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Cannabinoid Comparison Hub: Pharmacology and the EU Position

There are over a hundred cannabinoids in cannabis and around ten of them are sold to consumers. They act at different receptors, in different directions, and their evidence bases differ enormously, from three regulatory-grade trials at one end to zero human studies at the other.

FDA structure and function language No disease claims
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What actually separates these compounds.

Three things separate these compounds, and none of them is a flavour preference. Read them before you read any comparison, because they decide what a claim is worth.

Different receptors

CBD does not activate CB1 at all. THC is a partial agonist at it. CBC prefers CB2. The target decides the effect.

Different directions

Two cannabinoids can meet the same receptor and pull opposite ways. THCV blocks CB1 at low doses and activates it at high ones.

Different evidence

From three regulatory-grade trials at one end to zero human studies at the other. Most minor cannabinoid data is in vitro or rodent.

Start with the question you actually have.

Most comparison content treats cannabinoids as a menu of wellness options. They are not that. They act at different receptors, in different directions, and their evidence bases differ enormously.

CBDa vs CBD
CBDa reaches blood concentrations 19 to 25 times higher than CBD in humans. It also has different molecular targets and barely enters the brain. What the data shows.
Read comparison →
THCa vs CBD
THCa converts to THC when heated, which is why total-THC accounting exists. What that means for raw extracts in Europe, where member state limits differ sharply.
Read comparison →
Delta-8 vs CBD
Delta-8 is marketed as mild, half-strength THC. EFSA's 2025 assessment gave it a relative potency factor of one and applied the same reference dose as delta-9.
Read comparison →
CBDV vs CBD
CBDV is unusual among minor cannabinoids in having been properly tested in humans. Twice. Both trials failed. What that tells us, and how CBDV compares with CBD.
Read comparison →
THCV vs CBD
THCV blocks CB1 at low doses and activates it at high ones, which makes the non-intoxicating description conditional. The trials, the pharmacology and the EU position.
Read comparison →
CBD vs Melatonin
Melatonin is one of the few sleep-related substances with authorised EU health claims, at exact doses. CBD has none. The pharmacology, the evidence and the exact legal wording.
Read comparison →
CBD vs Ashwagandha
Ashwagandha has better stress trial data than CBD and a liver injury signal serious enough that European regulators have restricted it. Both facts belong together.
Read comparison →
CBN vs CBD
CBN forms when THC oxidises. The first controlled sleep trial reported in 2026 and missed its primary endpoint. What the research shows and how EU law treats both compounds.
Read comparison →
CBC vs CBD
CBC is the third branch of the cannabis pathway. Two respected laboratories disagree about whether it activates CB1, and no controlled human study of it exists.
Read comparison →
CBD vs CBG vs CBN
Three non-intoxicating cannabinoids sold as if interchangeable. They act at different receptors and their research bases differ enormously. A structured European comparison.
Read comparison →
Hemp Oil vs CBD Oil
Hemp seed oil contains no CBD and is not a novel food. CBD extract is a different product with a different legal status in the EU. How to tell them apart on a label.
Read comparison →
CBG vs CBN
CBG is the precursor everything else comes from. CBN is what THC becomes when it oxidises. How the two differ in mechanism, evidence and European regulatory position.
Read comparison →

No comparison matches that search.

The honest summary.

Every claim on this table is sourced on the individual pages. Binding affinity numbers for the minor cannabinoids are genuinely inconsistent between labs, so assay context matters.

Compound
CB1 receptor
CB2 receptor
Other target
Human evidence
Intoxicating
Where it comes from
CBD
No activation. Negative allosteric modulator
Ki 240 nM, low efficacy
ENT1 transporter under 250 nM; TRPA1 ~0.09 μM
Strong in rare epilepsy, negative in pain
No
CBDA, decarboxylated
THC
Partial agonist, Ki 20 to 36 nM
Ki 31 to 52 nM
TRPA1, 0.23 μM
Extensive, including approved medicines
Yes
THCA, decarboxylated
CBG
Weak, Ki around 1.3 μM
Weak partial, Ki 490 nM
Alpha-2 adrenoceptor, EC50 0.2 nM
One human trial
No
CBGA, the parent precursor
CBN
Weak partial, 29 percent max effect
Negligible
TRPA1, 0.18 μM
One polysomnography trial
Weakly, very high doses
Oxidation of THC
CBC
Disputed between studies
CB2-preferring, Ki 27 nM
TRPA1, approximately 0.09 μM
None
No
CBCA, decarboxylated
CBDa
Inactive, Ki above 10 μM
Low efficacy
COX-2, EC50 2 μM, 9-fold selective
No controlled trials
No
Native plant product
CBDV
Inactive
Ki 140 nM, EC50 5.0 nM
TRPA1, 0.42 μM
Two designed trials, both negative
No
CBDVA, propyl series
THCV
Antagonist at low dose, agonist at high
Partial agonist, Ki 47 to 63 nM
5-HT1A positive modulation
Limited early-stage work
Dose-dependent
THCVA, propyl series
THCa
Weak, EC50 above 10 μM
Disputed
PPAR-gamma, potent
Essentially none in humans
No, until heated
Native plant product
Delta-8 THC
Partial agonist, Ki around 36 nM
Around 50 nM, same as delta-9
Same profile as delta-9
Minimal; EFSA equates potency to delta-9
Yes
Acid conversion, usually from CBD
Showing 6 of 10 compounds

