The receptors, the two hydrolases, the contested transport step, and the botanical chemistry that acts on them — with the ceiling that separates enzyme inhibition from direct agonism.
10 pages · 83 citations (4 without a resolved identifier, marked on the page) · updated 2026-09-27
What this section is, and what it is not
Education and harm reduction. Not medical, legal or financial advice. Every factual claim carries a source; contested and single-source claims are marked as such on the page.
The boundary. This section teaches separation, purification, formulation, dosing arithmetic and analytical chemistry with real parameters, because withholding that detail from someone who will proceed anyway is the harm this library exists to prevent. It does not publish preparative routes for converting one cannabinoid into a more intoxicating one; those are described structurally and cited to the literature, without procedures.
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A retrograde, on-demand lipid signalling system with no vesicular storage: made when needed, released backwards across the synapse onto presynaptic CB1, and terminated by hydrolysis rather than by being pumped back into vesicles. Everything on this shelf follows from that architecture, including the single distinction that organises it — raising the tone of the system you already have is not the same intervention as adding an exogenous agonist.
7 sections · target
The serine hydrolase responsible for roughly 85 percent of 2-AG hydrolysis in the brain, and the junction at which the endocannabinoid system meets prostaglandin synthesis. Inhibiting it raises 2-AG and simultaneously starves the cyclooxygenase pathway of substrate — which makes MAGL inhibition a cannabinoid and an anti-inflammatory intervention in one move. The animal literature on complete chronic blockade is also the strongest available argument against maximal inhibition of anything on this shelf.
5 sections · enzyme
The hydrolase that terminates anandamide and the other fatty-acid amides. It has the best-characterised human genetic variant on this shelf, the most persuasive animal pharmacology, and the worst clinical record: repeated failure to reproduce animal analgesia in human trials, and one catastrophic phase 1 trial in 2016 that killed a volunteer. This page is not an endorsement of FAAH inhibition and should not be read as one.
7 sections · enzyme
A Gi/o-coupled seven-transmembrane receptor, the most abundant G-protein-coupled receptor in the mammalian brain, sitting presynaptically where it suppresses neurotransmitter release. Its distribution explains why cannabis has no lethal respiratory depression, and the partial-versus-full agonist distinction at this receptor explains why synthetic full agonists kill people anyway.
7 sections · target
The second cannabinoid receptor: Gi/o-coupled like CB1, but expressed principally on immune cells and in the periphery, and in the brain largely on microglia rather than on neurons. Agonism is anti-inflammatory and immunomodulatory without the psychoactivity that comes from neuronal CB1, which is why CB2 is the most industrially interesting target on this shelf — and why a common dietary sesquiterpene that hits it selectively matters.
5 sections · target
Endocannabinoids get from the extracellular space to their intracellular enzymes, and how they do it is not settled. This page lays out the three competing accounts, marks the mechanism contested, and then covers the compounds that block the process selectively — because whatever the mechanism is, it is pharmacologically addressable, and guineensine is the cleanest natural example of that on the whole shelf.
6 sections · target
Every botanical compound on this shelf in one table, with source, molecular target, reported potency with units, the assay level the number came from, and the citation. Then, as its own section rather than a footnote, the caveat that decides whether any of it means anything: a micromolar in-vitro IC50 against an enzyme says nothing about whether a dietary or infusion dose reaches that concentration at the enzyme in a person.
6 sections · botanical
The pepper family carries an unusual concentration of endocannabinoid-system-active chemistry: guineensine and piperine and β-caryophyllene in black pepper, the kavalactones and yangonin in kava, related amides across Piper longum and Piper guineense. The operator argues that black pepper hits four mechanisms at once. The evidence supports each mechanism individually; the family-level claim is a hypothesis, and the same convergence that makes it interesting makes black pepper a drug-interaction hazard rather than a free potentiator.
5 sections · botanical
The term began in 1998 as a specific claim about endogenous lipids and was later broadened into the idea that terpenes shape the effect of cannabis. The broadened version is contested and the negative evidence is good: two independent groups found no terpene modulation of CB1 or CB2 signalling at plausible concentrations. What survives is narrower and still real — cannabinoid-cannabinoid interaction, pharmacokinetic interaction, aroma-mediated expectancy, receptor-independent effects at high local concentration, and one genuine terpene-to-cannabinoid-receptor case in β-caryophyllene.
6 sections · target
Kava is the operator Oilahuasca thesis applied to a botanical that is already polypharmacological: GABA-A potentiation, reversible MAO inhibition, FAAH and MAGL inhibition, a CB1 ligand in yangonin, sodium and calcium channel block, noradrenaline uptake inhibition. The potentiator categories follow from that mechanism map. So does the hazard, and the hazard is the point of this page: kava carries a hepatotoxicity signal, and deliberately stacking CYP inhibitors onto it means slowing the clearance of the very thing loading the liver. No doses and no preparation methods appear here.
7 sections · safety