Home Ingredients Cannabidiolic Acid (CBDA)

Cannabidiolic Acid (CBDA)

Cannabis sativa
Evidence Level
Preliminary
6 Clinical Trials
4 Documented Benefits
1/5 Evidence Score

Cannabidiolic acid (CBDA) is the raw, acidic form of CBD made by the hemp plant. With heat, drying or age, CBDA loses a carbon dioxide group and turns into CBD, a change called decarboxylation, so finished CBD products hold little CBDA unless they are raw or cold-processed. Like CBD, it does not cause a high. There are essentially no human efficacy trials of CBDA. The interest in it comes from laboratory and animal work, where it reduced nausea, vomiting and anxiety-related behavior by enhancing a serotonin (5-HT1A) receptor and acted as a selective COX-2 enzyme blocker, in some tests more potently than CBD. It is also chemically unstable and little studied in people. In the United States, the FDA has concluded that CBD and THC products are excluded from the dietary supplement definition and has not recognized CBDA as a lawful dietary ingredient; federal hemp rules are also changing.

Studied Dose No oral dose has been established for any human use, and there are no human efficacy trials. The animal nausea and anxiety work used very low animal doses (roughly 0.01 to 5 mg/kg in rats), far below typical CBD amounts and not a guide for people; products list CBDA in mg alongside CBD.
Active Compound Cannabidiolic acid (CBDA), the carboxylic-acid precursor of cannabidiol (CBD); a non-intoxicating acidic cannabinoid in raw hemp that decarboxylates to CBD with heat.

Benefits

Nausea and vomiting signals in animal studies

In rats and in shrews, low injected doses of CBDA reduced vomiting from motion or a toxin and cut nausea-related behavior, including a model of anticipatory nausea. A serotonin (5-HT1A) receptor blocker reversed the effect while a cannabinoid receptor blocker did not. These are animal findings and have not been tested for nausea in people.

Supported by Trial 1, Trial 3

Anxiety-related behavior in animal studies

In rats stressed by foot shocks the day before, a very low injected dose of CBDA reduced anxiety-like responses in a light-dark test, an effect reversed by a serotonin (5-HT1A) receptor blocker; without that prior stressor CBDA changed nothing. A stable laboratory analog showed similar effects. This is animal work, not evidence in people.

Supported by Trial 4, Trial 3

Potency at the 5-HT1A serotonin receptor in laboratory tests

In cell-membrane binding assays, CBDA increased activation of the 5-HT1A serotonin receptor at very low concentrations and did so more strongly than CBD. Researchers link this receptor to the anti-nausea and anxiety-related effects seen in animals. Greater potency in a laboratory test does not mean a larger benefit in people.

Supported by Trial 1, Trial 3

COX-2 inflammation enzyme in laboratory tests

In enzyme assays, CBDA blocked COX-2, which makes inflammatory prostaglandins, about 9 times more selectively than COX-1, and a crude cannabis extract rich in CBDA showed the same selective block. A separate screen of six cannabinoids also found COX-inhibiting activity. These are test-tube findings, not evidence of reduced inflammation in people.

Supported by Trial 5

Mechanism of action

1

The acidic form that becomes CBD

The hemp plant builds its cannabinoids in acidic forms, making CBDA from the shared precursor cannabigerolic acid (CBGA), so fresh plant material is rich in CBDA rather than CBD. Heat, light, air and time strip a carbon dioxide group from CBDA and convert it to CBD, a reaction called decarboxylation, which is why raw or cold-pressed hemp holds more CBDA.

2

Enhances a serotonin receptor, weak at cannabinoid receptors

In laboratory tests CBDA boosts signaling through the 5-HT1A serotonin receptor rather than acting strongly on the CB1 cannabinoid receptor that produces the cannabis high, which fits its lack of intoxication. The animal anti-nausea and anxiety-related effects were blocked by a 5-HT1A blocker but not by a CB1 blocker.

3

Selective COX-2 enzyme inhibition

CBDA carries a salicylic-acid-like chemical group, similar to some anti-inflammatory drugs, and in enzyme tests it blocks COX-2 more than COX-1. In the laboratory, chemically modifying that acid group removed the selectivity, so the intact acid form matters for this action, and converting CBDA to CBD strips the group away entirely.

4

Unstable and poorly characterized in people

Because CBDA readily loses its acid group and turns into CBD, it is hard to keep stable in products and in the body, and human data on how much is absorbed are sparse. Reviews describe acidic cannabinoids as long overlooked and still mostly studied in cells and animals, so their behavior in people is uncertain.

