CBDA and CBGA: The Acidic Cannabinoids Explained

Scientifically reviewed by Chana Frenkel, Ph.D. · Edited by Nani Frenkel, chief editor.

Cannabis synthesizes its major cannabinoids primarily in acidic forms. Fresh CBD-rich flower contains mainly cannabidiolic acid (CBDA) rather than CBD, while CBG-rich flower contains mainly cannabigerolic acid (CBGA) rather than CBG; both molecules carry an extra carboxyl group and shed it only when heated or aged. That one chemical detail changes a lot: what a raw tincture or a glass of cannabis juice delivers, what a lab reports, and what the raw-cannabis health claims actually rest on. It also explains how a 2022 laboratory study that found these two acids blocking a coronavirus in a dish turned into a headline that cannabis prevents COVID. This article covers CBDA and CBGA: what they are, what the cell and animal research shows, how heat changes the answer, and how one cell-culture study became a wildly overstated COVID headline.

What Are CBDA and CBGA?

The plant builds CBGA first, from its terpene and polyketide building blocks. Three enzymes then convert CBGA into the acids of the familiar cannabinoids: CBDA synthase makes CBDA, CBCA synthase makes CBCA, and THCA synthase makes THCA, which has its own profile on this site.^[1] Each acid keeps a carboxyl group (a –COOH) that the neutral cannabinoids lack. Removing it as carbon dioxide is called decarboxylation, and it turns CBDA into CBD and CBGA into CBG. Heat accelerates decarboxylation, while storage can gradually convert and degrade the acidic cannabinoids.^[2] Our decarboxylation explainer covers the temperatures and times.

Two things follow. First, CBDA and CBGA are not considered intoxicating.^[1] Second, they are not inert. Both have pharmacology of their own, different from CBD and CBG, and that is what the rest of this article is about.

Why Do Raw Cannabis and Juicing Claims Rest on the Acids?

Because that is what raw cannabis contains. Juicing fresh leaves or eating unheated flower delivers CBDA and CBGA (and THCA) rather than CBD, CBG and THC. Anyone claiming a benefit from raw cannabis is, whether they know it or not, claiming a benefit from the acids. The claims usually cited are anti-inflammatory and anti-nausea effects. Those have a real basis in laboratory and animal work, described below, but no controlled human trial has tested raw cannabis or isolated CBDA or CBGA as a treatment for any condition. The 2026 review that surveyed the field called controlled human trials a “dearth” and listed chemical instability and low bioavailability as the obstacles to running them.^[1]

What Does CBDA Do, in the Lab?

CBDA is the better-studied of the two. Three findings carry most of its reputation, and each comes from a dish or an animal.

• COX-2 inhibition (enzyme assay): CBDA selectively inhibited cyclooxygenase-2, the enzyme targeted by anti-inflammatory drugs such as celecoxib, with about nine-fold selectivity over COX-1. The carboxyl group was essential: methylating it abolished the selectivity, and THCA was far weaker.^[3]
• Nausea and vomiting (shrews and rats): CBDA at very low doses prevented toxin- and motion-induced vomiting in shrews and suppressed nausea-like behavior in rats. The effect was blocked by a 5-HT1A antagonist and not by a CB1 antagonist, pointing to the serotonin receptor rather than the cannabinoid receptor. The authors reported CBDA as more potent than CBD on these measures.^[4]
• Absorption (people): Human evidence remains limited and does not establish therapeutic efficacy. In a 2025 placebo-controlled laboratory study, 15 healthy adults received a full-spectrum hemp extract containing roughly equal amounts of CBD and CBDA, along with THC, THCA and minor cannabinoids. CBDA reached substantially higher peak blood concentrations and peaked earlier than CBD. Because participants received a mixture, however, the study could not isolate CBDA’s effects, and at the higher doses the mixture produced subjective effects and impaired working memory that cannot be attributed to CBDA.^[5] Preclinical pharmacokinetic studies suggest that acidic cannabinoids generally have limited brain penetration and short half-lives, while formulation can substantially change exposure.^[1]

Our sister site’s comparison of CBD and CBDA covers the consumer side of that evidence.

What Does CBGA Do, in the Lab?

