The propyl homolog of CBG — the same cannabigerol scaffold built with a shorter three-carbon side chain. CBGV has been tested: in cell assays, and in mice. It has never been tested in a person. Everything below holds that line.
Cannabis builds two parallel cannabinoid series: the common pentyl series (five-carbon side chain) and a minor varin series (three-carbon side chain). CBGV is the varin-series counterpart of CBG — same geranyl core, shorter tail. Its acid, CBGVA, is the varin analog of CBGa, and decarboxylation yields neutral CBGV. That relationship is established chemistry; it is not a claim about effects.
A first-class reference is as clear about its limits as its knowledge. Here is the honest line for CBGV — established on the left, not-yet-established on the right.
CBGV has been studied. It has been put through receptor and ion-channel screens in cells, and it has been given to mice. What has never happened is a study of CBGV in a person: no trial of its effects, and no dedicated human pharmacokinetic or dose-ranging study of CBGV isolate. Separately, none of that preclinical work is a graded record in the gated registry — so it is cited below in prose, with the disclosure attached, and it carries no evidence grade here. Two different absences, named separately, because they mean different things.
Four published studies that tested CBGV by name. Every one is cells or animals; not one involved a person. Each entry leads with what was actually tested — species and preparation — because that is where most misreadings of this literature begin.
These papers are real, checkable, and not graded entries in the CBG Atlas registry. The registry's gated pipeline has not ingested them, so they carry no rung on our evidence ladder and nothing on this page is asserted on their authority. They are disclosed here so the scope of the answer is honest — the same treatment the CBG monograph gives the published human pharmacokinetic work it cannot grade. If and when they enter the registry through the gated pipeline, they will appear graded and cited like every other record.
What was actually tested: Human CB1 and CB2 receptors expressed in a laboratory cell system (heterologous expression). Cells in a dish — not people, and not an animal.
Across four different functional read-outs, every phytocannabinoid tested behaved agonist-like on its own but as an inverse agonist when a selective receptor agonist was already present. Of the compounds screened, “CBGV displayed enhanced potency in many of the functional outputs”, and the signalling was biased — which read-out a compound drove correlated with how it bound. This describes receptor behaviour in a controlled assay. It is not a measured effect in a person, and it supports no claim about what CBGV does in a body.
Read it with this: Conflict of interest: two of the authors are employed by Phytoplant Research S.L., a cannabinoid supplier. The result is disclosed with that affiliation attached rather than presented as neutral.
What was actually tested: Human TRPV1 in a transfected-cell calcium assay.
CBGV both stimulated and then desensitised human TRPV1 — one of the very few CBGV observations made on a human receptor rather than a rodent one. Desensitising a channel means the second exposure produces less response than the first; it is a property of the assay, not a described benefit.
Registry status: This paper IS a gated-registry record. But the finding the registry grades for it is the CBG one — TRPV1/TRPV2 desensitiser, TRPM8 antagonist. The CBGV observation above is read from the same publication and is NOT separately graded, so it is disclosed here in prose and carries no evidence grade.
What was actually tested: RAT recombinant TRPV3 and TRPV4 channels expressed in HEK-293 cells. Rat channels, not human ones, and not a whole animal.
CBGV and CBGA “were significantly more efficacious at desensitizing this channel [TRPV3] to the action of carvacrol than at activating it”, and the same pattern held at TRPV4, where “CBGA, CBGV, cannabinol and cannabigerol were significantly more efficacious at desensitizing this channel to the action of 4α-PDD than at activating it”. In plain terms: in this assay CBGV tended to quieten these channels rather than switch them on.
Read it with this: Published 2011, not 2012 — an external summary of this work carried the wrong year. And the species matters: a rat channel result does not establish the same behaviour at the human channel.
What was actually tested: Laboratory-synthesised side-chain variants of CBG — CBGV among them — tested on colorectal cancer cells in vitro and in a mouse model of chemotherapy-induced neuropathic pain.
All the side-chain lengths reduced chemotherapy-induced neuropathic pain in mice to a similar degree. The shorter chains — CBGV among them — were better at reducing colorectal cancer cell viability in the dish. Two limits are load-bearing: cell viability in a well is not a tumour responding in a patient, and a chemotherapy-induced pain model in mice is not a pain outcome in a person. This is a structure-activity observation, not evidence of benefit.
Read it with this: Penn State College of Medicine; no industry affiliation is declared on the author list. Compare with the glioblastoma caution below — the two in-vitro cancer-cell results do not point the same way.
A single 2021 mouse study reports a result for CBGV and a different result for CBGVA, its acid. They are not interchangeable, and the difference is the entire point — so they are set out side by side, in separate columns, and neither is summarised without the other.
| Property | CBGV — the neutral compound | CBGVA — the acid, a different molecule |
|---|---|---|
| What it is | Cannabigerovarin — the neutral compound this page is about | Cannabigerovarinic acid — a different molecule: the acid precursor CBGV is made from |
| In the Anderson 2021 mouse seizure screen | No effect on thresholds for hyperthermia-induced seizures at the single dose tested (100 mg/kg, intraperitoneal, given as a suspension) | One of three acids the same screen identified as having anticonvulsant properties (with CBGA and CBDVA) |
| The most that supports | “No effect at the dose tested.” One dose, one model, one formulation — a suspension, which limits how much compound reaches the circulation. It is not a finding that CBGV is inactive. | A preclinical signal in one mouse screen — in a paper whose lead compound, CBGA, was anticonvulsant in one test and PROCONVULSANT in another. The authors' own conclusion is that liabilities would need to be overcome. |
| Does the result carry across? | No. A finding about the acid is not a finding about the neutral form — they are different molecules with different handling in the body. | No. And neither column is a claim about either molecule in a person. |
| Human evidence | None published | None published |
Reading down the left column: at the one dose that was tried, in the one model that was used, CBGV changed nothing. That is “no effect at the dose tested” — it is not a finding that CBGV is inactive, and it is certainly not a finding that CBGV is active. The compound was given as a suspension, which limits how much of it reaches the circulation at all. Reading down the right column: the result there belongs to a different molecule and does not transfer left. Neither column is a claim about either compound in a human being, and CBG Atlas asserts no seizure-related property for CBGV or for CBGVA. This is educational information, not medical advice.