Clinical trials

1
CBDA for Nausea and Vomiting in Rats and Shrews (animal)
PubMed

Laboratory and animal study of CBDA on toxin-, motion- and lithium-induced vomiting and nausea-related gaping, with receptor-binding assays (Bolognini et al. 2013, Br J Pharmacol).

House musk shrews and rats, plus rat brainstem and mouse brain membrane assays.

Low injected CBDA (0.1 to 0.5 mg/kg in shrews; 0.01 to 0.1 mg/kg in rats) reduced vomiting and nausea-related gaping, including a model of anticipatory nausea, and enhanced 5-HT1A receptor activation in vitro. A 5-HT1A blocker reversed the effect while a CB1 blocker did not. CBDA was more potent than CBD. Animal and laboratory evidence only.

2
Tolerability and Behavior of Oral CBDA in Rats (animal)
PubMed

Animal study assessing oral CBDA for neuromotor tolerability (locomotion, coordination, grip strength), feeding and anxiety-related behavior; one author worked for a cannabinoid maker (Brierley et al. 2016, Psychopharmacology (Berl)).

Male Lister Hooded rats given oral CBDA 0.05 to 5 mg/kg.

CBDA caused no adverse effects on movement, coordination or strength and did not change normal feeding. It showed an anxiety-related behavior change in one test but not in two others, so the signal was inconsistent. The authors concluded CBDA was well tolerated and worth clinical study. Animal evidence only.

3
Stable CBDA Analog (HU-580) for Nausea and Anxiety in Rats (animal)
PubMed

Laboratory and animal comparison of CBDA and its stable methyl ester analog HU-580 on 5-HT1A activation, nausea-related gaping and stress-induced anxiety-like behavior (Pertwee et al. 2018, Br J Pharmacol).

Human 5-HT1A receptor cell membranes and rats in nausea and foot-shock-stress anxiety models.

Both CBDA and HU-580 enhanced 5-HT1A activation at very low concentrations and reduced acute and anticipatory nausea-related gaping. HU-580, more potent and more stable than CBDA, also reduced stress-induced anxiety-like behavior; both effects were blocked by a 5-HT1A blocker. Animal and laboratory evidence only.

4
THC, CBDA and CBD on Stress-Linked Anxiety Behavior in Rats (animal)
PubMed

Animal study of injected THC, CBDA and CBD on anxiety-like responding with and without prior foot-shock stress (Rock et al. 2017, Psychopharmacology (Berl)).

Rats in a light-dark emergence test, dosed acutely or for 21 days.

Without a stressor, CBDA produced neither anxiety-reducing nor anxiety-provoking effects, while THC was anxiety-provoking. After foot-shock stress the day before, a very low dose of CBDA (and CBD) prevented the stress-driven anxiety-like response, an effect reversed by a 5-HT1A blocker. The authors concluded CBDA's effect may require a specific stressor. Animal evidence only.

5
CBDA as a Selective COX-2 Inhibitor in the Laboratory (lab)
PubMed

Laboratory enzyme study of CBDA on cyclooxygenase activity and the chemical features behind it (Takeda et al. 2008, Drug Metab Dispos).

Cell-free cyclooxygenase (COX-1 and COX-2) enzyme assays and a cannabis extract.

CBDA inhibited COX-2 with an IC50 near 2 micromolar and was about 9 times more selective for COX-2 than COX-1, while THC's acid form was far weaker. A CBDA-rich cannabis extract was also selective for COX-2, and methylating the acid group removed the selectivity. Test-tube evidence only, not a measure of inflammation in people.

6
Decarboxylation and Stability of CBDA in Hemp Seed Oil (lab)
PubMed

Analytical chemistry study measuring cannabinoids in commercial hemp seed oils and the decarboxylation kinetics of CBDA at different temperatures (Citti et al. 2018, J Pharm Biomed Anal).

13 commercial hemp seed oil samples and laboratory decarboxylation reactions.

CBDA was the most abundant cannabinoid acid in the oils. Because these acids break down with light, air and heat, the authors measured how fast CBDA loses its acid group and converts to CBD at different temperatures, confirming that storage conditions strongly affect how much CBDA remains. Analytical evidence about stability, not a health outcome.

