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Plate 507 of 545Verified

Tetrahydrocannabinol (THC)

PubChem records this structure as Tetrahydrocannabinol.

Also known asDelta-9-tetrahydrocannabinol · Dronabinol · THC · Marinol · delta9-Tetrahydrocannabinol · delta9-THC · delta1-THC · delta-9-THC

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

PubChem CID
16078
ChEMBL
CHEMBL465
Measurements
65
InChIKey
CYQFCXCEBYINGO-IAGOWNOFSA-N

I · Summary

What is known

Published passages, each quoted whole and attributed to the database that published it. Two blocks are written here rather than quoted, and both say so where they stand: the synthesized summary at the top, which may draw only on the passages beneath it, and the history note, which cites the works it came from. Every claim in either carries a marker to its source.

No synthesized summary

31 passages, the most of any compound, and the largest share of them are dosing, formulation and regulatory detail for named pharmaceutical products. Summarizing those accurately means reproducing dose figures in synthesized prose, which is the one place a marker does not protect a reader who misreads the sentence.

What it is

  • delta-9-Tetrahydrocannabinol (Δ9-THC) can cause developmental toxicity according to an independent committee of scientific and health experts.
  • 1-trans-delta-9-tetrahydrocannabinol appears as brown amorphous semi-solid, viscous oil or chunky golden yellow solid. (NTP, 1992)

    CAMEO ChemicalsNational Toxicology Program, Institute of Environmental Health Sciences, National Institutes of Health (NTP). 1992. National Toxicology Program Chemical Repository Database. Research Triangle Park, North Carolina.

  • Delta(9)-tetrahydrocannabinol is a diterpenoid that is 6a,7,8,10a-tetrahydro-6H-benzo[c]chromene substituted at position 1 by a hydroxy group, positions 6, 6 and 9 by methyl groups and at position 3 by a pentyl group. The principal psychoactive constituent of the cannabis plant, it is used for treatment of anorexia associated with AIDS as well as nausea and vomiting associated with cancer chemotherapy. It has a role as a metabolite, a non-narcotic analgesic, a hallucinogen, an epitope and a cannabinoid receptor agonist. It is a diterpenoid, a polyketide, a benzochromene and a phytocannabinoid.
  • Dronabinol is a DEA Schedule II controlled substance. Substances in the DEA Schedule II have a high potential for abuse which may lead to severe psychological or physical dependence. It is a Hallucinogenic substances substance.

Recognized use

  • Hallucinogens Psychotropic Drugs Analgesics, Non-Narcotic Cannabinoid Receptor Agonists

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)National Library of Medicine's Medical Subject Headings online file (MeSH, 2017); Available from, as of September 13, 2017: https://meshb.nlm.nih.gov/record/ui?ui=D013759

  • Dronabinol capsules are indicated for the treatment of nausea and vomiting associated with cancer chemotherapy in patients who have failed to respond adequately to conventional antiemetic treatments. /Included in US product label/

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)US Natl Inst Health; DailyMed. Current Medication Information for DRONABINOL capsule (September 2015). Available from, as of September 13, 2017: https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=68b4168b-5782-4e68-a25a-5b4e4408dbce

  • Dronabinol is used for the treatment of anorexia associated with weight loss in patients with acquired immunodeficiency syndrome (AIDS). Dronabinol is designated an orphan drug by the US Food and Drug Administration (FDA) for use in this condition.

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)American Society of Health-System Pharmacists 2011; Drug Information 2011. Bethesda, MD. 2011

  • /EXPL THER/ BACKGROUND: Cannabis use disorder is associated with substantial morbidity and, after alcohol, is the most common drug bringing adolescents and adults into treatment. At present, there are no FDA-approved medications for cannabis use disorder. Combined pharmacologic interventions might be particularly useful in mitigating withdrawal symptoms and promoting abstinence. OBJECTIVE: The purpose of this study was to evaluate the safety and efficacy of dronabinol, a synthetic form of delta-9-tetrahydrocannabinol, a naturally occurring pharmacologically active component of marijuana, and lofexidine, an alpha-2 agonist, in treating cannabis dependence. METHODS: One hundred fifty six canna…

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)PMID 26711160Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4729291

  • Dronabinol is indicated for the treatment of anorexia associated with weight loss in patients with AIDS, and nausea and vomiting associated with cancer chemotherapy in patients who have failed to respond adequately to conventional antiemetic treatments.

    Drug Indication

    DrugBank

  • The Cannabis sativa plant produces numerous bioactive compounds with potential medical benefits, including terpenes, flavonoids, and cannabinoids. Among these, delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD) are the most extensively researched and studied compounds. THC is responsible for the psychoactive effects associated with cannabis consumption. Historically, cannabis was predominantly utilized for recreational purposes due to its psychoactive properties. However, more recently, there has been significant interest in its potential medical applications. The U.S. Food and Drug Administration (FDA) recognizes the potential value of cannabis for medical purposes and acknowledges th…

