Everything begins with CBG.
CBG is the precursor the plant builds the other cannabinoids from — and one of the least understood. CBG Atlas is the evidence-graded reference for what is actually known, told at your level and honest about its limits.
Someone, somewhere, is deciding whether to give this to a parent, a patient, themselves. They deserve the real state of the evidence — not the most hopeful reading of it.
The newest verified science.
The most recent studies on CBG, CBGA & CBGV — verified against PubMed, graded by study type, and traceable to source. Generated live from the Evidence Library.
Pharmacokinetic and pharmacodynamic properties of cannabigerol in male mice
Acute effects of cannabigerol on anxiety, stress, and mood: a double-blind, placebo-controlled, crossover, field trial
Cannabigerol modulates α-adrenoceptor and 5-HT1A receptor-mediated electrophysiological effects on dorsal raphe nucleus and locus coeruleus neurons and anxiety behavior in rat
The gap-map — coverage, not marketing.
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.
Most references show you their strongest page. The gap-map shows every tracked condition — including the ones with no primary evidence at all — with what would have to be done before a grade could move. A gap is not a promise, and nothing on it says CBG works for anything.
The compounds around CBG.
Each has its own record, held to the same standard as the monograph. Where the registry holds little, the page says so rather than filling the space.
Cannabigerolic acid
The acidic precursor CBG is decarboxylated from, and the branch point to THCA, CBDA and CBCA. Chemistry and biosynthesis are firm; the pharmacology catalogue is in progress.
Cannabigerovarin
The propyl (varin) homolog of CBG. Precise on identity and biosynthesis, and explicit that no CBGV-specific pharmacology or human data sits in the gated registry yet.
Tetrahydrocannabivarin
The propyl homolog of THC, anchored on one verified review of its receptor pharmacology — and honest that the popular claims made for it are not verified here.
Why CBG is the mother cannabinoid.
Not a marketing epithet — a description of the biosynthesis. Every well-known cannabinoid in the plant descends from one acid, and that is why this reference starts here.
A single branch point
Every well-known cannabinoid traces back through CBGA. Change what happens at the synthase step and you change which cannabinoid the plant makes.
Acid, then neutral
Plants make the acidic forms — THCA, CBDA, CBCA. Heat and time decarboxylate them into the neutral forms most people know.
Why it matters
Understanding the origin is the foundation for reading any claim about a cannabinoid's effects — and for seeing where the evidence is, or isn't.
Where CBG may act.
A guided map of where CBG’s known mechanisms could act — every region graded, hedged, and honest about what it does not show.
Original anatomical study. Decorative — every claim it points at is written out beside it.
CBG's most potent known interaction is at α2-adrenoceptors, alongside 5-HT1A antagonism and TRP-channel activity. One small acute human trial has measured anxiety, stress and mood; everything else here is laboratory or animal work.
Signals under study- Low
Anxiety & stress — one small, single-dose, placebo-controlled human trial (Cuttler 2024). Graded Low: acute, self-report endpoints, and two preclinical studies in our registry point the other way.
- Hypothesized
Mood — 5-HT1A antagonism is a plausible mechanism. No human trial has measured it.
- Preclinical
Neuroinflammation — TRP-channel activity seen in cell and animal studies only.
What the evidence does not establishWhether these receptor interactions produce a meaningful, measurable effect in people — and at what dose. The single human trial measured one acute dose in healthy volunteers.
- Low
The most safety-relevant thing our registry holds, and it is a mechanism, not an outcome. 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 — mechanistic plausibility only. The receptor activity is measured in the laboratory; the human effect is uncharacterised in both direction and size.
What the evidence does not establishWhether CBG raises, lowers or does not change blood pressure in people. If you take blood-pressure medication or have a cardiovascular condition, consult a clinician first.
- Hypothesized
The most-cited preclinical signal for CBG. In a mouse model of colitis it reduced inflammatory markers, with a CB2-modulated component — an animal result, not a human one.
Signals under study- Preclinical
Gut inflammation — reduced colonic inflammation in a murine DNBS model (Borrelli 2013).
- Preclinical
Oxidative stress — lowered nitric-oxide production in macrophages and reactive-oxygen-species formation in intestinal epithelial cells.
What the evidence does not establishAny effect on inflammatory bowel disease in people. No human study of CBG in any digestive condition sits in the registry.
