Cannabinoids: the compounds behind the plant

Where they come from

Nearly every cannabinoid starts as CBGA — cannabigerolic acid, the stem cell of the plant’s chemistry. Enzymes convert CBGA into three acidic siblings; heat then knocks a carbon-dioxide molecule off each acid — decarboxylation — leaving the neutral compounds you see on labels.

The six you’ll meet

Each card: what it is, where it comes from, and what research has recorded — with the evidence caveat up front, not buried.

THC

Δ⁹-tetrahydrocannabinol · C₂₁H₃₀O₂

What it is: The cannabinoid that made the plant famous — and its primary intoxicating compound. It’s the molecule most drug tests look for, and the number most labels lead with.
Where it comes from: The plant actually makes THCA (see the pathway above). Heat — a flame, a vaporizer, an oven — converts THCA into THC. Until heated, dried flower is mostly THCA.
What research has recorded: THC is a partial agonist at the body’s CB1 and CB2 receptors: it binds the same system the body’s own endocannabinoids use. CB1 binding is what produces intoxication. That receptor pharmacology is well established.
The caveat: How any individual responds to a given dose isn’t predictable from the molecule — set, setting, tolerance, and the rest of the chemistry all play in. A THC percentage on a label doesn’t translate into a predictable experience — which is exactly what our label guide is about.

THCV

Δ⁹-tetrahydrocannabivarin · C₁₉H₂₆O₂

What it is: THC’s shorter-chain cousin — the same three-ring skeleton, but with a 3-carbon propyl chain where THC carries five. Most cannabis makes only traces; some African landrace lines, like Durban Poison, make notably more.
Where it comes from: A parallel pathway: CBGVA → THCVA → THCV, with heat finishing the last step. “Varin” cannabinoids are simply the propyl-chain versions.
What research has recorded: In preclinical research (animals and cells), THCV behaves as a CB1 antagonist at low doses — it can block rather than activate the receptor — with different activity at higher doses.
The caveat: Human data is thin, and dose-dependence makes simple stories unreliable. The “diet weed” and appetite claims come from early-stage research, not human trials. Interesting, not established.

CBN

cannabinol · C₂₁H₂₆O₂

What it is: THC, aged. CBN forms as THC oxidizes — exposed to time, heat, light, and air. Old cannabis tests higher in CBN and lower in THC for exactly this reason.
Where it comes from: Not built by the plant at all — it’s a breakdown product. On the pathway above, THC → CBN is aging, not biosynthesis.
What research has recorded: Mildly psychoactive on its own, and much less potent than THC at CB1. Human studies of CBN alone are few and small.
The caveat: It’s marketed as “the sleep cannabinoid,” but that reputation traces mostly to old cannabis — THC plus CBN plus sedating terpenes like myrcene — rather than to CBN research specifically. A product promising CBN will make you sleepy is marketing ahead of the science.

CBD

cannabidiol · C₂₁H₃₀O₂

What it is: The second famous cannabinoid, and the one that isn’t intoxicating. CBD won’t get you high — which is why it appears in everything from oils to gummies to an actual prescription medicine (Epidiolex, for severe epilepsy).
Where it comes from: CBGA → CBDA → CBD, with heat doing the last step. “Hemp” is legally defined in the US as cannabis testing at or below 0.3% THC — plants bred to make CBDA instead of THCA.
What research has recorded: CBD has low affinity for CB1 and CB2 — it doesn’t intoxicate largely because it barely binds the receptors THC acts on. It’s the most-studied cannabinoid after THC: real clinical data supports specific uses, and research continues on others.
The caveat: “Non-intoxicating” doesn’t mean “no effects” or “risk-free” — CBD interacts with liver enzymes that metabolize many common medications. And the wellness industry’s CBD claims vastly outrun the clinical evidence. Talk to a clinician about interactions.

CBG

cannabigerol · C₂₁H₃₂O₂

What it is: The precursor — often called the “mother cannabinoid,” because its acidic form, CBGA, is the compound the plant converts into THCA, CBDA, and CBCA. By harvest, most CBGA has already been converted, so CBG itself is usually a minor component.
Where it comes from: Leftover CBGA, decarboxylated by heat. Breeders are now developing CBG-dominant lines selected to convert less CBGA onward.
What research has recorded: Non-intoxicating. Early-stage research — cells and animals, not people — has explored CBG across several targets. Human data is minimal. Researchers find it interesting mostly because of its central role in the plant’s chemistry.
The caveat: Nearly every CBG product claim is extrapolated from preclinical work. The honest summary: interesting chemistry, early science.