    Drug Indication

    StatPearls

  • Dronabinol is a synthetic form of tetrahydrocannabinol ('THC'), which obtained FDA approval in 1985 for the treatment of HIV/AIDs-induced anorexia and chemotherapy-induced nausea and vomiting ('CINV') in patients who do not successfully respond to conventional antiemetics. Dronabinol also has off-label use to treat obstructive sleep apnea with mixed and unclear efficacy (only Phase II trials). Therefore, the American Academy of Sleep Medicine does not support its use until reliable data is available (such as Phase III trials). Recent studies also utilized dronabinol in chronic pain patients, which showed efficacy compared to placebo, but further research is necessary. Additionally, current f…

    Drug Indication

    StatPearls

  • The primary psychoactive component of cannabis; Used therapeutically as antiemetic and appetite stimulant; [Merck Index]

    Use Classification

    Haz-Map, Information on Hazardous Chemicals and Occupational DiseasesMerck Index - O'Neil MJ, Heckelman PE, Dobbelaar PH, Roman KJ (eds). The Merck Index, An Encyclopedia of Chemicals, Drugs, and Biologicals, 15th Ed. Cambridge, UK: The Royal Society of Chemistry, 2013.

  • Tetrahydrocannabinols (DEA Code Number: 7370) is a Schedule I contolled substance. /Tetrahydrocannabinols/

    Use Classification

    Hazardous Substances Data Bank (HSDB)21 CFR 1308.11(d) (USDEA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of October 19, 2017: https://www.ecfr.gov

  • Marihuana (DEA Code Number: 7360) is a Schedule I controlled substance. /Marihuana/

    Use Classification

    Hazardous Substances Data Bank (HSDB)21 CFR 1308.11(d) (USDEA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of October 19, 2017: https://www.ecfr.gov

  • Dronabinol [(-)-delta-9-trans tetrahydrocannabinol] in an oral solution in a drug product approved for marketing by the U.S. Food and Drug Administration (DEA Code Number: 7365) is a Schedule II controlled substance. /Dronabinol/

    Use Classification

    Hazardous Substances Data Bank (HSDB)21 CFR 1308.12(f) (USDEA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of October 19, 2017: https://www.ecfr.gov

How it acts

  • Dronabinol is a synthetic form of delta-9-tetrahydrocannabinol (Δ⁹-THC), the primary psychoactive component of cannabis (marijuana). THC demonstrates its effects through weak partial agonist activity at Cannabinoid-1 (CB1R) and Cannabinoid-2 (CB2R) receptors, which results in the well-known effects of smoking cannabis such as increased appetite, reduced pain, and changes in emotional and cognitive processes.
  • The availability of potent synthetic agonists for cannabinoid receptors has facilitated our understanding of cannabinoid actions on synaptic transmission in the central nervous system. Moreover, the ability of these compounds to inhibit neurotransmitter release at many central synapses is thought to underlie most of the behavioral effects of cannabinoid agonists. However, despite the widespread use and misuse of marijuana, and recognition of its potential adverse psychological effects in humans, comparatively few studies have examined the actions of its primary psychoactive constituent, delta(9)-tetrahydrocannabinol (THC), at well-defined synaptic pathways. Here we examine the recent literat…

    Hazardous Substances Data Bank (HSDB)PMID 23209160Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3721267

Behavior carries the pharmacological classes and the acute-effect durations, with plasma half-life kept separate from duration of effect.

In the body

  • Dronabinol is almost completely absorbed (90 to 95%) after a single oral dose. Due to the combined effects of first-pass hepatic metabolism and high lipid solubility, only 10 to 20% of the administered dose reaches systemic circulation. Relative bioavailability data from healthy male and female subjects suggest that a dose of 4.2 mg of SYNDROS provides comparable systemic exposure (Cmax and AUC) to a 5 mg dronabinol capsule, under fasted conditions, with the Cmax and AUCinf of 1.9 ± 1.3 ng/mL and 3.8 ± 1.8 ng.h/mL respectively. The concentrations of both dronabinol and its major active metabolite (11-hydroxy-delta-9-THC) peak at approximately 0.5 to 4 hours after oral dosing with SYNDROS and…

    Absorption, Distribution and Excretion

    DrugBank

  • Dronabinol and its biotransformation products are excreted in both feces and urine. Biliary excretion is the major route of excretion with about half of a radiolabeled oral dose being recovered from the feces within 72 hours as contrasted with 10 to 15% recovered from urine. Less than 5% of an oral dose is recovered unchanged in the feces. Due to its redistribution, dronabinol and its metabolites may be excreted for prolonged periods of time. Following single-dose administration, dronabinol metabolites have been detected for more than 5 weeks in the urine and feces. In a study of dronabinol capsules involving AIDS patients, urinary cannabinoid/creatinine concentration ratios were studied b…

    Absorption, Distribution and Excretion

    DrugBank

  • Dronabinol has a large apparent volume of distribution, approximately 10 L/kg, because of its lipid solubility.

    Absorption, Distribution and Excretion

    DrugBank

  • The value for clearance average is about 0.2 L/kg-hr but is highly variable due to the complexity of cannabinoid distribution.