Important context: Human trials showing effects for CBD used 100 to 1,600 mg a day. Consumer products typically deliver 10 to 50 mg. No trial evidence supports scaling those findings down.

Eight cannabinoids, eight evidence bases.

Receptor figures are in vitro and vary between laboratories. The evidence bar counts human trials, not cell studies.

CBD Non-intoxicating
Cannabidiol
CB1No activation
CB2Ki 240 nM
OriginCBDA, decarboxylated
Human evidence Dozens of trials
THC Intoxicating
Delta-9-tetrahydrocannabinol
CB1Partial agonist, 20 to 36 nM
CB2Ki 31 to 52 nM
OriginTHCA, decarboxylated
Human evidence Extensive
CBG Non-intoxicating
Cannabigerol
CB1Weak, Ki 1.3 μM
CB2Weak partial, 490 nM
OriginCBGA, the precursor
Human evidence One trial
CBN Intoxicating
Cannabinol
CB1Weak partial, 29 percent
CB2Negligible
OriginOxidation of THC
Human evidence One sleep trial
CBC Non-intoxicating
Cannabichromene
CB1Disputed
CB2CB2-preferring, 27 nM
OriginCBCA, decarboxylated
Human evidence None
CBDa Non-intoxicating
Cannabidiolic acid
CB1Inactive above 10 μM
CB2Ki 12 nM, low efficacy
OriginNative plant product
Human evidence None controlled
CBDV Non-intoxicating
Cannabidivarin
CB1Inactive
CB2Ki 140 nM
OriginCBDVA, propyl series
Human evidence Two, both negative
THCV Intoxicating
Tetrahydrocannabivarin
CB1Antagonist low, agonist high
CB2Partial, 47 to 63 nM
OriginTHCVA, propyl series
Human evidence Limited

One precursor. Several directions.

Understanding the biosynthesis makes the table easier to read. Cannabis makes one precursor, CBGA. Three enzymes compete for it. THCA synthase produces THCA. CBDA synthase produces CBDA. CBCA synthase produces CBCA. Whatever CBGA is left becomes CBG.

Heat and time then strip a carbon dioxide group from each acid, giving THC, CBD, CBC and CBG.

One precursor. Several directions.
Two compounds sit outside that scheme

CBN has no synthase; it is what THC becomes when it oxidises. Delta-8 THC is barely present in natural hemp and is generally manufactured by acid conversion from CBD.

And a separate branch makes the varins

Built from a shorter starting molecule, it produces CBDV and THCV. That branch is genetically segregated, which is why varin content is rare in ordinary hemp.

Three things worth knowing first.

Each one changes what a claim on the pages ahead is actually worth.

Three things worth knowing first.
01
The dose gap

Human trials showing effects for CBD used 100 to 1,600 mg a day. Consumer products typically deliver 10 to 50 mg, and EFSA’s provisional safe level sits at around 2 mg. No trial evidence supports scaling those findings down.

02
Most minor cannabinoid data is preclinical

CBC, CBDa and THCa have essentially no controlled human data at all. Binding affinity numbers are also genuinely inconsistent between labs, and any single figure quoted without its assay context is misleading.

03
The entourage effect is not established

Two studies designed specifically to test whether cannabis terpenes modulate cannabinoid receptor activity found they do not. A 2024 scoping review concluded there is limited evidence for it as a stable and predictable phenomenon.

