Author: Luke Sholl
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With over a decade of experience writing about CBD and cannabinoids, Luke is an established journalist working as the lead writer for Cibdol and other cannabinoid publications. Committed to presenting factual, evidence-based content, his fascination with CBD also extends to fitness, nutrition, and disease prevention.
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What Is THCA (Tetrahydrocannabinolic Acid)?

Keep reading for a summary of THCA's critical attributes, side effects, supporting research, and legal status.

What is THCA?

Tetrahydrocannabinolic acid (THCA) is a raw cannabinoid found in the Cannabis sativa species. It is an acidic, non-psychotropic cannabinoid that results from the biosynthesis of precursor cannabinoid CBGA. When THCA is exposed to heat, it loses one carboxyl group and becomes THC, the cannabinoid most commonly associated with marijuana.

Side effects

In its acidic form, THCA doesn't appear to have any notable side effects. However, THCA is unstable and will naturally decarboxylate into the psychotropic cannabinoid THC over time.

Summary of THCA

• Analogue of THC
• Non-psychotropic
• Found in live cannabis plants (leaves)
• Most abundant non-psychotropic cannabinoid
• Appears to be an agonist of TRPV receptors
• Limited amount of supporting research

THCA and supporting research

Large-scale studies and clinical trials into the possible benefits of THCA are incredibly limited. There are, however, early indications that the cannabinoid may have anti-inflammatory and neuroprotective qualities.

In 2011, researchers at Leiden University published a study[1] outlining the interaction between THC, THCA, CBD, CBDA, CBG, and CBGA with cyclooxygenase enzymes (COX-1 and COX-2). These enzymes are important because they influence the production of prostaglandins, a lipid compound involved in inflammation. Results showed that all six cannabinoids "inhibited cyclooxygenase enzyme activity".

The neuroprotective qualities of THCA were tested in a 2012 animal study[2] published in Phytomedicine. The effect of THCA, alongside THC and CBD, was examined against the neurotoxin MPP+, an organic chemical responsible for cell death. Researchers concluded that "THC and THCA protect dopaminergic neurons", with THCA significantly increasing cell counts.

The British Journal of Pharmacology published a 2013 study[3] that outlined the potential impact of non-THC cannabinoids on cancer cells. In an effort to understand underlying mechanisms, researchers focused on cannabinoids that didn't bind with cannabinoid receptors but instead showed an affinity for TRP channels. THCA was found to inhibit androgen receptor cells involved in prostate cancer.

Legal status

Although THCA is not scheduled under the UN Convention on Psychotropic Substances, local regulations may vary due to its chemical similarity to THC.

Sources

[1] Ruhaak, L. R., Felth, J., Karlsson, P. C., Rafter, J. J., Verpoorte, R., & Bohlin, L. (2011). Evaluation of the Cyclooxygenase Inhibiting Effects of Six Major Cannabinoids Isolated from Cannabis sativa. Biological and Pharmaceutical Bulletin, 34(5), 774–778. https://doi.org/10.1248/bpb.34.774 [Source]

[2] Moldzio, R., Pacher, T., Krewenka, C., Kranner, B., Novak, J., Duvigneau, J. C., & Rausch, W. D. (2012). Effects of cannabinoids Δ(9)-tetrahydrocannabinol, Δ(9)-tetrahydrocannabinolic acid and cannabidiol in MPP+ affected murine mesencephalic cultures. Phytomedicine, 19(8–9), 819–824. https://doi.org/10.1016/j.phymed.2012.04.002 [Source]

[3] de Petrocellis, L., Ligresti, A., Schiano Moriello, A., Iappelli, M., Verde, R., Stott, C. G., Cristino, L., Orlando, P., & di Marzo, V. (2012). Non-THC cannabinoids inhibit prostate carcinoma growthin vitroandin vivo: pro-apoptotic effects and underlying mechanisms. British Journal of Pharmacology, 168(1), 79–102. https://doi.org/10.1111/j.1476-5381.2012.02027.x [Source]

Sources

[1] Ruhaak, L. R., Felth, J., Karlsson, P. C., Rafter, J. J., Verpoorte, R., & Bohlin, L. (2011). Evaluation of the Cyclooxygenase Inhibiting Effects of Six Major Cannabinoids Isolated from Cannabis sativa. Biological and Pharmaceutical Bulletin, 34(5), 774–778. https://doi.org/10.1248/bpb.34.774 [Source]

[2] Moldzio, R., Pacher, T., Krewenka, C., Kranner, B., Novak, J., Duvigneau, J. C., & Rausch, W. D. (2012). Effects of cannabinoids Δ(9)-tetrahydrocannabinol, Δ(9)-tetrahydrocannabinolic acid and cannabidiol in MPP+ affected murine mesencephalic cultures. Phytomedicine, 19(8–9), 819–824. https://doi.org/10.1016/j.phymed.2012.04.002 [Source]

[3] de Petrocellis, L., Ligresti, A., Schiano Moriello, A., Iappelli, M., Verde, R., Stott, C. G., Cristino, L., Orlando, P., & di Marzo, V. (2012). Non-THC cannabinoids inhibit prostate carcinoma growthin vitroandin vivo: pro-apoptotic effects and underlying mechanisms. British Journal of Pharmacology, 168(1), 79–102. https://doi.org/10.1111/j.1476-5381.2012.02027.x [Source]

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