    Absorption, Distribution and Excretion

    DrugBank

  • THC is primarily metabolized in the liver by microsomal hydroxylation and oxidation reactions catalyzed by Cytochrome P450 enzymes. 11-hydroxy-▵9-tetrahydrocannabinol (11-OH-THC) is the primary active metabolite, capable of producing psychological and behavioural effects, which is then metabolized into 11-nor-9-carboxy-▵ 9-tetrahydrocannabinol (THC-COOH), THC's primary inactive metabolite. Dronabinol and its principal active metabolite, 11-OH-delta-9-THC, are present in approximately equal concentrations in plasma. Concentrations of both parent drug and metabolite peak at approximately 0.5 to 4 hours after oral dosing and decline over several days.

    Metabolism/Metabolites

    DrugBank

  • The analgesic activity of delta-8- and delta-9-THC is mainly due to the 11-hydroxy metabolite.

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)Wilson RS, May EL; J Med Chem 18: 700-3 (1975) as cited in DHHS/NIDA; Research Monograph Series 52: Testing Drugs for Physical Dependence Potential and Abuse Liability p.71 (1984) DHHS Pub No. (ADM)87-1332

  • The metabolism of delta(9)-tetrahydrocannabinol (THC) is relatively complex, and over 80 metabolites have been identified. However, much less is known about the formation and fate of cannabinoid conjugates. Bile excretion is known to be an important route for the elimination of phase II metabolites. A liquid chromatography-tandem mass spectrometry LC-MS/MS procedure for measuring cannabinoids in oral fluid was adapted, validated and applied to 10 bile samples. THC, 11-hydroxy-delta(9)-tetrahydrocannabinol (11-OH-THC), 11-nor-9-carboxy-delta(9)-tetrahydrocannabinol (THCCOOH), cannabinol (CBN), cannabidiol (CBD), delta(9)-tetrahydrocannabinolic acid A (THC-A), 11-nor-9-carboxy-delta(9)-tetrahy…

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 22980143Fabritius M et al; Forensic Sci Int 223 (1-3): 114-8 (2012)

  • The presence of the metabolite 11-nor-9-carboxy-delta-9-tetrahydrocannabinol (C-THC) in hair is generally accepted as the definitive proof of delta-9-tetrahydrocannabinol (THC) ingestion. During hair analysis, the removal of any potential C-THC external contamination that could result from marijuana smoke or close personal contact via a wash procedure is critical. Here, we performed a series of experiments to demonstrate that C-THC is the reliable indicator of marijuana ingestion when paired with the correct washing procedure to remove potential external contamination.

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 27185816Hill VA et al; J Anal Toxicol 40 (5): 345-9 (2016)

History, discovery and cultural use

— Not in this archive. PubChem, ChEMBL and the Human Protein Atlas publish pharmacology, regulation and toxicology, and none of them publishes a heading for when Tetrahydrocannabinol (THC) was first made, by whom, or how it has been used. That is a gap in the databases this site reads and not a gap in the literature — the history of these compounds is written, at length and under peer review, in the works below. This site does not summarize them; it says where they are. Where a published passage above happens to touch origin or traditional use, it appears inside the entry that carries it.

Histories of this field

Scholarship on psychedelics generally, not on Tetrahydrocannabinol (THC) specifically. Whether any of these treats this compound is a question for the book, not for this page.

  • Mescaline: A Global History of the First Psychedelic

    Traces mescaline and the peyote and San Pedro cacti from pre-Columbian ritual use through nineteenth-century chemistry to twentieth-century psychiatry and the counterculture.

    Jay M. Mescaline: A Global History of the First Psychedelic. Yale University Press, New Haven and London; 2019. ISBN 9780300231076.

  • Expanding Mindscapes: A Global History of Psychedelicsopen access

    Essays on the international and cross-cultural history of psychedelic science, deliberately decentring the standard North American and European account.

    Dyck E, Elcock C, editors. Expanding Mindscapes: A Global History of Psychedelics. The MIT Press, Cambridge MA; 2023. ISBN 9780262546935 (paper), 9780262376891 (open access). doi:10.7551/mitpress/14417.001.0001.

  • Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers

    Botany, ethnography and chemistry of the principal hallucinogenic plants, by the founder of modern ethnobotany and the chemist who first synthesized LSD.

    Schultes RE, Hofmann A, Rätsch C. Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers. 2nd ed. Healing Arts Press, Rochester VT; 2001. ISBN 9780892819799.

  • Psychonauts: Drugs and the Making of the Modern Mind

    The tradition of scientific self-experimentation with psychoactive drugs, and its part in the emergence of psychology and of modernism.

    Jay M. Psychonauts: Drugs and the Making of the Modern Mind. Yale University Press, New Haven; 2023. ISBN 9780300257946.

  • Ancient Psychoactive Substances

    Archaeological and bioarchaeological evidence for psychoactive plant use across the ancient world.

    Fitzpatrick SM, editor. Ancient Psychoactive Substances. University Press of Florida, Gainesville; 2018. ISBN 9780813056708.

  • History and Current Status of Psychedelics and Entactogens for the Treatment of Psychiatric Disorders

    A chapter tracing psychedelic and entactogen research from earlier ritual use through the mid-century research period to current clinical trials.

    Stroud C, Posey Norris SM, Matney C, editors. History and Current Status of Psychedelics and Entactogens for the Treatment of Psychiatric Disorders. In: Exploring Psychedelics and Entactogens as Treatments for Psychiatric Disorders: Proceedings of a Workshop. National Academies Press, Washington DC; 2022. NBK587225.

