01 — The flagship
The mother cannabinoid
Everything begins with CBG.
CBG (cannabigerol) is the neutral form of CBGa, the acid the plant makes first and branches into THCA, CBDA and CBCA; CBGa decarboxylates to CBG, and both occur in the plant. grade: Established CBG is non-intoxicating, and in laboratory (in vitro) assays it behaves as an antagonist at the CB1 cannabinoid receptor (Cascio et al., 2010, PMID 20002104). study type: In vitro
Now CBG has shelf space of its own, and the controlled human research on what it does amounts to a few small trials. CBG Atlas reads that research and grades every claim against it, so you don't have to take the label's word.
Every claim sourced and graded21 PubMed-verified studiesEditorially independent
Pl. II — Cannabis sativa L.Follow THC, CBD or CBC back far enough and you arrive at the same acid, the one this plant makes first: CBGA. How one acid becomes the family, with its studies
Start reading
Three ways into the Atlas.
Frequently asked questions
Common questions about CBG.
The six questions people ask first, answered on the monograph and repeated here word for word, with the grade and the hedge kept inside each answer where an answer engine can't drop them.
Is CBG intoxicating?
No. CBG (cannabigerol) is non-intoxicating. In laboratory (in vitro) assays it behaves as an antagonist at the CB1 cannabinoid receptor, blocking it rather than switching it on (Cascio et al., 2010, PMID 20002104). That result is validated in vitro: receptor pharmacology from controlled lab assays, which carries no human clinical evidence grade and is not a measured clinical effect in people.
Why is CBG called the mother cannabinoid?
Because its acid form, cannabigerolic acid (CBGa), is the single precursor that three synthase enzymes convert into the THC, CBD and CBC lines. The name comes from that position in the plant's biosynthesis. It describes a family tree, and only a family tree.
Is CBG antibacterial?
So far, only in the lab and in mice. In laboratory (in vitro) tests and in a mouse infection model, CBG was active against methicillin-resistant Staphylococcus aureus (MRSA), acting on the bacterial membrane and on biofilms (Appendino et al., 2008, PMID 18681481; Farha et al., 2020, PMID 32017534). Both findings are preclinical. CBG has not been tested for this in humans, so the results are not evidence of benefit as an anti-infective. Evidence grade: Low.
Is there any human evidence for CBG?
Very little on effects. The one published human trial of CBG's effects on anxiety and stress was a double-blind, placebo-controlled crossover study that gave a single 20 mg oral dose to 34 healthy adults (Cuttler et al., 2024, PMID 39003387). Evidence grade: Low. One small acute study is a starting point, and it supports no treatment claim. More human CBG research is in print, and our registry leaves it ungraded. It goes beyond pharmacokinetics to studies that measured effects, among them a repeated-dose trial whose primary endpoint was null. A hand-kept list of those papers would go stale the moment the literature moved, so our safety page keeps the off-registry human record instead, with its disclosures.
Does CBG help with anxiety?
Not on current evidence. In the only human trial of CBG's effects on anxiety and stress, a one-time 20 mg oral dose was associated with lower self-reported anxiety and stress in healthy adults, who showed no intoxication or measurable impairment (Cuttler et al., 2024, PMID 39003387). The animal work tells a messier story. One study found no effect and another reported an anxiety-increasing effect, so the preclinical picture is mixed and leaves any benefit unconfirmed. Evidence grade: Low. Read the human result as an early signal; it does not show clinical efficacy.
Can CBG affect blood pressure?
This is the main safety caution on the platform. In vitro, CBG is a potent agonist at the α2-adrenoceptor (Cascio et al., 2010, PMID 20002104), and α2 agonism can lower blood pressure. Whether that produces a measurable change in people, and how large a change, is uncharacterized. Evidence grade: Hypothesized. Anyone taking blood-pressure or other cardiovascular medication should consult a clinician before use. This is educational information, not medical advice.
