are federally legal, individual US states set their own rules — some restrict or ban specific hemp cannabinoids, novel forms, or intoxicating derivatives. CBDV's status can differ by state and change over time. Check your state's current law. This is not legal advice.
Broadly: in the UK and EU, extracted cannabinoids like CBDV fall under novel-food rules and generally require authorization before sale as food. In Canada, phytocannabinoids are regulated under the Cannabis Act. Rules vary and change; CBDV is not a free-market supplement in these regions. Not legal advice — verify officially.
No benefit has been established in people — and that is a finding, not a gap. CBDV has been through randomised controlled trials: a Phase 2 trial in adults with inadequately controlled focal seizures did not separate from placebo, and a crossover trial in HIV-associated neuropathic pain ran the other way, with pain scores numerically higher on CBDV (Brodie 2021; Eibach 2021). In laboratory research it inhibits the enzyme DAGLα and activates/desensitizes the TRPV2 ion channel (De Petrocellis 2011) — a mechanism in a dish, not a benefit in a person. Marketed benefits are not confirmed. Not medical advice.
Mainly research. CBDV has been given to people in registered clinical trials — for focal seizures, and for HIV-associated neuropathic pain — and neither trial met its primary efficacy endpoint (Brodie 2021; Eibach 2021). The remaining human studies are 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, and none is approved in any jurisdiction. Consumer products sell it as a minor cannabinoid. Not medical advice.
No — and this one was tested properly. In a Phase 2 randomised controlled trial, 162 adults with inadequately controlled focal seizures added CBDV to their existing medication, titrated to 800 mg twice daily: seizures fell in both arms — 40.5% on CBDV against 37.7% on placebo — with no significant difference on any seizure subtype or any secondary measure (Brodie 2021). Earlier animal work had reported anticonvulsant activity (Hill et al. 2012); the trial in people did not confirm it. That is graded Not-supported — tested, primary endpoint not met — and CBDV is not a substitute for prescribed antiseizure medication. Not medical advice.
Not established — and unlike seizures, autism has never been tested as a clinical question for CBDV. The two published human studies gave a single dose and scanned the brain (Pretzsch 2019; Pretzsch 2021), measuring scanner signals rather than symptoms, so no trial has asked whether CBDV changes anything a family would notice. That is an absence of testing, not a tested-and-null result: our registry holds no primary evidence either way. CBDV is not a therapy for autism. Not medical advice.
Yes — more than for most minor cannabinoids, and none of it established a benefit. A Phase 2 randomised controlled trial in 162 adults with inadequately controlled focal seizures did not separate from placebo on its primary endpoint, 40.5% against 37.7% (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). Trials exist; efficacy does not, and that is graded Not-supported. CBD's clinical record belongs to a different molecule and is not carried across. Not medical advice.
Yes, once — in an open-label study of five girls with Rett syndrome, with no control group. That paper reports two different seizure-reduction figures for the same cohort, and the EEG worsened in two of the five children (Hurley 2022). Two further single-dose brain-imaging studies in men measured scanner signals rather than symptoms (Pretzsch 2019; Pretzsch 2021). None of this is controlled efficacy evidence, so CBDV in Rett syndrome remains no primary evidence rather than a finding in either direction. Not medical advice.
Not fully established — and not benign by default. In the Phase 2 focal-seizure trial, 72.8% of people taking CBDV reported at least one treatment-emergent adverse event against 48.1% on placebo, most commonly diarrhoea, nausea and somnolence; serum transaminases rose above three times the upper limit of normal in three people taking CBDV, two of whom stopped treatment (Brodie 2021). A transient transaminase rise also prompted a dose reduction in the Rett syndrome study (Hurley 2022) — two studies, the same liver signal. Long-term and general consumer safety are catalogue in progress here. If you take medications or have health conditions, consult a clinician. Not medical advice.
Adverse effects have been recorded in trials, so this is not an empty file. In the Phase 2 focal-seizure trial the three most common treatment-emergent adverse events on CBDV were diarrhoea, nausea and somnolence, and 72.8% of that group reported at least one against 48.1% on placebo; liver transaminase elevations occurred in three participants, two of whom discontinued (Brodie 2021). A small open-label study saw a transient transaminase rise and EEG worsening in two of five children (Hurley 2022). What does not exist is a side-effect profile for consumer products at consumer amounts — that part is catalogue in progress, an absence of testing rather than a clean result. Consult a clinician about your situation. Not medical advice.
There is no established safe or maximum dose for CBDV, so "too much" cannot be defined from verified evidence. No standard consumer dosing guidelines exist. As with any cannabinoid, more is not necessarily better, and effects and safety vary by person and product. Consult a clinician. Not medical or dosing advice.