    Workshop proceedings record what participants said; they are not a consensus statement of the National Academies.

  • Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions

    Peer-reviewed review covering the isolation, synthesis, pharmacology and ritual use of peyote and mescaline.

    Dinis-Oliveira RJ, Pereira CL, da Silva DD. Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions. Current Molecular Pharmacology 12(3):184–194; 2019. doi:10.2174/1874467211666181010154139.

Institutional archives

  • Heffter Research Institute Funds and coordinates clinical research on psilocybin, and keeps records of the studies it has supported since 1993. Sponsors the research it archives.
  • Multidisciplinary Association for Psychedelic Studies (MAPS) Sponsors clinical research, chiefly on MDMA-assisted therapy, and publishes an archive of historical and contemporary documents. A sponsor and an advocacy organization, not a disinterested archive; its clinical programme has a commercial arm.

The rest of this dossier

  • Affinity — 65 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — 15 published passages, plus any assay in this archive bearing on toxicity.
  • Legal — DEA Schedule II and III, with the passage it was read from.
  • Systems — where this compound’s targets are transcribed, by brain region and tissue.

Passages via PubChem descriptive sections, aggregating DrugBank, LiverTox, FDA, DEA, HSDB, EPA. Each is quoted whole and attributed to the database that published it. The only prose written here about Tetrahydrocannabinol (THC) is the history note, which says so on its face and carries a reference for every claim in it.

II · Identity

Structure and descriptors

Descriptors are computed here with RDKit from the structure PubChem returns — not from the archive's stored copy, so an edited local structure cannot reach this table.

2D structural depiction of Tetrahydrocannabinol
Depiction served by PubChem for CID 16078. Not redrawn here, so the picture and the identity come from the same record.
Formula
C21H30O2R
Molecular weight
314.47g/molR
Exact mass
314.2246DaR
cLogP
5.74R
TPSA
29.5ŲR
H-bond donors
1R
H-bond acceptors
2R
Rotatable bonds
4R
Aromatic rings
1R
Heavy atoms
23R
Fraction sp³
0.619R
Formal charge
0R

Computed with RDKit 2025.09.2 from the SMILES returned by PubChem. Audit run 26/09/2026.

III · Behavior

Behavioral summary

Class, mechanism, and the duration of acute effects — each quoted from the record or trial that publishes it. Duration of effects and plasma half-life are shown separately, because they are different quantities and diverge by a factor of three or four.

Classification

Duration of acute subjective effects

3.3–4.3 h

vaporized cannabis, 2.9% and 6.7% Δ9-THC; 19 healthy adults

“Subjective effects persisted through 3.3-4.3 h, with alcohol potentiating the duration of the cannabis effects”
Hartman RL et al., Drug testing and analysis 2016. PMID 26257143

~5 h to recovery of driving-related cognitive skills

inhaled 20 mg Δ9-THC

“The latter model predicted that most driving-related cognitive skills would 'recover' (Hedges' g=-0.25) within ∼5-hs (and almost all within ∼7-hs) of inhaling 20 mg of Δ9-THC; oral Δ9-THC-induced impairment may take longer to subside”
Impairment recovery, not duration of subjective effects — a related but distinct measure.McCartney D et al., Neuroscience and biobehavioral reviews 2021. PMID 33497784

Plasma elimination half-life

How fast the body clears the drug — not how long the effects last. The two diverge sharply: LSD is cleared with a half-life of about 2.6 h while its subjective effects run 8–12 h.

  • The elimination phase of dronabinol can be described using a two-compartment model with an initial (alpha) half-life of about 4 hours and a terminal (beta) half-life of 25 to 36 hours.
    DrugBank
  • After the pseudo-equilibrium is reached, THC is then slowly eliminated. This slow elimination is primarily due to the slow return of THC from sequestered tissues to blood. The terminal half-life of THC is approximately 1 day. /Several investigators have/ suggested terminal half-life /ranging between/ 19 to 36 hours. There are no significa…
    Hazardous Substances Data Bank (HSDB)DHHS/NIDA; Research Monograph Series 79: Structure-Activity Relationships of the Cannabinoids p.XX (1987) DHHS Pub No. (ADM)90-1534
  • The elimination half-life of dronabinol (delta-1-tetrahydrocannabinol) in 3 chronic marihuana users following smoking 4 cigarettes over a 2 day period is reported. The elimination half-life in blood plasma was calculated to be 4.1 days (range 2.9-5.0 days).
    Hazardous Substances Data Bank (HSDB)Johansson E et al; J Pharm Pharmcol 40: 374-5 (1988)

Primary pharmacological drivers

  • Cannabinoid CB1 receptor agonist16570099

Mechanism, as published

Quoted verbatim from the database named after each passage, never summarized.