Latest research
The newest verified science.
The newest papers on CBG, its acid and its varin, each checked against PubMed, graded by how the study was run and traceable to source. The list updates itself as the library grows.
Study type: Animal · preclinical2026
Pharmacokinetic and pharmacodynamic properties of cannabigerol in male mice
Open in the library →
Study type: Human trial2024
Acute effects of cannabigerol on anxiety, stress, and mood: a double-blind, placebo-controlled, crossover, field trial
Open in the library →
Study type: Animal · preclinical2023
Cannabigerol modulates α-adrenoceptor and 5-HT1A receptor-mediated electrophysiological effects on dorsal raphe nucleus and locus coeruleus neurons and anxiety behavior in rat
Open in the library →
Sources verified·21 studies·updated 9 August 2026·How we check
What we don't know
The gap-map, condition by condition.
Across 10 tracked conditions, CBG has 0 with established or demonstrated human efficacy, 1 with any human data at all, and 1 with no primary evidence. The rest are preclinical or mechanistic only. This is the honest state of the evidence.
What the gap-map shows
Most references lead with their strongest page. The gap-map starts from the other end: every condition we track, including the ones with no primary study behind them, and what it would take to move each grade. Read it as an inventory of the science, and never as a list of things CBG treats.
The family
The compounds around CBG.
CBG doesn't travel alone. Its acid, its varin and THC's varin cousin each get a page held to the same standard, and where the research is thin, the page is short.
The cannabinoid family, in brief
Numerals count studies in our registry; a plain node is catalogue in progress. The whole family, mapped →
CBGa — the acid
Cannabigerolic acid
The acid the plant actually makes. Heat turns it into CBG; the plant's enzymes turn it into THCA, CBDA and CBCA. The chemistry is settled, while what it does in the body is still being catalogued.
CBGV — the varin
Cannabigerovarin
CBG with a shorter tail: three carbons on the side chain instead of five. Chemists know it well. It has been tested in cells and mice, never in people.
THCV — the propyl THC
Tetrahydrocannabivarin
THC's propyl homolog, sold as “diet weed”. The mouse study the appetite claim traces to reported no significant effect on food intake, and none of the popular claims made for it has been verified. Its receptor pharmacology rests on one verified review.
The origin
Why CBG is the mother cannabinoid.
The nickname sounds like marketing, but it's chemistry. Follow THC, CBD or CBC back far enough and you arrive at the same acid, CBGA. So this reference starts where the plant does.
Figure E · biosynthesis
The making of the mother cannabinoid
i
A single branch point
The plant's synthases all work on the same pool of CBGA, and the one doing the work decides which acid the flower builds up.
ii
Acid, then neutral
Raw flower is mostly acids. Heat and time knock a molecule of CO₂ off each one, turning THCA into THC, CBDA into CBD and CBCA into CBC, which is why the numbers on a COA move as material sits in storage.
iii
Why it matters
A claim about “CBG” can mean the acid, CBGA, or the neutral form, and they are different molecules. Before trusting any claim, check which one the study used.
Six grades, strongest first
- grade: grade: Established“is shown to”
- grade: grade: Demonstrated“has been shown to”
- grade: grade: Emerging“may · early evidence suggests”
- grade: grade: Low“limited evidence · unclear”
- grade: grade: Hypothesized“proposed mechanism”
- grade: grade: Not supported“evidence does not support”
Signature instrument
Where CBG may act.
Where in the body could CBG do something? Its receptor activity points to seven places. Open them up and, for most, the answer so far is a cell dish, a mouse, or nothing at all.
Original anatomical drawing, for orientation only. The claims it points to are written out in full beside it.
Body regionSelect to expand
Start with the strongest chemistry. CBG's most potent known action is at α2-adrenoceptors, and it also antagonises 5-HT1A receptors and acts on TRP channels. One small acute human trial in our registry has measured anxiety, stress and mood; the rest comes from laboratory or animal work.
