THCA-AΔ9-Tetrahydrocannabinolic acid A
The acid form of Δ9-THC made by the plant; almost no affinity for CB1 and CB2 receptors.
C₂₂H₃₀O₄
CAS 23978-85-0
- Family
- PhytocannabinoidPrincipal
- Origin
- Biosynthesis (plant)
- First described
- 1967
- Molar mass
- 358.48 g/mol
Updated on
In plain terms
THCA is the form in which the plant makes THC. It binds very little to the brain's CB1 and CB2 receptors. Heat or time turn it into THC.
Receptors and activity
Target network
- Activates
- Blocks or inhibits
The lower the cited value, the closer the target sits to THCA-A: one ring per factor of 100. A target with no measured value stays on the edge.
Where these targets live
Where each target has been found in humans, according to the cited studies. The map shows the target, not an effect of THCA-A.
CB1CB1 found in 7 regions of the body
- Basal gangliadenseMost dense in basal ganglia outflow nuclei1
- CerebellumdenseVery dense in the cerebellum1
- HippocampusdenseVery high concentrations in the hippocampus2
- AmygdaladenseHigh concentrations in the amygdala2
- CortexpresentPresent throughout the neocortex2
- Adipose tissuepresentExpressed in adipose tissue3
- GutpresentColonic epithelium, smooth muscle and plexus4
Map sources
- Herkenham M et al. Cannabinoid receptor localization in brain. Proc Natl Acad Sci U S A, 1990 (new tab)
- Glass M et al. Cannabinoid receptors in the human brain: a detailed anatomical and quantitative autoradiographic study in the fetal, neonatal and adult human brain. Neuroscience, 1997 (new tab)
- Engeli S et al. Activation of the peripheral endocannabinoid system in human obesity. Diabetes, 2005 (new tab)
- Wright K et al. Differential expression of cannabinoid receptors in the human colon: cannabinoids promote epithelial wound healing. Gastroenterology, 2005 (new tab)
Cited values
- CB1AgonistKi = 3.1 µM · human25 out of 100
McPartland et al. 2017, Cannabis Cannabinoid Res: affinity and efficacy of THCA-A (new tab) · [3H]CP55,940, HEK-hCB1; approximate Ki, reference standard containing 2% THC; weak cAMP inhibition at 10 µM; agonist and PAM according to Palomares 2020
- CB2Inverse agonistKi = 12.5 µM · human15 out of 100
Palomares et al. 2020, Br J Pharmacol: collagen-induced arthritis, PPARγ and CB1 (new tab) · [3H]CP55,940, HEK-hCB2 (McPartland 2017, no efficacy measured); inverse agonism according to Palomares 2020
- PPARγPartial agonistIC50 = 470 nM · not specified39 out of 100
Nadal et al. 2017, Br J Pharmacol: THCA, PPARγ agonist (new tab) · PolarScreen competition assay; GAL4-PPARγ transactivation in HEK-293T, max. efficacy 6× lower than rosiglitazone
- TRPM8AntagonistIC50 = 150 nM · rat47 out of 100
De Petrocellis et al. 2011, Br J Pharmacol: TRP channels (new tab) · inhibition of the icilin response, HEK-293 rat TRPM8
- TRPA1AgonistEC50 = 2.7 µM · rat26 out of 100
De Petrocellis et al. 2011, Br J Pharmacol: TRP channels (new tab) · intracellular Ca2+, HEK-293 rat TRPA1; efficacy 41.6%
- TRPV2AgonistEC50 = 18.4 µM · rat12 out of 100
De Petrocellis et al. 2011, Br J Pharmacol: TRP channels (new tab) · intracellular Ca2+, HEK-293 rat TRPV2
Measured effects
Not characterised. No placebo-controlled human trial has measured the effects of THCA-A, so no level is shown.
Levels computed from placebo-controlled human trials: difference from placebo on 100, at the dose and route stated. Read the method
Pharmacology
Δ9-tetrahydrocannabinolic acid A is the form in which cannabis produces THC: THCA synthase, an FAD-dependent oxidocyclase, forms it from CBGA (Sirikantaramas et al., 2004), then heat or ageing decarboxylate it to Δ9-THC. It was isolated in 1967 (Yamauchi et al., Chem. Pharm. Bull. 15:1075). Hanuš et al. (2016) count it, with the acids of the three other major cannabinoids, among the plant's major constituents. Its affinity for cannabinoid receptors is very low: McPartland et al. (2017) estimated Ki values of about 3.1 µM at human CB1 and 12.5 µM at human CB2, with weak CB1 agonism at 10 µM and no measurable efficacy at CB2; the standard tested contained 2% THC, which, according to the authors, probably explains part of the binding measured. Palomares et al. (2020), by contrast, describe it as an orthosteric agonist and positive allosteric modulator of CB1, and an inverse agonist at CB2. It binds PPARγ (IC50 0.47 µM) and activates it with a maximal efficacy six times lower than rosiglitazone (Nadal et al., 2017). In vitro it activates rat TRPA1 (EC50 2.7 µM) and TRPV2 (EC50 18.4 µM) and blocks rat TRPM8 (IC50 0.15 µM; De Petrocellis et al., 2011). In mice it reduced striatal lesions induced by 3-NPA through a PPARγ-dependent pathway (Nadal et al., 2017) and attenuated collagen-induced arthritis (Palomares et al., 2020); no controlled human data were found.