Side effects and drug interactions

Common Potential side effects

CBDA has not been tested for safety in people in any dedicated trial, so its side-effect profile is essentially unknown; almost all information comes from short-term animal and laboratory work.
CBDA is not intoxicating and does not cause a high on its own. Products sold as raw or full-spectrum hemp may also contain trace THC, which is where any intoxication or impairment would come from.
CBDA is chemically unstable and converts to CBD with heat, light, air and time, so the amount in a product can change during storage, and some reported effects may come from CBD rather than CBDA.
CBDA products are often blends that also contain CBD, CBN or trace THC; a cannabis drug test can turn positive from the THC in these blends, so avoid them if you are tested for work or sport, or ask about confirmatory testing.
Long-term safety is unknown, and safety in pregnancy and breastfeeding has not been studied, so avoid it then.

Important Drug interactions

No formal human drug-interaction studies of CBDA exist, so check with a pharmacist or doctor before combining it with any regular medicine.
Other cannabinoids and cannabis products: CBDA is usually sold with CBD and sometimes THC or CBN, which carry their own interactions; CBD in particular can affect the liver enzymes that clear many medicines and has been reported to interact with blood thinners such as warfarin and the seizure medicine clobazam.
Sedatives and alcohol: like other hemp products marketed for calm, CBDA blends may add to drowsiness, especially if they contain THC or CBN; ask your doctor before combining.
Because CBDA can convert to CBD, any interaction known for CBD may apply to a CBDA product that has partly decarboxylated.

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Frequently asked questions about Cannabidiolic Acid (CBDA)

What is CBDA and does it make you high?

CBDA (cannabidiolic acid) is the raw, acidic form of CBD that the hemp plant actually makes. It is not intoxicating and does not cause a high. When hemp is heated, dried or aged, CBDA slowly converts to CBD, so raw or cold-pressed hemp products contain more CBDA while most standard CBD products contain little.

What does the research actually show for CBDA?

Almost nothing in people. There are essentially no human efficacy trials of CBDA for any health outcome. The interest comes from laboratory and animal work, where it reduced nausea, vomiting and anxiety-related behavior in rats and shrews by enhancing a serotonin (5-HT1A) receptor and blocked the COX-2 inflammation enzyme in test tubes, in some tests more potently than CBD. No dose has been established.

How is CBDA different from CBD?

CBDA is the chemical parent of CBD. The plant builds CBDA first; heat, light, air and time strip away a carbon dioxide group and turn it into CBD, a reaction called decarboxylation. That makes CBDA unstable, and it means a CBDA product can partly become CBD during storage or heating. CBD has far more human research than CBDA. See our CBD page for its own evidence.

Is CBDA legal as a dietary supplement?

Its status is unsettled. The FDA has concluded that CBD and THC products are excluded from the dietary supplement definition, and it has not recognized CBDA as a lawful dietary ingredient. A federal law passed in November 2025 redefines hemp from November 2026, excludes products with more than 0.4 mg THC per container and excludes cannabinoids made outside the plant. State rules also vary, so check before you buy.

Will CBDA show up on a drug test?

It can. CBDA products are often blends that contain trace THC or other cannabinoids, which can trigger a positive cannabis urine screen. If you are drug tested for work or sport, avoid these products or ask about confirmatory testing.

What is Cannabidiolic Acid?

Cannabidiolic acid (CBDA) is the raw, acidic form of CBD made by the hemp plant. With heat, drying or age, CBDA loses a carbon dioxide group and turns into CBD, a change called decarboxylation, so finished CBD products hold little CBDA unless they are raw or cold-processed. Like CBD, it does not cause a high.

What is Cannabidiolic Acid used for?

Cannabidiolic Acid has several researched uses. In rats and in shrews, low injected doses of CBDA reduced vomiting from motion or a toxin and cut nausea-related behavior, including a model of anticipatory nausea.

What is the recommended dosage of Cannabidiolic Acid?

The clinically studied dose is No oral dose has been established for any human use, and there are no human efficacy trials. The animal nausea and anxiety work used very low animal doses (roughly 0. Always follow the product label and check with a healthcare provider for personal advice.

Is Cannabidiolic Acid safe, and does it have side effects?

For most healthy adults, Cannabidiolic Acid is well tolerated at studied doses. Reported effects can include: CBDA has not been tested for safety in people in any dedicated trial, so its side-effect profile is essentially unknown; almost all information comes from short-term animal and laboratory work. CBDA is not intoxicating and does not cause a high on its own. It may also interact with some medications. Cannabidiolic Acid is not right for everyone, so check with a healthcare provider first if you are pregnant or breastfeeding, have a medical condition, or take prescription medication.

Does Cannabidiolic Acid interact with any medications?