CBGA is the branch point of the whole cannabinoid family, and most of its research is recent.

• Seizures (mice): In a mouse model of Dravet syndrome, CBGA was the most potent of the acids screened against heat-triggered seizures and strengthened the effect of the anti-seizure drug clobazam. But it cut both ways: at high doses it increased spontaneous seizures, and in a separate electrical test it was pro-convulsant. The authors concluded it could be a lead molecule, not a replacement for CBD.^[6]
• Aldose reductase (enzyme assay): Extracts rich in CBG and CBGA inhibited aldose reductase, an enzyme involved in diabetic complications, with the acid-rich fractions the most active. This is the source of the “CBGA and diabetes” claim; it is an enzyme in a tube, not a patient.^[7]
• Coronavirus entry (cells): see the next section.

No controlled human trial has tested isolated CBGA as a treatment. The plant’s own CBGA is scarce because the synthases convert most of it; the high-CBGA chemovars described in our CBG profile carry a defective synthase gene.

Did CBDA and CBGA Really Block SARS-CoV-2?

In a dish, yes. In people, nobody knows, and the doses make it unlikely.

In 2022, a team at Oregon State University screened hemp extracts against the SARS-CoV-2 spike protein using magnetic beads and mass spectrometry, then tested the strongest binders in cells. CBDA and CBGA bound the spike protein’s receptor-binding domain with micromolar affinity, prevented a spike-carrying pseudovirus from entering ACE2-expressing human cells, and blocked live virus, including the alpha and beta variants, in monkey kidney cells. In the live-virus experiment, inhibition required concentrations in the tens of micrograms per milliliter, far above the blood concentration reported after the small oral dose cited by the authors. Neutral cannabinoids such as THC, CBD and CBG showed weak or no binding; THCA was not carried into the cell experiments.^[8] That is the whole finding. It was done in cell culture, by a group with no commercial conflict, and it was a good piece of chemistry.

What it did not show is that taking CBDA or CBGA prevents or treats COVID-19. The authors themselves noted that the effective concentrations were high and that the one human measurement available, 0.21 micromolar after an oral dose, was far below them.^[8] One subsequent commentary estimated that maintaining comparable concentrations might require roughly 500 to 800 mg of CBDA several times daily; that calculation was illustrative, not a tested human dose, and the commentary concluded that cannabinoids including CBDA and CBGA are not recommended for preventing or treating SARS-CoV-2 infection.^[9] We found no animal or human follow-up to the study. The chemistry was sound; the headline that traveled around the world was not.

Is There Any Human Evidence?

Almost none that tests the acids themselves. We searched the clinical literature for randomized trials of CBDA and for human trials of CBGA and found no controlled trial that has tested isolated CBDA or CBGA as a treatment. The clearest CBDA-specific information is pharmacokinetic: the 2025 mixed-extract study showed that CBDA reached the bloodstream, but because participants received several cannabinoids together, it could not establish CBDA’s effects or benefits.^[5] The acid cannabinoids are, in the words of the 2026 review, an “underutilized yet potentially valuable class” that has not yet been put through the trials that would tell us whether the lab results mean anything in people.^[1]

How Does Heat Change the Answer?

Completely. Decarboxylation is not a switch but a rate: the acids convert faster at higher temperatures, and they differ in how quickly they go and how much is lost to side reactions along the way.^[2] Smoking, vaping and sufficiently prolonged baking can convert much or most of the acid to the neutral form, depending on temperature, time and the product matrix; a properly prepared raw tincture or fresh juice retains more of the acidic forms. So the same hemp flower can deliver CBDA or CBD depending on what you do with it, and any claim about “CBD” from raw material has to say which molecule it means.

This matters for testing too. Conventional GC analysis without derivatization heats the sample in the inlet, causing acidic cannabinoids to decarboxylate. It therefore measures some CBD that existed as CBDA in the original sample and may underestimate total cannabinoid content when conversion is incomplete.^[10] HPLC runs at room temperature and measures the acids and neutrals separately. That is why potency labels list CBDA and CBD as separate lines, and why two methods can disagree. Our articles on how HPLC measures potency and gas chromatography for cannabis explain the difference.

Are CBDA and CBGA Affected by the 2026 Hemp Redefinition?