Key sources.
- Sirikantaramas et al. 2004, J Biol Chem: THCA synthase (new tab)PMID 15190053
- Yamauchi et al. 1967, Chem Pharm Bull 15:1075: isolation (new tab)DOI 10.1248/cpb.15.1075
- McPartland et al. 2017, Cannabis Cannabinoid Res: affinity and efficacy of THCA-A (new tab)PMID 28861508
- Palomares et al. 2020, Br J Pharmacol: collagen-induced arthritis, PPARγ and CB1 (new tab)PMID 32510591
- Nadal et al. 2017, Br J Pharmacol: THCA, PPARγ agonist (new tab)PMID 28853159
- De Petrocellis et al. 2011, Br J Pharmacol: TRP channels (new tab)PMID 21175579
- ANSM, consolidated list of narcotics (26/06/2026) (new tab)
History
- Source
- Cannabis: the acid form in which the plant produces Δ9-THC (THCA synthase)
Biosynthetic pathway
Formed by THCA synthase, an FAD-dependent oxidocyclase, from CBGA (Sirikantaramas et al., 2004). Heat or ageing decarboxylate it to Δ9-THC (Radwan et al., 2021).
Legal framework
- European Union
Not named in the schedules of the UN conventions: the 1971 Convention covers Δ9-THC and six THC isomers (INCB Green List 2024). No EU instrument specific to THCA was found.
- France
The generic 'benzo[c]chromene nucleus' class (ANSM decisions of 22 May and 3 June 2024) excludes tetrahydrocannabinolic acid 'subject to compliance with the content set in article 1 of the arrêté of 30 December 2021' (0.30% Δ9-THC). The exact reach of this proviso is a matter for a lawyer. Checked 19/10/2026.
Sources: EUR-Lex, UNODC, CND, ANSM, IUPHAR/BPS, ChEBI, EUDA. Our method.
Classification
Family, origin and source verification
- Family
Phytocannabinoid › Principal
- Presence in the plant
Enzymatic biosynthesis in the plant
- Chemistry
Type Δ9-THC · C5 side chain · acid form
- Verification
Every fact on this entry was checked against its primary sources on 20 October 2026.
- Wikipedia (English)
Tetrahydrocannabinolic acid (new tab)
Article paired by the molecule's structure (InChIKey), revision read on 19 October 2026. Read as a second opinion, never cited as a source.
References
- Sirikantaramas et al. 2004, J Biol Chem: THCA synthase (new tab)PMID 15190053
- Yamauchi et al. 1967, Chem Pharm Bull 15:1075: isolation (new tab)DOI 10.1248/cpb.15.1075
- McPartland et al. 2017, Cannabis Cannabinoid Res: affinity and efficacy of THCA-A (new tab)PMID 28861508
- Palomares et al. 2020, Br J Pharmacol: collagen-induced arthritis, PPARγ and CB1 (new tab)PMID 32510591
- Nadal et al. 2017, Br J Pharmacol: THCA, PPARγ agonist (new tab)PMID 28853159
- De Petrocellis et al. 2011, Br J Pharmacol: TRP channels (new tab)PMID 21175579
- ANSM, consolidated list of narcotics (26/06/2026) (new tab)
Identifiers
Names
- Common name
- Δ9-Tetrahydrocannabinolic acid A
- IUPAC name
- (6aR,10aR)-1-hydroxy-6,6,9-trimethyl-3-pentyl-6a,7,8,10a-tetrahydrobenzo[c]chromene-2-carboxylic acid
- Other names
- THCA · Δ9-THCA-A · delta-9-tetrahydrocannabinolic acid A
Identifiers
- Formula
- C₂₂H₃₀O₄
- CAS
- 23978-85-0
- PubChem CID
- 98523(new tab)
- ChEBI
- 67078(new tab)
- InChIKey
- UCONUSSAWGCZMV-HZPDHXFCSA-N
- SMILES
- CCCCCC1=
CC2= C([C@@H] 3C= C(CC[C@H] 3C(O2) (C) C) C) C(= C1C(= O) O) O
LLM ingestion format: a structured superset of the entry (identifiers, binding, versioned legal status). Full corpus.