  • The availability of potent synthetic agonists for cannabinoid receptors has facilitated our understanding of cannabinoid actions on synaptic transmission in the central nervous system. Moreover, the ability of these compounds to inhibit neurotransmitter release at many central synapses is thought to underlie most of the behavioral effects…
    Hazardous Substances Data Bank (HSDB)PMID 23209160Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3721267
  • Cannabis has potential therapeutic use but tetrahydrocannabinol (THC), its main psychoactive component, appears as a risk factor for ischemic stroke in young adults. We therefore evaluate the effects of THC on brain mitochondrial function and oxidative stress, key factors involved in stroke. Maximal oxidative capacities V max (complexes I…
    Hazardous Substances Data Bank (HSDB)PMID 25654095Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4310259
  • MDSCs are potent immunosuppressive cells that are induced during inflammatory responses, as well as by cancers, to evade the antitumor immunity. We recently demonstrated that marijuana cannabinoids are potent inducers of MDSCs. In the current study, we investigated the epigenetic mechanisms through which THC, an exogenous cannabinoid, ind…
    Hazardous Substances Data Bank (HSDB)PMID 25713087Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4370051
  • Dronabinol is a synthetic form of delta-9-tetrahydrocannabinol (Δ⁹-THC), the primary psychoactive component of cannabis (marijuana). THC demonstrates its effects through weak partial agonist activity at Cannabinoid-1 (CB1R) and Cannabinoid-2 (CB2R) receptors, which results in the well-known effects of smoking cannabis such as increased ap…
    DrugBank
  • Dronabinol-induced sympathomimetic activity may result in tachycardia and/or conjunctival injection. Its effects on blood pressure are inconsistent, but subjects have experienced orthostatic hypotension and/or syncope upon abrupt standing. Dronabinol also demonstrates reversible effects on appetite, mood, cognition, memory, and perceptio…
    DrugBank

IV · Clinical

Clinical description

Where this compound's substance class sits in ICD-11 and DSM-5-TR, and how much of the recorded literature speaks to each domain of a mental status examination.

Filed under Hallucinogens

  • 6C49Disorders due to use of hallucinogens

Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR): Hallucinogen-Related Disorders. Category names only — the manual is in copyright and no diagnostic criterion is reproduced here.

Filed under Cannabinoid Receptor Agonists

  • 6C41Disorders due to use of cannabis
  • 6C42Disorders due to use of synthetic cannabinoids

Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR): Cannabis-Related Disorders. Category names only — the manual is in copyright and no diagnostic criterion is reproduced here.

MeSH does not separate plant cannabinoids from synthetic agonists; ICD-11 does. Both chapters are listed because the class alone does not decide which applies.

How much has been written about each domain

The clinical domains, and how many of the records this archive holds for this compound say something under each. What the terms mean, and the word list behind every spoke, are set out in the method.

Affect0Mood3Perception0Cognition4Thought process0Thought content0Psychomotor activity0Insight and judgment0
This measures the literature, not the compound. Each spoke counts how many of the 26 records this archive holds for this compound say something under that domain — 4 at the widest ring. A long spoke means the subject has been written about, not that the effect is strong, and a spoke at the center means nothing here discusses it rather than that nothing happens. The terms behind each domain are listed in the method.
Mood 3
matched on “elation”, “mood” · in Pharmacology: Pharmacodynamics; Toxicology: Hazardous Substances Data Bank (HSDB); PMID 24281276
Cognition 4
matched on “cognitiv”, “memory” · in Pharmacology: Mechanism of Action; Pharmacology: Pharmacodynamics; Toxicology: Hazardous Substances Data Bank (HSDB); PMID 33497784

V · Systems

Systems physiology

Where the targets this compound binds are transcribed — brain regions on the left, peripheral and autonomic tissues on the right. A join of two measurements, not a claim about what the compound does to either.

0846 nTPM

Square-root ramp · shared scale across both plates

Shading is transcript level — not affinity, and not affinity combined with expression. Outlined but unshaded organs hold none of this compound’s resolved targets above the atlas’s detection threshold. Anatomy from EMBL-EBI Anatomogram (Apache License 2.0); regions identified by Uberon (uberon.org), CC BY 3.0.

Brain regions

Regions where this compound's measured targets are transcribed. Linked from the plate above.

  1. retina

    411.4 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX411.4
    • CB1CNR17.5 pX1.1
    • CB2CNR28.5 pX0.1
    • Nuclear receptor subfamily 1 group I member 2NR1I24.9 pX0.1
  2. cerebral cortex

    201.5 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX201.5
    • CB1CNR17.5 pX18.6
  3. hypothalamus

    168.6 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX168.6
    • CB1CNR17.5 pX9.0
    • Nuclear receptor subfamily 1 group I member 2NR1I24.9 pX0.3
  4. midbrain

    149.5 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX149.5
    • CB1CNR17.5 pX2.1
  5. basal ganglia

    148.1 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX148.1
    • CB1CNR17.5 pX15.1
    • Nuclear receptor subfamily 1 group I member 2NR1I24.9 pX0.1
  6. amygdala

    124.7 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX124.7
    • CB1CNR17.5 pX13.3
  7. cerebellum

    122.7 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX122.7
    • CB1CNR17.5 pX18.3
  8. hippocampal formation

    120.5 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX120.5
    • CB1CNR17.5 pX13.2
  9. spinal cord

    115.7 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX115.7
    • CB1CNR17.5 pX1.7
  10. pituitary gland

    91.0 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX91.0
    • CB1CNR17.5 pX17.3

Peripheral & autonomic

Tissues outside the CNS expressing the same targets — where a compound's bodily effects become possible.