- Preclinical
Two threads: an anti-inflammatory signal measured in cells and mice, and antibacterial activity against MRSA characterised in vitro.
Signals under study- Preclinical
Inflammatory markers — 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 systemic-infection model. No human efficacy data.
What the evidence does not establishWhether CBG affects infection or inflammation in people. Antibacterial activity in a dish is not an antibiotic.
- Preclinical
CBG activates and then rapidly desensitises TRPV1 and TRPV2 — the thermo-sensory channels behind most topical hypotheses. The channel behaviour is characterised; the skin outcome is 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 here.
What the evidence does not establishAnything about CBG on human skin. This region is on the map because the receptor is, not because the outcome is.
- No primary evidence
Frequently claimed, and 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. That is not a negative finding; it is an absence, and we will not fill it.
What the evidence does not establishWhether CBG affects intraocular pressure at all. Claims to the contrary are not supported by anything in this registry.
- No primary evidence
Proposed by extension from the gut and immune work rather than measured. No study in our registry examines joints.
Signals under study- No primary evidence
Joint inflammation — inferred from anti-inflammatory activity measured elsewhere. Inference is not evidence, and we grade it 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 are on the map because the receptor is, not because the outcome is — and a map that showed only regions with findings would be a marketing diagram.
Trust you can verify — not trust you’re asked to grant.
Hash-pinned snapshots
Every published snapshot carries a SHA-256 registry hash (154671f50c4a…) and every study its own provenance hash. Download the exact snapshot and check what you read against it.
Download & verify →Contradicting evidence, shown
Where the literature conflicts, we say so. Studies that contradict a claim are counted on the gap-map beside the ones that support it. We never manufacture consensus.
See the conflicts →Contractual independence
Funded by Peregrine Biopharma, which holds no editorial authority — a firewall written into the funding agreement, not a promise.
Read the standard →One scale. Honest about every rung.
Every claim on CBG Atlas carries a grade, and the grade governs the language it is allowed to use. The two move together — so the tone can never outrun the evidence.
- Established
Settled science — replicated human data, or biochemistry that is not in dispute.
“is shown to” - Demonstrated
Shown reproducibly in controlled experiments — typically laboratory (in-vitro) work.
“has been shown to” - Emerging
An early signal — preclinical (animal) work, or human evidence too limited to settle the question.
“may · early evidence suggests” - Low
Limited and low-confidence — sparse, indirect, or single-source data.
“limited evidence · unclear” - Hypothesized
Proposed and plausible — but not yet shown.
“proposed mechanism” - Not supported
Tested, and the evidence does NOT support it. This is a finding against the claim — not an absence of evidence.
“evidence does not support”
Three ways into the Atlas.
The CBG monograph
The compound record at two depths — consumer and researcher. The same evidence, told at your level.
Research Library
Every verified study, graded by type and traceable to its DOI and PubMed record — and downloadable as open data.
How we grade
The six-rung evidence ladder and the hedge language bound to each rung.
What to require before you buy.
Our directories are empty on purpose: a listing appears only when its verification can be checked. Until then, here is what to demand of anyone selling to you.
ConsumerChoosing a product
What a certificate of analysis has to show before a label on the front means anything.
See the criteria →
FormulatorSourcing an ingredient
The specifications and documentation to require from a supplier, and the checks that make a claim auditable.
See the criteria →
ResearcherReference-grade material
What separates reference-grade from retail, and what a research COA must state to be usable.
See the criteria →Photographs — Kadarius Seegars · Madeline Liu · National Cancer Institute. Unsplash License; licence and source recorded per file in the repository.
Three directories, by who you are.
Educational listings, never endorsements. Each entry shows the verification it actually carries, and no listing is a health claim.
Consumer products
Brands, retailers and marketplaces listed for third-party testing and plain milligram labeling — the checks to make before you buy.
Compounds to formulate
Manufacturers, distributors and toll formulators for CBG actives, judged on the documentation, purity and traceability they publish.
Research compounds
Neat standards, certified solutions and reference materials for quantitation, calibration and method validation. Research use only.
Atlas is not open yet, and nothing on this site answers questions today. When it opens it will answer only from this verified registry, cite every source, carry the grade with the claim, and say “we don't know” where the registry is silent. Read what Atlas will and will not do.