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Tetrahydrocannabinol (THC) Cannabinoid Research

Tetrahydrocannabinol (THC) Research Dashboard

1001

Primary Studies

413

Related Studies

1414

Total Studies

Clinical Studies

27

Clinical Meta-analyses

150

Double-blind human trials

99

Clinical human trials

Pre-Clinical Studies

336

Meta-analyses/Reviews

263

Animal studies

126

Laboratory studies

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CannaKeys has 1414 studies associated with Tetrahydrocannabinol (THC).

Here is a small sampling of Tetrahydrocannabinol (THC) studies by title:

  • THC and CBD: Similarities and differences between siblings
  • Oral THC: CBD cannabis extract in main symptoms of Alzheimer disease: agitation and weight loss
  • Reversible cerebral vasoconstriction syndrome associated with probable drug poisoning
  • Cannabis-opioid interaction in the treatment of fibromyalgia pain: an open-label, proof of concept study with randomization between treatment groups: cannabis, oxycodone or cannabis/oxycodone combination-the SPIRAL study
  • Characterization of the Antitumor Potential of Extracts of Cannabis sativa Strains with High CBD Content in Human Neuroblastoma

Components of the Tetrahydrocannabinol (THC) Research Dashboard

  • Top medical conditions associated with Tetrahydrocannabinol (THC)
  • Proven effects in clinical trials for Tetrahydrocannabinol (THC)
  • Receptors associated with Tetrahydrocannabinol (THC)
  • Individual study details for Tetrahydrocannabinol (THC)

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Overview - Tetrahydrocannabinol (THC)

Description of Tetrahydrocannabinol (THC)

The plant-based (phytocannabinoid) delta-9-tetrahydrocannabinol (delta-9-THC) was discovered in 1964, and by 2016 thirty-one distinct members of this family had been identified. THC is primarily (but not exclusively) responsible for many therapeutic and adverse mind-altering effects of the plant. THC is the most studied of all cannabis constituents. THC is exclusive to cannabis, but it is also produced synthetically.


Here we focus on delta-9-THC.

Other Names:

Delta 9-Tetrahydrocannabinol

Delta-9-THC


Dronabinol (Marinol®, Syndros®) are a synthetic version of delta-9-THC (other supplier-based synonyms)


IUPAC Name: (6aR,10aR)-6,6,9-trimethyl-3-pentyl-6a,7,8,10a-tetrahydrobenzo[c]chromen-1-ol


Molecular Formula: C21H30O2


Source–PubChem


Nabilone (Cesamet®) is a synthetic version of delta-9-THC (other supplier-based synonyms)


IUPAC Name: (6aR,10aR)-1-hydroxy-6,6-dimethyl-3-(2-methyloctan-2-yl)-7,8,10,10a-tetrahydro-6aH-benzo[c]chromen-9-one 


Molecular Formula: C24H36O3


Source–PubChem


 

Tetrahydrocannabinol (THC) Properties and Effects

Delta-9-THC is a multi-target molecule. THC-abundant cannabis plants (i.e., chemotype I) or products have proven effects such as bronchodilation (CB1 inhibits cholinergic contraction of bronchi), appetite stimulation, down-regulation of the body’s immune responses, and potent analgesic properties in cases of central pains. In addition, they have been employed therapeutically in patients with asthma, HIV/AIDS-related anorexia, rheumatoid arthritis, or spinal cord injuries.


THC's multiple and simultaneous effects can produce many safe and therapeutic results when understood and used with its complexity in mind. But, unfortunately, cannabis (especially THC-abundant types) can worsen things, especially in THC-sensitive individuals or several specific cases.


For instance, while THC has been shown to work via several pathways by which it can create apoptotic (anti-cancer) effects, various pre-clinical trials have discovered that colon, ovarian, and metastasizing breast cancer cell lines rely, at least in part, on GPR-55 for proliferation. Since THC is an agonist at GPR-55, these early study results suggest caution in using a THC-rich type of cannabis for these particular cancers. While it might turn out that THC’s positive effects via CB1 or CB2 outweigh the potential pitfalls of GPR-55 activation on possible proliferation, a Chemotype II balanced type of cannabis or cannabis-based therapeutic may be the advisable option until the science becomes more discerning for this specific situations.


Other examples of using caution when using a type of cannabis containing primarily THC include patients with pancreatitis, individuals with vulnerabilities to developing psychosis, adolescents, or during pregnancy, all of which especially warrant caution and careful discernment.


Most common dose-dependent delta-9-THC-associated adverse effects:


For evidence-based information on reducing the risk of cannabis use, click on the following link: Cannabis Use Guideline to Reduce Risk.


Adverse Effects of Synthetic Versions of Delta-9-THC: Dronabinol (Marinol) and Nabilone (Cesamet)

While Dronabinol (Marinol) and Nabilone (Cesamet) are synthetic forms of delta-9-THC, both have different molecular formulas (see names text box), resulting in diverse adverse effects potential.


In this systematic review and meta-analyses of clinical trials (2022), Dronabinol presented 111 "diverse but not severe" adverse effects, while Nabilone presented 40.