Possible interactions include: No formal human drug-interaction studies of CBDA exist, so check with a pharmacist or doctor before combining it with any regular medicine. Other cannabinoids and cannabis products: CBDA is usually sold with CBD and sometimes THC or CBN, which carry their own interactions; CBD in… If you take prescription medication, check with a pharmacist or doctor before using it.

How strong is the scientific evidence for Cannabidiolic Acid?

NutraSmarts rates the evidence for Cannabidiolic Acid as Preliminary (1 out of 5). It is backed by 6 clinical trials and 12 cited references summarized on this page. A higher rating reflects more, larger, and better-designed human studies.

References(12 citations)

Evidence ratings on NutraSmarts are based on the totality of human clinical research, with emphasis on randomized controlled trials, meta-analyses, and systematic reviews. The references below directly support claims made throughout this page.

  1. Bolognini D, Rock EM, Cluny NL, Cascio MG, Limebeer CL, Duncan M, Stott CG, Javid FA, Parker LA, Pertwee RG. Cannabidiolic acid prevents vomiting in Suncus murinus and nausea-induced behaviour in rats by enhancing 5-HT1A receptor activation. Br J Pharmacol. 2013;168(6):1456-70. doi: 10.1111/bph.12043.PubMedUsed to support: Laboratory and animal study: low injected CBDA reduced toxin- and motion-induced vomiting in shrews and nausea-related gaping in rats, including a model of anticipatory nausea, and enhanced 5-HT1A receptor activation in membrane assays. A 5-HT1A blocker reversed the effect while a CB1 blocker did not, and CBDA was more potent than CBD. Animal and laboratory evidence only.
  2. Brierley DI, Samuels J, Duncan M, Whalley BJ, Williams CM. Neuromotor tolerability and behavioural characterisation of cannabidiolic acid, a phytocannabinoid with therapeutic potential for anticipatory nausea. Psychopharmacology (Berl). 2016;233(2):243-54. doi: 10.1007/s00213-015-4100-1.PubMedUsed to support: Animal study in rats given oral CBDA 0.05 to 5 mg/kg (one author employed by a cannabinoid maker): CBDA had no adverse effect on movement, coordination or grip strength and did not change normal feeding; an anxiety-related behavior change appeared in one of three tests. The authors concluded CBDA was very well tolerated and justified clinical investigation. Animal evidence only.
  3. Pertwee RG, Rock EM, Guenther K, Limebeer CL, Stevenson LA, Haj C, Smoum R, Parker LA, Mechoulam R. Cannabidiolic acid methyl ester, a stable synthetic analogue of cannabidiolic acid, can produce 5-HT(1A) receptor-mediated suppression of nausea and anxiety in rats. Br J Pharmacol. 2018;175(1):100-112. doi: 10.1111/bph.14073.PubMedUsed to support: Laboratory and animal study: both CBDA and its stable methyl ester analog HU-580 enhanced 5-HT1A receptor activation at very low concentrations and reduced acute and anticipatory nausea-related gaping in rats. HU-580, more potent and more stable than CBDA, also reduced stress-induced anxiety-like behavior; both effects were blocked by a 5-HT1A antagonist. Animal and laboratory evidence only.
  4. Rock EM, Limebeer CL, Petrie GN, Williams LA, Mechoulam R, Parker LA. Effect of prior foot shock stress and Δ(9)-tetrahydrocannabinol, cannabidiolic acid, and cannabidiol on anxiety-like responding in the light-dark emergence test in rats. Psychopharmacology (Berl). 2017;234(14):2207-2217. doi: 10.1007/s00213-017-4626-5.PubMedUsed to support: Animal study in rats: without a stressor CBDA produced neither anxiety-reducing nor anxiety-provoking effects, while THC was anxiogenic. After foot-shock stress 24 hours earlier, a very low dose of CBDA (and CBD) prevented the stress-driven anxiety-like response, an effect reversed by the 5-HT1A antagonist WAY100635. The authors concluded CBDA's anxiolytic effect may require a specific stressor. Animal evidence only.
  5. Takeda S, Misawa K, Yamamoto I, Watanabe K. Cannabidiolic acid as a selective cyclooxygenase-2 inhibitory component in cannabis. Drug Metab Dispos. 2008;36(9):1917-21. doi: 10.1124/dmd.108.020909.PubMedUsed to support: Cell-free enzyme study: CBDA inhibited COX-2 with an IC50 around 2 micromolar and was about 9 times more selective for COX-2 than COX-1, while the acid form of THC was a much weaker inhibitor. A CBDA-rich cannabis extract was also selective for COX-2, and methylating the carboxylic-acid group removed the selectivity. Laboratory evidence only.