No drug-interaction study of CBDV has been done in people, so nothing is established about what happens in a body. What does exist is laboratory enzyme work: CBDV inhibited the drug-metabolising enzymes CYP2C19 (Jiang et al. 2013) and CYP1A1 (Yamaori et al. 2013) in the test tube — in both cases as a comparator compound in studies about CBD, and less potently than CBD. There is no published CBDV data at all for CYP1A2, CYP2B6 or CYP2C9, so we assert nothing about those. Anyone taking other medicines should consult a clinician or pharmacist before use. Not medical advice.
Standard workplace drug tests look for THC and its metabolite, not CBDV, so pure CBDV is not the target. Anti-doping testing is a different matter: CBDV is prohibited in sport by the World Anti-Doping Agency — CBD is the exempt cannabinoid and CBDV is not — and after ten weeks of a broad-spectrum CBD product it was detected in 68% of pre-exercise and 84% of post-exercise urine samples (Gillham et al. 2025). Full- or broad-spectrum hemp products can also contain trace THC, which could trigger a positive on a standard test. A product's true content depends on its lab test (COA). Not legal or medical advice.
CBDV is a distinct compound from THC and is non-intoxicating — CBDV itself is not THC. But a CBDV product may contain trace THC depending on its source and formulation: full-spectrum hemp products include small amounts, while isolates should not. Always check the certificate of analysis (COA). Not legal advice.
On a standard workplace test, pure CBDV should not, because those tests target THC. The real risk there is trace THC in some full- or broad-spectrum hemp products, which could cause a positive result. In sport the opposite applies: CBDV itself is on the prohibited list and has been detected in athletes' urine (Gillham et al. 2025), so a competing athlete should regard it as a risk in its own right. If this matters to you, choose a product with a COA confirming its content. Not legal or medical advice.
CBDV products are used much like other cannabinoids — commonly as oils or tinctures (held under the tongue), capsules, or within full-spectrum hemp extracts. Because there are no established dosing guidelines or verified human-use protocols for CBDV, we describe formats only and give no usage recommendation. Not medical or dosing advice.
CBDV is sold as a minor or "specialty" cannabinoid — most often in oils and tinctures, capsules, or as part of full- and broad-spectrum hemp extracts; occasionally as isolate. It is far rarer than CBD. Product quality and actual CBDV content vary, so a certificate of analysis (COA) matters.
There is no established dose for CBDV. No verified consumer dosing guidelines exist, and clinical-trial amounts were research protocols, not recommendations — we do not provide them as advice. Effects and safety vary by person and product. Consult a qualified clinician before use. This is not medical or dosing advice.
Onset and duration in consumer use are not established, and we do not publish figures we cannot confirm. CBDV's pharmacokinetics have been measured in people once: an open-label study in five girls with Rett syndrome tracked blood levels of CBDV and two of its breakdown products, 7-OH-CBDV and 7-COOH-CBDV (Hurley 2022) — five participants, no control group, and a clinical dose rather than a consumer one. In general, sublingual and inhaled routes tend to act sooner than swallowed ones. And "work" is the harder word here: the randomised trials that tested benefit did not find it, and consumer onset and duration remain catalogue in progress. Not medical advice.
CBDV is the propyl homolog of CBD: chemically identical except CBDV's side chain is two carbons shorter (three-carbon propyl vs CBD's five-carbon pentyl), giving CBDV the formula C₁₉H₂₆O₂ versus CBD's C₂₁H₃₀O₂. Both are non-intoxicating. CBD is far more studied; CBDV's effects are largely unestablished. Not medical advice.
CBDV and THC are very different. THC is intoxicating — it activates the CB₁ receptor to produce a "high." CBDV is non-intoxicating and does not. Structurally, CBDV is the propyl homolog of CBD, not THC. THC is extensively studied; CBDV's human effects are largely unestablished. Not medical advice.
Both CBDV and CBG are non-intoxicating cannabinoids, but they differ in structure and lineage: CBDV is the propyl homolog of CBD, while CBG (the "mother cannabinoid") derives from CBGA and has its own distinct receptor profile. Their verified activities differ, and neither has an established human benefit. Not medical advice.
Neither can be called "better" from verified evidence, because no trial has compared them head to head. CBD is much more researched, and there is an approved purified-CBD medicine for specific rare seizure disorders — a regulatory fact about a different molecule, which we do not extend to CBDV. CBDV has been through its own randomised trials, and they did not meet their primary endpoints. "Better" depends on undefined goals and lacks comparative human data. Not medical advice.
CBDV's molecular formula is C₁₉H₂₆O₂, with a molecular weight of 286.41 g/mol and CAS number 24274-48-4. Structurally it is cannabidiol (CBD) with a three-carbon propyl side chain in place of CBD's five-carbon pentyl chain — hence two fewer carbons and the "varin" designation.
CBDV is obtained from cannabis/hemp — especially propyl-rich ("varin") chemotypes — using standard cannabinoid extraction (for example CO₂ or solvent extraction) followed by purification. It can also form when its acid, CBDVA, is heated (decarboxylation). Because plant levels are usually low, CBDV is comparatively difficult and costly to produce.
