C₂₂H₃₀O₄ · 358.47 g/mol
2-[(1R,6R)-6-isopropenyl-3-methylcyclohex-2-en-1-yl]-5-pentyl-4-(propan-2-yl)benzene-1,3-diol-6-carboxylic acid
Raw CBD precursor — potent antiemetic, COX-2 inhibitor, 5-HT1A agonist
CBDA is the acidic precursor to CBD found in raw, unheated cannabis. When cannabis is heated (smoked, vaporized, or cooked), CBDA undergoes decarboxylation to become CBD. Despite being the most abundant cannabinoid in high-CBD cannabis plants, CBDA has been largely overlooked in research — but emerging evidence suggests it may be more potent than CBD for certain applications, particularly nausea and vomiting, where it shows activity at doses 100-1000x lower than CBD.
Studies Indexed
180+
Half-Life
Converts to CBD upon heating; stability in raw form varies
Primary Receptors
5-HT1A (high affinity agonist), COX-1/COX-2 inhibitor, CB1/CB2 (low affinity)
Last Updated
June 2026
CBDA is produced in cannabis glands as the primary biosynthetic product before decarboxylation. In raw cannabis juice, smoothies, or cold-pressed extracts, CBDA is the dominant cannabinoid. Unlike CBD, CBDA is a potent 5-HT1A receptor agonist with approximately 100-fold higher affinity than CBD — this may explain its superior antiemetic potency in preclinical models. CBDA also inhibits COX-2 (cyclooxygenase-2), the same enzyme targeted by NSAIDs like ibuprofen, suggesting anti-inflammatory properties. GW Pharmaceuticals developed CBDA methyl ester (HU-580) as a more stable CBDA derivative with enhanced antiemetic properties. CBDA's instability (it converts to CBD at room temperature over time) has historically limited research, but new formulation technologies are enabling more rigorous study.
Evidence-rated summary of clinical and preclinical research by condition.
CBDA is 100-1000x more potent than CBD as an antiemetic in rat models of anticipatory nausea and chemotherapy-induced nausea. Acts via 5-HT1A agonism. GW Pharmaceuticals' CBDA methyl ester (HU-580) is in development.
CBDA inhibits COX-2 enzyme activity, reducing prostaglandin synthesis. Anti-inflammatory effects demonstrated in cell culture and animal models. May be relevant for inflammatory pain and fever.
CBDA's high-affinity 5-HT1A agonism suggests anxiolytic potential. Preclinical evidence shows CBDA reduces anxiety-like behavior at lower doses than CBD.
CBDA may have anticonvulsant properties, potentially contributing to the efficacy of whole-plant CBD extracts. Mechanism may involve 5-HT1A activation and COX-2 inhibition.
Peer-reviewed research with DOI links
Bolognini D, Rock EM, Cluny NL, et al.
British Journal of Pharmacology
Demonstrated that CBDA prevents vomiting and nausea-induced behavior via 5-HT1A receptor activation, with potency 100-1000x greater than CBD in these models.
DOI: 10.1111/bph.12043Rock EM, Limebeer CL, Parker LA
British Journal of Pharmacology
CBDA methyl ester (HU-580) suppressed nausea and anxiety in rat models at doses far lower than CBD, supporting development of stable CBDA derivatives as antiemetic and anxiolytic agents.
DOI: 10.1111/bph.15324Known interactions with pharmaceutical drugs. Consult a healthcare provider before combining. Full interactions database →
| Drug / Class | Severity | Mechanism | Clinical Effect |
|---|---|---|---|
| NSAIDs (ibuprofen, naproxen) | minor | Additive COX-2 inhibition | Potential additive anti-inflammatory and GI effects; clinical significance unknown |
| Serotonergic drugs (SSRIs, triptans) | moderate | Additive 5-HT1A agonism | Theoretical serotonin syndrome risk at high doses; clinical data lacking |
| Antiemetics (ondansetron, metoclopramide) | minor | Additive antiemetic effects via different mechanisms | Potential additive antiemetic benefit; no clinical interaction data |
Critical questions that remain unanswered in the current literature — representing the frontier of CBDA (Cannabidiolic Acid) research.
Explore the clinical and preclinical evidence for CBDA (Cannabidiolic Acid) across these therapeutic areas.
