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Review
. 2022 Mar 19;23(6):3344.
doi: 10.3390/ijms23063344.

Cannabinoids: Therapeutic Use in Clinical Practice

Cristina Pagano  1 , Giovanna Navarra  1 , Laura Coppola  1 , Giorgio Avilia  1 , Maurizio Bifulco  1 , Chiara Laezza  2
Affiliations
Review

Cannabinoids: Therapeutic Use in Clinical Practice

Cristina Pagano et al. Int J Mol Sci. .

Abstract

Medical case reports suggest that cannabinoids extracted from Cannabis sativa have therapeutic effects; however, the therapeutic employment is limited due to the psychotropic effect of its major component, Δ9-tetrahydrocannabinol (THC). The new scientific discoveries related to the endocannabinoid system, including new receptors, ligands, and mediators, allowed the development of new therapeutic targets for the treatment of several pathological disorders minimizing the undesirable psychotropic effects of some constituents of this plant. Today, FDA-approved drugs, such as nabiximols (a mixture of THC and non-psychoactive cannabidiol (CBD)), are employed in alleviating pain and spasticity in multiple sclerosis. Dronabinol and nabilone are used for the treatment of chemotherapy-induced nausea and vomiting in cancer patients. Dronabinol was approved for the treatment of anorexia in patients with AIDS (acquired immune deficiency syndrome). In this review, we highlighted the potential therapeutic efficacy of natural and synthetic cannabinoids and their clinical relevance in cancer, neurodegenerative and dermatological diseases, and viral infections.

Keywords: cancer; cannabinoids; neurodegenerative diseases; skin disorders; viral infections.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Main components of the endocannabinoid system (ECS). Biosynthesis of AEA and 2-AG take place on demand from membrane phospholipids by NAPE-PLD or calcium-dependent NAT and DAGL, respectively. The reuptake of endocannabinoids into cells occurs across the cell membrane by putative endocannabinoid protein transporters (EMT). FAAH is the main enzyme responsible for AEA degradation, while MAGL is the key enzyme in the hydrolysis of the 2-AG releasing arachidonic acid. Receptor targets of AEA and 2-AG on the plasma membrane are various: CB1, CB2, GPR18, GPR55, GPR119, and TRPs and in the nucleus PPARs. Abbreviations: EA: ethanolamine; AA: arachidonic acid; CB1: cannabinoid receptor 1, CB2: cannabinoid receptor 2, TRPs: transient receptor potential channels (V1-3, A1, and M8 types). GPRs: G-protein-coupled receptor (18, 55, and 119), and PPARs: peroxisome proliferator-activated nuclear receptors α, γ, or δ; PEA: palmitoylethanolamide; OEA: oleoylethanolamide.
Figure 2
Figure 2
Diseases in which cannabinoids exhibit their therapeutic effects.
See this image and copyright information in PMC

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