  1. skeletal muscle

    845.9 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX845.9
    • CB1CNR17.5 pX1.8
    • CB2CNR28.5 pX1.5
  2. liver

    658.2 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX658.2
    • Nuclear receptor subfamily 1 group I member 2NR1I24.9 pX44.3
    • CB1CNR17.5 pX0.1
    • CB2CNR28.5 pX0.1
  3. kidney

    355.4 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX355.4
    • CB1CNR17.5 pX0.6
    • Nuclear receptor subfamily 1 group I member 2NR1I24.9 pX0.1
  4. adrenal gland

    323.8 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX323.8
    • CB1CNR17.5 pX4.6
    • Nuclear receptor subfamily 1 group I member 2NR1I24.9 pX0.1
  5. heart muscle

    321.8 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX321.8
    • CB1CNR17.5 pX0.8
  6. small intestine

    273.2 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX273.2
    • Nuclear receptor subfamily 1 group I member 2NR1I24.9 pX29.4
    • CB1CNR17.5 pX8.1
    • CB2CNR28.5 pX3.1
  7. colon

    262.4 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX262.4
    • Nuclear receptor subfamily 1 group I member 2NR1I24.9 pX11.5
    • CB1CNR17.5 pX10.0
    • CB2CNR28.5 pX0.2
  8. salivary gland

    242.3 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX242.3
    • CB1CNR17.5 pX1.8
    • CB2CNR28.5 pX0.1
  9. lung

    232.6 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX232.6
    • CB1CNR17.5 pX2.8
    • CB2CNR28.5 pX0.1
  10. urinary bladder

    210.6 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX210.6
    • CB1CNR17.5 pX3.4
    • CB2CNR28.5 pX0.3
  11. spleen

    176.6 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX176.6
    • CB2CNR28.5 pX8.4
    • CB1CNR17.5 pX1.4
    • Nuclear receptor subfamily 1 group I member 2NR1I24.9 pX0.1
  12. thyroid gland

    172.7 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX172.7
    • CB1CNR17.5 pX3.9
    • CB2CNR28.5 pX0.2
  13. stomach 1

    170.7 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX170.7
    • CB1CNR17.5 pX3.4
    • Nuclear receptor subfamily 1 group I member 2NR1I24.9 pX1.6
    • CB2CNR28.5 pX0.4
  14. duodenum

    148.7 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX148.7
    • Nuclear receptor subfamily 1 group I member 2NR1I24.9 pX26.5
    • CB1CNR17.5 pX0.6
    • CB2CNR28.5 pX0.1
  15. pancreas

    140.2 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX140.2
    • CB1CNR17.5 pX1.2
    • Nuclear receptor subfamily 1 group I member 2NR1I24.9 pX0.1
  16. smooth muscle

    116.0 nTPM
    • L-lactate dehydrogenase A chainLDHA4.9 pX116.0
    • CB1CNR17.5 pX2.3
    • Nuclear receptor subfamily 1 group I member 2NR1I24.9 pX0.5

Each row joins two published measurements and nothing else: the affinity this archive holds for the compound at that target, and the transcript level the Human Protein Atlas reports for that target’s gene in that region. Bars scale with expression only. Expression is not activation — a receptor transcribed in a region is a receptor available to be bound there, which is a weaker and more defensible claim than saying the region is affected.

2 of this compound’s targets could not be resolved to a gene and are absent from both columns: Cannabinoid receptor, Transient receptor potential cation channel subfamily M member 8.

Expression data from Human Protein Atlas (CC BY-SA 3.0), RNA expression, nTPM (normalized transcripts per million), consensus tissue dataset. Uhlén M, et al. Tissue-based map of the human proteome. Science. 2015;347(6220):1260419.

VI · Profile

Affinity rosette

The strongest measurement at each of 6 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.

CB1 — Ki 8.54 pXCB2 — Ki 8.48 pXCannabinoid receptor — Ki 7.39 pXTransient receptor potential cation channel subfamily M member 8 — IC50 6.80 pXNuclear receptor subfamily 1 group I member 2 — EC50 4.90 pXL-lactate dehydrogenase A chain — Ki 4.85 pXCB1CB2Cannabinoid rece…Transient recept…Nuclear receptor…L-lactate dehydr…579
Fig. Radius is pX = −log₁₀(value in M), that is 9 − log₁₀(value in nM), computed from the normalized measurement. Hatched wedges are equilibrium binding constants (Ki, Kd); dashed outlines are functional readouts (IC₅₀, EC₅₀, AC₅₀, potency), which answer a different question and are not pooled with them. Rings mark whole pX units from 5 to 10, labeled every second ring in the gutter at the top. Where a target carries several measurements, the strongest is drawn.

VII · Toxicology

Toxicological profile

What has been measured, and what has been published — kept apart, and neither scored. There is no risk rating on this page; the archive once carried one, identical for every compound, produced by a stub.

Measured in this archive

Assays that bear on toxicity, drawn from the same ChEMBL records as everything else on this page. They are measurements of what a compound binds or does to cells — not verdicts about what it does to a person.