  6. Citti C, Pacchetti B, Vandelli MA, Forni F, Cannazza G. Analysis of cannabinoids in commercial hemp seed oil and decarboxylation kinetics studies of cannabidiolic acid (CBDA). J Pharm Biomed Anal. 2018;149:532-540. doi: 10.1016/j.jpba.2017.11.044.PubMedUsed to support: Analytical chemistry study of 13 commercial hemp seed oils: CBDA was the most abundant cannabinoid acid, and because these acids decompose with light, air and heat, the authors measured the decarboxylation kinetics of CBDA to CBD at different temperatures, showing that storage conditions strongly affect how much CBDA remains. Supports the stability and decarboxylation statements; not a health outcome.
  7. Rava A, Di Trapano M, Tse C, Ji L, Bid HK, Trezza V. Acidic cannabinoids in brain disorders: Neurobiological mechanisms, preclinical evidence, and translational challenges. Neurosci Biobehav Rev. 2026;191:107005. doi: 10.1016/j.neubiorev.2026.107005.PubMedUsed to support: Review of acidic cannabinoids including CBDA: long considered inactive precursors, they are now studied as bioactive molecules with distinct stability, pharmacokinetic and receptor properties and reduced psychotropic liability, acting on serotonergic and endocannabinoid signalling, neuroinflammation and oxidative stress. The authors stress that the evidence is preclinical and that major methodological and translational challenges remain. Two authors are employees of Essentia Scientific.
  8. Schwark WS, Wakshlag JJ. A One Health perspective on comparative cannabidiol and cannabidiolic acid pharmacokinetics and biotransformation in humans and domestic animals. Am J Vet Res. 2023;84(5):ajvr.23.02.0031. doi: 10.2460/ajvr.23.02.0031.PubMedUsed to support: Review of the pharmacokinetics of CBD and its lesser-known precursor CBDA in humans and domestic animals: summarizes that oral absorption and metabolism of these cannabinoids vary and that CBDA is far less studied than CBD. Supports the statement that human data on CBDA absorption are limited; much of the review concerns veterinary dosing.
  9. Rock EM, Sticht MA, Limebeer CL, Parker LA. Cannabinoid Regulation of Acute and Anticipatory Nausea. Cannabis Cannabinoid Res. 2016;1(1):113-121. doi: 10.1089/can.2016.0006.PubMedUsed to support: Review of the nausea literature: notes that clinical trials of cannabinoids for chemotherapy-induced nausea are sparse, that most evidence comes from preclinical rat models, and that the animal data on cannabidiol and cannabidiolic acid point to a need to test them in human trials. Supports the statement that CBDA's anti-nausea evidence is preclinical.
  10. Ruhaak LR, Felth J, Karlsson PC, Rafter JJ, Verpoorte R, Bohlin L. Evaluation of the cyclooxygenase inhibiting effects of six major cannabinoids isolated from Cannabis sativa. Biol Pharm Bull. 2011;34(5):774-8. doi: 10.1248/bpb.34.774.PubMedUsed to support: Laboratory study of six cannabinoids, including CBDA, in cyclooxygenase inhibition assays: the cannabinoids inhibited COX enzyme activity in vitro with IC50 values in the micromolar range. Corroborates that CBDA has COX-inhibiting activity in the test tube; laboratory evidence only.
  11. U.S. Food and Drug Administration. FDA Regulation of Cannabis and Cannabis-Derived Products, Including Cannabidiol (CBD). U.S. Food and Drug Administration (fda.gov). 2024;Web page, content current as of 07/16/2024..SourceUsed to support: Not PubMed-indexed; official FDA page read 2026-10-10. States that FDA has concluded THC and CBD products are excluded from the dietary supplement definition under section 201(ff)(3)(B) of the FD&C Act unless FDA issues a regulation finding otherwise, which it has not. The page does not name CBDA, so CBDA has not been recognized as a lawful dietary ingredient and its status is unsettled.
  12. Congressional Research Service. Change to Federal Definition of Hemp and Implications for Federal Enforcement (IN12620). Congressional Research Service Insight. 2025;December 3, 2025..SourceUsed to support: Not PubMed-indexed; Congressional report read 2026-10-10. Explains that P.L. 119-37 (enacted November 12, 2025) redefines hemp effective November 12, 2026, applying limits to total THC, excluding final products with more than 0.4 mg THC per container and cannabinoids synthesized or manufactured outside the plant, and requiring FDA to publish lists of cannabinoids. CBDA occurs naturally in the plant and is not named.