CBC

cannabichromene · C₂₁H₃₀O₂

What it is: The quiet third sibling. CBCA is one of the three main things the plant makes from CBGA, alongside THCA and CBDA — but CBC rarely reaches the label in quantity, because most breeding selects hard for THC or CBD lines.
Where it comes from: CBGA → CBCA → CBC, with heat finishing the job.
What research has recorded: Non-intoxicating. Preclinical work has noted activity at TRP channels — involved in sensing pain and temperature — rather than strong CB1/CB2 binding. Human research is essentially absent.
The caveat: CBC is the least-studied of the six on this page. Anyone selling you specific CBC benefits is guessing.

Your endocannabinoid system

Where your cannabinoid receptors live

This is a map of receptors — the docking stations your body already builds for its own endocannabinoids — not a map of what each cannabinoid does to each body part. Cannabinoids you inhale or ingest ride the bloodstream and act systemically; they don’t target organs like guided missiles. Tap a region to see which receptors live there, what the system does, and what that doesn’t prove.

Tap a region. Six regions, two receptor types — pick one to see which receptors live there, what your endocannabinoid system does with them, and what that doesn’t prove.

Read all six regions as plain text (no clicking needed)

Brain

CB1 — dense · CB2 — low

What the ECS does here: CB1 is one of the most abundant receptors in the human brain — dense in the cerebral cortex, hippocampus, basal ganglia, and cerebellum. Its signature move is retrograde signaling: the receiving neuron sends endocannabinoids backward to quiet the sending neuron, fine-tuning how much neurotransmitter gets released.

What this doesn’t mean: A dense receptor map is not a map of effects. It doesn’t mean THC “targets” memory or mood — it means the brain’s own tuning system is everywhere, so outside cannabinoids can nudge many dials at once.

Evidence note: Most distribution data comes from human and animal tissue studies. Connecting a receptor’s location to a felt effect still requires clinical trials.

Spine & nerves

CB1 — dense · CB2 — present (microglia)

What the ECS does here: CB1 is dense in the spinal cord’s dorsal horn — the relay where sensory signals, including pain signals, first enter the cord — and on peripheral sensory neurons. CB2 shows up mainly on microglia, the nervous system’s resident immune cells.

What this doesn’t mean: A receptor sitting on a pain pathway is not a painkiller. Presence is anatomy; relief is a clinical claim that needs trials.

Eyes

CB1 — confirmed · CB2 — reported, debated

What the ECS does here: The eye runs a working endocannabinoid system: endocannabinoids and their enzymes are found across ocular tissue, and CB1 is confirmed in the retina, ciliary body, trabecular meshwork, and cornea. CB2 has been reported in the retina by several groups, with pharmacological and genetic evidence of a functional role.

What this doesn’t mean: This doesn’t make cannabis an eye treatment. “Cannabis treats glaucoma” is far ahead of what the evidence supports.

Evidence note: CB2’s presence in the eye is still debated — antibody studies disagree on exactly where it is, so treat any CB2-and-vision claim as unsettled science.

Gut

CB1 — dense · CB2 — present (immune tissue)

What the ECS does here: The gut has its own nervous system — the enteric nervous system, the so-called “second brain” — and it is rich in CB1, which helps regulate motility, nausea signaling, and appetite. CB2 sits mainly with the immune cells lining the gut wall.

What this doesn’t mean: This is why appetite and nausea come up in cannabis conversations — but it doesn’t make any product a gut treatment.

Immune system

CB2 — dense · CB1 — low

What the ECS does here: CB2 is the immune system’s cannabinoid receptor: dense on B cells, natural killer cells, monocytes, macrophages, and microglia, plus the spleen and lymph nodes. Its main job is modulating immune signaling — especially the release of cytokines, the immune system’s chemical messengers.

What this doesn’t mean: “Supports immunity” is a marketing phrase, not a finding. Immune modulation is real biology; health claims need human trials.

Evidence note: CB2 is nearly absent from neurons in a healthy brain — which is why researchers study it as a possible non-intoxicating target. That research is still early.

Skin

CB1 + CB2 — present

What the ECS does here: Skin runs a local endocannabinoid system of its own: both receptors are found in keratinocytes, sebaceous (oil) glands, and cutaneous nerve endings, helping regulate barrier function, oil production, and local immune responses.

What this doesn’t mean: Local receptors are still not a proven treatment for any skin condition.

What’s recorded, what’s not

This guide describes what research has recorded about these compounds. It isn’t medical advice, dosing guidance, or a prediction of how any product will affect you. Most human data covers THC and CBD; research on the minor cannabinoids is early and largely preclinical — cells and animals, not people.

If you have a health question, talk to a qualified clinician — ideally one familiar with cannabis. Cannabis laws vary by place and change often; check yours.

Read the label guide ↗Open the terpene glossary ↗

Cannabinoids: the compounds behind the plant.