No hERG, cytochrome, cytotoxicity or transport measurement exists for Tetrahydrocannabinol (THC) in this archive.

Lethal-dose values — animal studies

These are not human doses. An LD50 is the dose killing half of a group of animals of one species by one route, and it is a poor predictor of human risk for these compounds. Each value is printed whole, with the species and route it was measured in, because a lethal dose separated from those two facts is worse than no figure at all. Nothing here supports inferring a safe dose for anyone.

  • LD50 Rat male oral 1270 mg/kg

    Hazardous Substances Data Bank (HSDB)Budavari, S. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 1996., p. 1573

  • LD50 Rat female oral 730 mg/kg

    Hazardous Substances Data Bank (HSDB)Budavari, S. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 1996., p. 1573

  • LD50 Rat male oral 800 mg/kg (sesame oil emulsion)

    Hazardous Substances Data Bank (HSDB)O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 1584

  • LD50 Rat male iv 35.5 mg/kg (sesame oil emulsion)

    Hazardous Substances Data Bank (HSDB)O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 1584

  • For more Non-Human Toxicity Values (Complete) data for delta 9-Tetrahydrocannabinol (12 total), please visit the HSDB record page.

    Hazardous Substances Data Bank (HSDB)

As published

Quoted verbatim from the database named after each passage, never summarized — a summary of a toxicology statement is a new claim.

Toxicity Summary

  • IDENTIFICATION AND USE: delta 9-tetrahydrocannabinol (THC, dronabinol) is light yellow resinous oil. This is a Schedule I controlled substance in the USA. The only legal medical application for marijuana is to reduce the adverse effects of chemotherapy for cancer patients, some patients have been given THC to reduce the pressure in the eye from glaucoma. HUMAN STUDIES: An oral dose of 20 mg of delta-9-THC or the smo…
  • The median lethal dose (LD50) of THC has been determined in various animal species through oral administration and ranges from 800 to 9000 mg/kg. In humans, there have been no recorded instances of fatal overdoses resulting from acute THC use. However, estimates for a potentially lethal human dose range from 4 to 15 g.
  • Toxicity
  • The mechanism of action of marinol is not completely understood. It is thought that cannabinoid receptors in neural tissues may mediate the effects of dronabinol and other cannabinoids. Animal studies with other cannabinoids suggest that marinol's antiemetic effects may be due to inhibition of the vomiting control mechanism in the medulla oblongata.

Hepatotoxicity

  • Serum aminotransferase elevations during dronabinol therapy were reported to occur in 6% of treated patients compared to 4.3% in controls who receiving cancer chemotherapy. The aminotransferase elevations were transient, mild-to-moderate in severity, and not associated with symptoms or jaundice. There have been no convincing cases of clinically apparent liver injury attributable to dronabinol published in the literat…

Human Toxicity Excerpts

  • /HUMAN EXPOSURE STUDIES/ In a study of the pharmacodynamics of chronic dronabinol exposure, healthy male volunteers (N=12) received 210 mg/day dronabinol, administered orally in divided doses, for 16 days. An initial tachycardia induced by dronabinol was replaced successively by normal sinus rhythm and then bradycardia. A decrease in supine blood pressure, made worse by standing, was also observed initially. These v…

    Hazardous Substances Data Bank (HSDB)US Natl Inst Health; DailyMed. Current Medication Information for DRONABINOL capsule (September 2015). Available from, as of September 13, 2017: https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=68b4168b-5782-4e68-a25a-5b4e4408dbce

  • /HUMAN EXPOSURE STUDIES/ Tetrahydrocannabinol, even in amounts equivalent to small doses of cannabis, impaired immediate memory in 8 young men.

    Hazardous Substances Data Bank (HSDB)Reynolds, J.E.F., Prasad, A.B. (eds.) Martindale-The Extra Pharmacopoeia. 28th ed. London: The Pharmaceutical Press, 1982., p. 354

  • /HUMAN EXPOSURE STUDIES/ BACKGROUND: Many cannabinoid medications are approved in North America or in phase III trials, such as dronabinol, nabilone, or nabiximols. Little is known about their subjective psychoactive effects when used for pain management. We hypothesized that when used for pain, dronabinol has psychoactive effects in a dose-response relationship, whose peak effects are comparable with smoking marijua…

    Hazardous Substances Data Bank (HSDB)PMID 24281276Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4013220

  • /HUMAN EXPOSURE STUDIES/ Subacute pulmonary effects of heavy marijuana smoking (five 2% delta-9-THC cigarettes for 60 days) include mild decreases in FEV1, maximal midexpiratory flow rate, large-airway conductance and diffusion capacity.

    Hazardous Substances Data Bank (HSDB)Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing Co., Inc. 1988., p. 680

  • For more Human Toxicity Excerpts (Complete) data for delta 9-Tetrahydrocannabinol (70 total), please visit the HSDB record page.

Published passages via PubChem toxicology sections, aggregating Hazardous Substances Data Bank (HSDB), RTECS, LiverTox. No figure on this page is scored, ranked or combined into a risk level.

VIII · Evidence

Every measurement

One row per published value. The identifier in the last column resolves to the ChEMBL assay record it was read from.