Mostly indirectly. The redefinition scheduled to take effect on December 11, 2026 switches federal hemp to a total-THC standard that counts THCA, which mainly affects high-THCA flower sold as hemp. CBDA and CBGA are not THC and are not counted, but products containing them must still meet the THC limit, including a 0.4-milligram cap on total THC per container of finished product, and the separate exclusion of cannabinoids synthesized outside the plant does not apply to acids extracted from hemp. Bills to delay or repeal the provision are pending in Congress.^[11] Our guide to the 2026 hemp redefinition has the details.

What Is the Bottom Line?

CBDA and CBGA are real, distinct molecules with their own pharmacology, not inactive precursors. CBDA inhibits an inflammatory enzyme and blocks nausea in animals through a serotonin receptor; CBGA has both anti- and pro-seizure effects in mice; both bound a coronavirus protein in a dish. None of that has established a medical benefit in a controlled human trial. The antiviral concentrations were far above the blood concentration reported after the oral dose cited in that study, while the acids’ chemical instability, formulation-dependent exposure and apparently limited brain penetration complicate their development. Treat them as the promising, under-studied half of cannabis chemistry, and treat any product that says otherwise as ahead of the evidence.

References

1. Singh SK, Antoine C, Tse C, Ji L, Reed M, Carter WG, Trezza V, et al. Therapeutic potential of acidic cannabinoids: an update. Journal of Cannabis Research. 2026;8:25.
2. Wang M, et al. Decarboxylation study of acidic cannabinoids: a novel approach using ultra-high-performance supercritical fluid chromatography/photodiode array-mass spectrometry. Cannabis and Cannabinoid Research. 2016;1(1):262–271.
3. Takeda S, Misawa K, Yamamoto I, Watanabe K. Cannabidiolic acid as a selective cyclooxygenase-2 inhibitory component in cannabis. Drug Metabolism and Disposition. 2008;36(9):1917–1921.
4. 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-HT_1A receptor activation. British Journal of Pharmacology. 2013;168(6):1456–1470.
5. Elder HJ, Zamarripa CA, Klausner M, Wakshlag J, Davis R, Dresser B, Kjaer C, Weerts EM, Vandrey R, Spindle TR. The pharmacokinetics and pharmacodynamics of a hemp-derived “full-spectrum” oral cannabinoid product with a 1:1 ratio of cannabidiol to cannabidiolic acid and delta-9-tetrahydrocannabinol to delta-9-tetrahydrocannabinolic acid: a double-blind, placebo-controlled, within-subjects human laboratory study. Cannabis and Cannabinoid Research. 2025;10(2):e299–e313.
6. Anderson L, Heblinski M, Absalom N, Hawkins N, Bowen M, Benson M, Zhang F, Bahceci D, Doohan P, Chebib M, et al. Cannabigerolic acid, a major biosynthetic precursor molecule in cannabis, exhibits divergent effects on seizures in mouse models of epilepsy. British Journal of Pharmacology. 2021;178(24):4826–4841.
7. Smeriglio A, Giofrè SV, Galati EM, Monforte MT, Cicero N, D’Angelo V, Grassi G, Circosta C. Inhibition of aldose reductase activity by Cannabis sativa chemotypes extracts with high content of cannabidiol or cannabigerol. Fitoterapia. 2018;127:101–108.
8. van Breemen RB, Muchiri RN, Bates TA, Weinstein JB, Leier HC, Farley S, Tafesse FG. Cannabinoids block cellular entry of SARS-CoV-2 and the emerging variants. Journal of Natural Products. 2022;85(1):176–184.
9. Brown JD, Goodin AJ. Will cannabis or cannabinoids protect you from SARS-CoV-2 infection or treat COVID-19?. Medical Cannabis and Cannabinoids. 2022;5(1):32–35.
10. Franzin M, et al. Incomplete decarboxylation of acidic cannabinoids in GC-MS leads to underestimation of the total cannabinoid content in cannabis oils without derivatization. Pharmaceutics. 2025;17(3):334.
11. Congressional Research Service. Changes to the statutory definition of hemp and implications for agricultural policy. In Focus IF13136, updated September 28, 2026.

This article is for information only and is not medical advice.