CBDV is the "varin" (propyl) homolog of CBD — neither its precursor nor a breakdown product of CBD. It arises on its own biosynthetic branch: the plant makes the acid CBDVA, which decarboxylates to CBDV. So CBDV and CBD are structural siblings built by parallel pathways, not one from the other.
Yes. In the living plant CBDV exists mainly as its acid, CBDVA (cannabidivarinic acid, C₂₀H₂₆O₄, CAS 31932-13-5). Heat drives off carbon dioxide (decarboxylation), converting CBDVA to CBDV — a change reported as near-complete at about 130 °C for 30 minutes. So raw and heated products differ chemically.
CBDV is sold by some specialty hemp and cannabinoid retailers, usually online, as oils, isolates, or within broad/full-spectrum extracts. It is far less common than CBD. Availability and legality depend on your jurisdiction and product class. Choose sellers who provide third-party lab results (a COA). Not legal or purchasing advice.
CBDV occurs at low levels in most cannabis, concentrating mainly in specific propyl-rich ("varin") chemotypes, so sourcing and isolating it takes selective plants and extra purification. Limited demand and small-scale production add cost. That rarity is also why verifying real content with a certificate of analysis (COA) matters.
Look for a current certificate of analysis (COA) from an accredited third-party lab. It should list the actual CBDV content (matching the label), confirm THC is within legal limits, and screen for contaminants like pesticides, solvents, and heavy metals. No COA, or a mismatched one, is a red flag. Not purchasing advice.
That's your call, and here is what is checkable about CBDV. It is not an untested compound; it is a tested one that did not work, graded Not-supported. Two randomised controlled trials measured benefit — in focal seizures and in HIV-associated neuropathic pain — and neither met its primary endpoint (Brodie 2021; Eibach 2021), while adverse events were more common on CBDV than on placebo. Buying it means accepting that. If you proceed, prioritize lab-tested products and consult a clinician. Not medical or purchasing advice.
Look for: a current third-party COA confirming CBDV content and legal THC levels; contaminant screening (pesticides, heavy metals, solvents); a clear label matching the COA; transparent hemp sourcing; and no disease or "cure" claims (a legal red flag). Verify legality for your jurisdiction. Not medical, legal, or purchasing advice.
Not an empty box, and not a request for work that has already been done. A clear specification of the evidence that would move CBDV off a null — any of which would enter through the gated pipeline and appear here, graded and cited.
The Phase 2 focal-seizure trial did not, and the neuropathic-pain trial ran the wrong way. What would move CBDV off a null is a controlled trial, in a defined population, that beats placebo on a pre-specified clinical endpoint. Until one exists, no efficacy claim is available for any indication.
The two imaging studies show CBDV can shift brain chemistry and brain connectivity after one dose, in men, in a scanner. Nobody has shown that either shift corresponds to a change in symptoms — the authors say so themselves. Work linking the biomarker to a clinical outcome is the missing step.
Transaminase elevations appeared in two independent studies, and the interaction evidence is laboratory enzyme work in which CBDV was a comparator rather than the subject. Dedicated human safety and interaction studies — including CYP1A2, CYP2B6 and CYP2C9, for which no CBDV data exists at all — would let this page say something firmer than “uncharacterized”.
Two lists, kept apart on purpose. First the single registry-graded record this page relies on — biosynthesis, and not CBDV-specific. Then every CBDV-specific paper cited above: real, published, checkable, and ungraded here.
Phase 2 RCT · in people · primary endpoint not met
Randomised crossover trial · in people · endpoint not met
Phase 1 · open-label, non-randomised, no control · n = 5
Imaging biomarker · pilot · not a clinical endpoint
Imaging biomarker · partial nulls · not a clinical endpoint
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. Not completed, and it supports no efficacy statement. NCT03849456 — CBDV in autism spectrum disorder (paediatric): TERMINATED, with 1 participant enrolled. The reason for termination is unverified and is deliberately not stated here. It supports no efficacy statement.
For the other varin pillar see CBGV, for the family see the varin cannabinoids, and for the platform's deepest graded record see the CBG monograph. Peregrine Biopharma funds the platform and holds no editorial authority.
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 — it is CBGa that the three synthases branch into THC, CBD and CBC. The best-evidenced compound on this platform.
The acid CBG comes from, and the shared substrate the three branch synthases compete for. Decarboxylates to CBG with heat.
The propyl (varin) analogue of CBG — a three-carbon side chain instead of five.
Non-intoxicating, and one of the three branch products off the shared CBGA substrate.
Forms as THC ages and oxidises, so it accumulates in stored material rather than being made by the plant directly.
The propyl analogue of THC, with receptor behaviour that differs from it in laboratory work.