Signals under study- Low
Anxiety & stress: one small, single-dose, placebo-controlled human trial (Cuttler 2024), held at Low because the dose was acute, the endpoints were self-reported, and two preclinical studies in our registry point the other way.
- Hypothesized
Mood: 5-HT1A antagonism is a plausible mechanism, but no human trial has measured it.
- Preclinical
Neuroinflammation: TRP-channel activity, seen only in cell and animal studies.
What the evidence does not establishWhether these receptor interactions produce a meaningful, measurable effect in people, and at what dose. Our registry's one human trial of CBG's effects measured a single acute dose in healthy volunteers, and only for anxiety and stress.
- Low
This is the most safety-relevant finding in our registry, and it is a mechanism. α2-adrenoceptor agonism can influence vascular tone; no study has measured a blood-pressure effect of CBG in a person.
Signals under study- Hypothesized
Blood pressure: plausible from the mechanism alone. The receptor activity was measured in the laboratory, and the direction and size of any human effect are uncharacterised.
What the evidence does not establishWhether CBG raises blood pressure in people, lowers it, or leaves it unchanged. If you take blood-pressure medication or have a cardiovascular condition, consult a clinician first.
- Hypothesized
CBG's most-cited preclinical signal comes from the gut. In a mouse model of colitis, CBG reduced inflammatory markers, and part of the effect was CB2-modulated. The result belongs to the mice and has not been shown in people.
Signals under study- Preclinical
Gut inflammation: CBG reduced colonic inflammation in a murine DNBS model (Borrelli 2013).
- Preclinical
Oxidative stress: CBG lowered nitric-oxide production in macrophages and the formation of reactive oxygen species in intestinal epithelial cells.
What the evidence does not establishAny effect on inflammatory bowel disease in people. Our registry contains no human study of CBG in any digestive condition.
- Preclinical
Two lines of evidence meet here: an anti-inflammatory signal measured in cells and mice, and antibacterial activity against MRSA characterised in vitro.
Signals under study- Preclinical
Inflammatory markers: effects on macrophage nitric oxide and oxidative balance, in cell and animal models.
- Preclinical
Antibacterial: activity against methicillin-resistant Staphylococcus aureus in vitro and in a mouse model of systemic infection. There are no human efficacy data.
What the evidence does not establishWhether CBG affects infection or inflammation in people. Activity against bacteria in a dish does not make CBG an antibiotic.
- Preclinical
Most topical hypotheses rest on two thermo-sensory channels, TRPV1 and TRPV2, which CBG activates and then rapidly desensitises. The channel behaviour has been characterised. The effect on skin has not.
Signals under study- No primary evidence
Skin inflammation: our registry holds no study of CBG in skin, in any model. The mechanism is real; the application is untested in our registry.
What the evidence does not establishAnything about CBG on human skin. The region is on the map because the receptors are there; no skin outcome has been studied.
- No primary evidence
Eye claims turn up often, and they open one of the clearest gaps in the record: our registry holds no primary study of CBG and intraocular pressure.
Signals under study- No primary evidence
Intraocular pressure: no verified study either way, which makes this an absence of data rather than a negative finding.
What the evidence does not establishWhether CBG affects intraocular pressure at all. Nothing in our registry supports claims that it does.
- No primary evidence
Joint claims are borrowed from the gut and immune work and have not been measured. Our registry holds no study that examines joints.
Signals under study- No primary evidence
Joint inflammation: inferred from anti-inflammatory activity measured in other tissues. An inference falls short of evidence, so the evidence here is graded as absent.
What the evidence does not establishAny effect on joint pain, stiffness or inflammation, in any species.
- No primary evidence
Three of seven regions hold no primary evidence at all. They earn their place on the map because CBG’s receptor targets sit there, and no study in our registry has measured an outcome in any of them.
Built to be trusted
Check our work yourself.