What was actually tested: Mouse models of epilepsy — a phytocannabinoid screen against seizure thresholds.
The source of both columns of the table above. Its title names the divergence: the same paper reports a compound that was anticonvulsant in one test and proconvulsant in another. Read the table, not this line, for what it says about CBGV and CBGVA.
Read it with this: ⚠ Do not quote the CBGV result and the CBGVA result apart from one another. Separated, either half misleads.
What was actually tested: Mouse intraperitoneal pharmacokinetics of six phytocannabinoid ACIDS, CBGVA among them. Animal only, and about the acid — not about CBGV.
CBGVA's pharmacokinetics were characterised alongside five other phytocannabinoid acids. Brain penetration of the acids AS A CLASS was low. That is the whole of what this paper supports about CBGVA here.
Read it with this: This is a study of the acid, not of CBGV, and it measures exposure in mice — not effect, and not in people. It does not give CBGV a pharmacokinetic profile.
The honest contrast between the propyl homolog and its well-studied pentyl parent:
| Property | CBGV | CBG |
|---|---|---|
| Relationship | Propyl (C₃) side-chain homolog | Pentyl (C₅) side chain |
| Molecular formula | C₁₉H₂₈O₂ · ≈ 288.4 | C₂₁H₃₂O₂ · 316.48 |
| Acidic precursor | CBGVA (varin series) | CBGa (pentyl series) |
| Biosynthetic role | Varin-series analog of the CBG branch point — parallel inferred from the verified pentyl pathway, not verified for CBGV | The pentyl “mother cannabinoid” |
| Characterized pharmacology | Included in a small number of in-vitro screens (CB1/CB2, TRPV1, TRPV3/TRPV4) — no graded registry record; the platform asserts no target profile | α2-adrenoceptor, 5-HT1A, CB1, TRP channels (in vitro) |
| Human evidence | None — no human study of CBGV has been published, for effects or for exposure | One small acute trial (Low) |
| Depth of the record | A handful of preclinical reports, largely one laboratory each, none independently replicated | A multi-study preclinical base plus one human trial |
| Intoxicating | Expected no — inferred, not verified | No |
No CBGV study is a graded record in the gated registry — the CBGV literature above is cited in prose and carries no grade. What the registry does hold nearby is the family biosynthesis that explains where CBGV comes from.
These studies characterize the pentyl-series biosynthesis of the cannabinoid family. The varin series that CBGV belongs to is understood to run in parallel — but these are not CBGV-specific, and the parallel is inference, not measurement.
Not an empty box — a clear specification of the evidence we are watching for. Any of it would enter through the gated pipeline and appear here, graded and cited.
Any study of CBGV in people — a tolerability and exposure study before anything else. No human pharmacokinetic, dose-ranging or efficacy work on CBGV isolate has been published, and that single absence is what caps everything else on this page.
The existing in-vitro results are essentially one laboratory each, and the CB1/CB2 work has authors employed by a cannabinoid supplier. Reproduction by unaffiliated groups would move these from observations to findings.
One laboratory report has CBGV reducing colorectal cancer cell viability; another has cannabinoids including CBGV blunting treatment-induced death in glioblastoma cells. Work that reconciles those — or shows they are answering different questions — matters more than another single-lab screen.
CBGV is expected to be non-intoxicating — inferred from the cannabigerol scaffold it shares with CBG, not verified for CBGV in our registry. Its safety profile is not characterized: there is no human safety, tolerability or drug-interaction data of any kind, and the preclinical work above was not designed to answer safety questions. Treat it as a research-stage compound. Any cardiovascular or interaction cautions elsewhere on CBG Atlas apply to CBG, not CBGV. This is educational information, not medical advice.
What was tested: Glioblastoma cells in the laboratory (Harvard / Dana-Farber). Cells in a dish — no animals, no patients. The direction of effect is why this sits in the safety section: treatment-induced cancer-cell death went down, not up. Cannabinoids including CBGV made glioblastoma cells less likely to die when exposed to chemotherapy and radiation, by lowering what the authors call apoptotic priming — how close a cell already sits to its own death threshold. Whether anything comparable happens in a person receiving cancer treatment is unknown and untested. This is not a reason to use CBGV in cancer care, and anyone undergoing cancer treatment should discuss any cannabinoid product with their oncology team. Cited by DOI because it is not yet indexed in PubMed, and it is an early accepted version that may change. Note also that it does not sit comfortably with the colorectal-cell result above: one report has CBGV reducing cancer-cell viability, another has it blunting treatment-induced cancer-cell death in a different tumour type. Two small, unreplicated laboratory findings pointing opposite ways is what an unsettled literature looks like — neither is a basis for use.
Cited by DOI alone. Off-registry, ungraded, and an early accepted version that may change before final publication.
Two lists, kept apart on purpose. First the registry-graded records this page relies on — family biosynthesis, not CBGV-specific. Then every CBGV-specific paper cited above, which is real, published and checkable, but ungraded here.
For grounded, graded reading, see CBGa and the CBG monograph.
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.
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 CBD, and the varin with the largest published human trial record.
The propyl analogue of THC, with receptor behaviour that differs from it in laboratory work.