  • Occurrences of dizziness and dry mouth were most commonly noted in both Dronabinol and Nabilone treatment groups. Similarly, nausea, drowsiness, and fatigue occurred with similar frequency.

  • However, adverse effects of dizziness, dry mouth, and headache were significantly higher in patients treated with Dronabinol.

  • Drowsiness was >7 x as frequent in patients treated with nabilone than in the placebo group. 

Tetrahydrocannabinol (THC) Receptor Binding

Endocannabinoid System (ECS) and THC:


  1. CB1 moderate agonist with a mean ~Ki 25nM (using human tissue data from 16 trials)  (J. McPartland et al., 2007)

  2. CB2 moderate agonist with a mean ~Ki 35nM (using human tissue data from 16 trials)  (J. McPartland et al., 2007)


Endocannabinoidome (eCBome) and THC:

In addition, when THC binds with CB1 and CB2, it also co-activates, either in part or significantly, a diverse group of receptor sites (incomplete list), enzymes, neurotransmitters, hormones, and other signaling pathways:



  1. Acetylcholine (e.g., memory, wakefulness) E. Murillo-Rodríguez et al., 2018

  2. A1 (Adenosine1) (inhibitor)

  3. Cortisol (e.g., stress response) Kathmann et al., 2006

  4. Cytokines (anti-inflammatory) L. Jean-Gilles et al., 2010

  5. Cytokines (pro-inflammatory) F. Zádor et al., 2021

  6. Dopamine (e.g., motivation, reward) A. Terzian et al., 2011 Dopamine neurons contain CB2 receptors posited to be responsible for the tetrad effect associated with the use of cannabis (Q. R. Liu et al., 2020)

  7. Endogenous opioids (e.g., analgesia) M. Kathmann et al., 2006

    1. DOR (δ-Delta) (Delta opioid receptor)

    2. MOR (μ-Mu) (Mu opioid receptors)



  8. Epinephrine (e.g., fight, flight, or freeze) N. Niederhoffer et al., 2001

  9. Gamma-aminobutyric acid (GABA) (e.g., calming) S. Lee et al., 2010

  10. Ghrelin (e.g., hunger, angry) L. Senin et al., 2013

  11. Glucagon (e.g., hungry, angry) K. Patel et al., 2014

  12. Glutamate:(e.g., excitement, excitotoxicity) A. Köfalvi et al., 2020

  13. GlyRs (Glycine receptors) (N. Hejazi et al., 2006)–THC directly potentiates the function of GlyRs through an allosteric mechanism

  14. GPR18 (agonist)

  15. GPR55 (agonist) (the reader is also reminded that CBD is an antagonist at GPR55)

  16. Insulin (e.g., hungry, angry) A. Laguerre et al., 2021

  17. Leptin (e.g., satiated) B. Bosier et al., 2013

  18. Norepinephrine (e.g., stress, attention) R. Wyrofsky et al., 2019

  19. Oxytocin (e.g., trust, intimacy) D. Wei et al., 2015

  20. PPAR γ (agonist)

  21. Serotonin (e.g., happiness, well-being) I. Ibarra-Lecue et al., 2021

  22. Testosterone (e.g., confidence, aggression) J. Lim et al., 2023

  23. TRPV2 (agonist)

  24. TRPV3 (antagonist)

  25. TRPV4

  26. TRPM8 (antagonist)

  27. Vasopressin (e.g., social recognition, aggression) V. Luce et al., 2014

  28. Signaling Pathways:

    1. cAMP (cyclic adenosine monophosphate) (inhibition) (P. J. Little et al., 1991)–Dysfunction of cAMP signaling can contribute to some pathologies, including cancer



  29. Enzymes inhibited by THC

    1. ATX-β and ATX-γ (inhibition) (Autotaxin-β and -γ contribute to form lysophosphatidic acid (LPA), associated with neuropathies, fibrosis, immune disorders, MS, breast cancer, atherosclerosis (M. C. Eymery et al., 2023)

    2. CYP1A2 (inhibition) (S. Nasrin et al., 2021)

    3. CYP2B6 (inhibition) (S. Nasrin et al., 2021)

    4. CYP2C9 (inhibition) (S. Nasrin et al., 2021)

    5. CYP2D6 (inhibition) (S. Nasrin et al., 2021)





Ki legend:



  • Full/strong agonist Ki ~1-9nM

  • Moderate agonist Ki ~10-99nM

  • Weak agonist Ki ~100-999nM

  • Very weak agonist Ki ~1,000-up nM


(The reader is reminded that a smaller Ki is associated with the most potent effects.)

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Information on this site is based on scientific studies (human, animal, or in vitro), clinical experience, or traditional usage as cited in each article. The results reported may not necessarily occur in all individuals. For many of the conditions discussed, treatment with prescription or over-the-counter medication is also available. Consult your physician, nutritionally oriented health care practitioner, and/or pharmacist for any health problem and before using any supplements or before making any changes in prescribed medications.