Hash-pinned snapshots
Trust, then check. Every published snapshot carries a SHA-256 registry hash (154671f50c4a…) and every study its own provenance hash, so you can download the snapshot and hold it up against what you read here.
Download & verify →Contradicting evidence, shown
Studies disagree, and a reference that hides the arguments is selling something. The gap-map counts the studies against each claim beside the studies for it, and calls a consensus only where one exists.
See the conflicts →Contractual independence
Peregrine Biopharma funds the platform and holds no editorial authority. That firewall is written into the funding agreement itself.
Read the standard →Corrections, published
We get things wrong. When we do, the correction records what the page said, what was wrong and when it was fixed, and then it stays on the record.
Read the corrections → Instruments
Pick the evidence up and turn it over.
Reading about a lab report is one thing. Taking one apart is another. These pages put the material in your hands: the family tree, a Definition: certificate of analysisGlossaryCertificate of Analysis (COA)grade: grade: EstablishedA Certificate of Analysis (COA) is the lab report that states what a product actually contains, ideally issued by an independent third-party laboratory. It reports the measured cannabinoid content (does it match the label?), the THC level (which bears on legality and drug testing), and screening for contaminants: pesticides, residual solvents, heavy metals and microbes.Read the full entry →, a label, the chemistry of heat and time, and the road a claim has to travel.
01 — The map
The cannabinoid family, mapped
Every route from the mother acids to the shelf: enzyme branches, heat, and the slow chemistry of ageing. Each compound coloured by how much of it our registry holds.
02 — The paperwork
Read a COA
A specimen certificate of analysis, line by line: the total-THC arithmetic, what “ND” means, and where a weak report hides its gaps.
03 — The label
Label Lab
Type a claim. See which kind it is, whether it carries a hedge, and what grade the record behind it holds. The same rules the site applies to its own answers.
04 — The chemistry
Heat, time and light
Why THCA flower is contested, why old product moves on a drug test, why aged stock carries CBN. An illustrative simulator, with its limits printed on it.
05 — The road
How a claim climbs
From a dish to a mouse to a trial to replication, with the real CBG claims placed where their evidence stops.
06 — The system
The endocannabinoid system, in motion
The system shown working, step by step in motion: a signal arriving, a messenger sent backwards to turn the sender down, the enzymes that end it, and where CBG’s laboratory record touches it, each step with its grade.
07 — The reading order
Paths by role
A formulator, a brand owner, a lab and a buyer each need a different seven pages. Each path ends with a short check of your own judgement.
Also: molecule pairs · the research timeline · the shelf vs the record
Who this is for
One directory for each kind of reader.
Written for the people who have to stand behind a claim: the formulator choosing an active, the brand owner signing off a label, the lab reading a COA, and the buyer who asks all three for proof. And for anyone who has heard of CBG and wants the record, gaps included. Each kind of reader gets a directory of its own. A supplier earns a place in it once someone can check its verification, and so far one is listed, the platform's own sponsor, disclosed as such. Listings are there to educate, not to endorse, and until the lists fill up these pages say what to require of any seller.
ConsumerChoosing a product
The front of the jar makes the promise. The certificate of analysis has to back it up, and here is what it must show.
See the criteria →
FormulatorSourcing an ingredient
Which specs and paperwork to demand from a supplier, and the checks that let an auditor follow a claim back to its batch.
See the criteria →
ResearcherReference-grade material
Reference-grade material answers to a stricter standard than retail. Where that line falls, and what a research COA must state before the material goes into a method.
See the criteria →Photographs: Kadarius Seegars · Madeline Liu · National Cancer Institute. Unsplash License; licence and source recorded per file in the repository.
Coming later: Atlas, an assistant that answers from the registry
Atlas is not open yet, and nothing on this site answers questions today. When it opens, it will draw its answers from our verified registry alone, cite its sources and carry the grade of every claim it makes. Ask it something the registry can't support and it will say “we don't know”. Read what Atlas will and will not do.