Why we publish it this way

We grow our own hemp in Europe, run our own supercritical CO2 extraction and publish a third-party certificate of analysis for every batch. Under EU rules, that measured laboratory data is close to the entirety of what we are lawfully permitted to tell you about a cannabinoid product.

It is also, in our view, the most useful thing we could tell you. A company selling these compounds has an obvious incentive to overstate what they do. We would rather publish the trials that failed alongside the ones that succeeded.

What European law permits anyone to say

This is the section most CBD sites omit, and its absence is usually how you can tell a page has not been written carefully.

Under Regulation (EC) No 1924/2006, a health claim may only be made if it appears on the Union list of authorised claims. No health claim for CBD, cannabidiol, hemp extract or any cannabinoid is authorised. None.

Article 10(3) reaches further than most people realise. References to general, non-specific benefits are permitted only alongside a specific authorised claim. Because no cannabinoid claim exists, phrases such as “supports wellbeing”, “helps you relax”, “for balance” or “supports the endocannabinoid system” are not lawful on a cannabinoid product in the EU either.

Regulation (EU) No 1169/2011, Article 7(3), separately prohibits attributing to any food the property of preventing, treating or curing a human disease. Under Directive 2001/83/EC, a product presented as having therapeutic properties can be reclassified as an unauthorised medicinal product, which is a considerably more serious outcome than a labelling breach.

Enforcement authorities treat implied claims as claims: product names, category names such as a “sleep range”, imagery, testimonials, influencer content, meta descriptions and links to clinical studies about effects.

What remains lawful is factual information: botanical origin, extraction method, measured cannabinoid content, purity, third-party laboratory analysis, allergen and ingredient declarations, and instructions for use.

Every page in this hub is built from that narrow palette. It is why they describe receptors and trials rather than benefits.

 

The EU regulatory position, in short

CBD and all cannabinoid-containing extracts are unauthorised novel foods under Regulation (EU) 2015/2283. No CBD novel food has been authorised anywhere in the EU. Hemp seeds, hemp seed oil and hemp seed protein are not novel and are unaffected.

EFSA published a provisional safe level in February 2026: 0.0275 mg per kilogram of body weight per day, roughly 2 mg for a 70 kg adult, for CBD isolate of at least 98 percent purity. Safety could not be established for anyone under 25, for pregnant or breastfeeding women, or for people taking medication.

The Kanavape judgment, stated correctly. In Case C-663/18 the Court of Justice held that CBD lawfully produced from the whole plant is not a narcotic drug, and that member states cannot ban lawfully produced CBD on narcotics grounds alone without justification. It did not authorise CBD as a food. Novel food, food information and medicines rules apply independently. The frequently repeated line that the EU Court made CBD legal across Europe conflates narcotics law with food law.

THC limits are three separate things. The 0.3 percent figure is a cultivation eligibility criterion for hemp varieties, raised from 0.2 percent in January 2023. Regulation (EU) 2022/1393 sets THC maxima only for hemp seed products, at 3.0 mg/kg and 7.5 mg/kg for the oil. Finished-product limits for extracts are national and diverge sharply.

Member states differ substantially. Germany’s BVL considers CBD food supplements not marketable. Denmark requires novel food authorisation and publishes THC action limits. Sweden combines novel food classification with a narcotics ruling covering THC-containing extracts. Spain’s enforcement has channelled the category into external-use products. The Netherlands operates an informal tolerance conferring no legal certainty.

01
Our own fields Organically grown hemp, cultivated by us rather than bought in.
02
Our own extraction CO2 extraction in our own labs, so the process is ours end to end.
03
A COA per batch Measured cannabinoid content published against the code on your bottle.
04
Negative results too We publish the trials that failed alongside the ones that worked.

References

Each comparison page carries its own reference list. The primary sources behind the master table are:

01 Zagzoog A et al. Sci Rep 2020;10:20405.
02 Walsh KB, McKinney AE, Holmes AE. Front Pharmacol 2021;12:777804
03 De Petrocellis L et al. Br J Pharmacol 2011;163:1479-1494.
04 Pertwee RG. Br J Pharmacol 2008;153:199-215.
05 Ibeas Bih C et al. Neurotherapeutics 2015;12:699-730.
06 EFSA CONTAM Panel. EFSA Journal 2025;23(11):e9735.
07 EFSA. Provisional safe level for cannabidiol. EFSA Journal 2026;24:9862
08 Court of Justice of the European Union, Case C-663/18, 19 November 2020
09 Regulation (EC) No 1924/2006 and Commission Regulation (EU) No 432/2012.