Equilibrium binding constants 57

Ki and Kd — a concentration at equilibrium. Directly comparable across rows at the same target.

TargetClassTypeValue (nM)pXOrganismAssay
CB1Cannabinoid receptorsKi2.908.54Homo sapiensCHEMBL953973
CB2Cannabinoid receptorsKi3.308.48Homo sapiensCHEMBL895424
CB2Cannabinoid receptorsKi9.208.04Mus musculusCHEMBL896543
CB1Cannabinoid receptorsKi15.307.82Mus musculusCHEMBL3541169
CB1Cannabinoid receptorsKi17.007.77Homo sapiensCHEMBL895425
CB1Cannabinoid receptorsKi18.007.74Homo sapiensCHEMBL5527146
UncheckedUnclassifiedKi20.007.70— organism not recordedCHEMBL828819
CB2Cannabinoid receptorsKi24.007.62Homo sapiensCHEMBL1952637
CB2Cannabinoid receptorsKi30.007.52Homo sapiensCHEMBL6083333
CB1Cannabinoid receptorsKi32.007.49RATPMID 10991998
CB1Cannabinoid receptorsKi36.007.44Rattus norvegicusCHEMBL3782512
CB2Cannabinoid receptorsKi36.007.44Homo sapiensCHEMBL921109
CB2Cannabinoid receptorsKi36.007.44Homo sapiensCHEMBL4430873
CB2Cannabinoid receptorsKi36.007.44Homo sapiensCHEMBL658959
CB2Cannabinoid receptorsKi36.007.44Homo sapiensCHEMBL2210674
CB2Cannabinoid receptorsKi36.007.44Homo sapiensCHEMBL658878
CB2Cannabinoid receptorsKi36.007.44Homo sapiensCHEMBL1065037
CB2Cannabinoid receptorsKi36.007.44Homo sapiensCHEMBL828769
CB2Cannabinoid receptorsKi36.407.44Homo sapiensCHEMBL4714300
CB2Cannabinoid receptorsKi36.407.44Homo sapiensCHEMBL3239823
CB2Cannabinoid receptorsKi36.407.44Homo sapiensCHEMBL5360494
CB1Cannabinoid receptorsKi37.007.43RATPMID 10991998
CB1Cannabinoid receptorsKi37.007.43Rattus norvegicusCHEMBL828818
CB1Cannabinoid receptorsKi38.007.42RATPMID 10991998
CB1Cannabinoid receptorsKi39.007.41Homo sapiensCHEMBL6083332
CB1Cannabinoid receptorsKi39.507.40Homo sapiensCHEMBL3873281
CB1Cannabinoid receptorsKi39.507.40Rattus norvegicusCHEMBL3266181
CB1Cannabinoid receptorsKi40.007.40Homo sapiensCHEMBL1069625
CB1Cannabinoid receptorsKi40.007.40Mus musculusCHEMBL896544
CB1Cannabinoid receptorsKi40.007.40Homo sapiensCHEMBL4344064
CB2Cannabinoid receptorsKi40.007.40Homo sapiensCHEMBL3873282
CB2Cannabinoid receptorsKi40.007.40Mus musculusCHEMBL4714299
CB1Cannabinoid receptorsKi40.707.39Homo sapiensCHEMBL5360493
CB1Cannabinoid receptorsKi40.707.39Homo sapiensCHEMBL3239822
Cannabinoid receptorCannabinoid receptorsKi41.007.39Homo sapiensCHEMBL661062
CB1Cannabinoid receptorsKi41.007.39Rattus norvegicusCHEMBL1287584
CB1Cannabinoid receptorsKi41.007.39Homo sapiensCHEMBL875683
CB1Cannabinoid receptorsKi41.007.39Homo sapiensCHEMBL2210675
CB1Cannabinoid receptorsKi41.007.39Rattus norvegicusCHEMBL921108
CB1Cannabinoid receptorsKi41.007.39Homo sapiensCHEMBL4430872
CB1Cannabinoid receptorsKi41.007.39Homo sapiensCHEMBL657905
CB1Cannabinoid receptorsKi41.007.39Mus musculusCHEMBL659663
CB1Cannabinoid receptorsKi41.007.39Homo sapiensCHEMBL658061
CB1Cannabinoid receptorsKi41.007.39Rattus norvegicusCHEMBL828768
CB1Cannabinoid receptorsKi41.007.39Rattus norvegicusCHEMBL1219989
CB2Cannabinoid receptorsKi41.007.39Homo sapiensCHEMBL953972
CB2Cannabinoid receptorsKi42.007.38Homo sapiensCHEMBL5527148
Cannabinoid receptorCannabinoid receptorsKi46.007.34Rattus norvegicusCHEMBL657995
CB1Cannabinoid receptorsKi47.607.32Rattus norvegicusCHEMBL659693
CB1Cannabinoid receptorsKi66.507.18Rattus norvegicusCHEMBL658891
Cannabinoid receptorCannabinoid receptorsKi82.007.09Rattus norvegicusCHEMBL4360722
CB1Cannabinoid receptorsKi1106.96RATPMID 10991998
CB1Cannabinoid receptorsKi1306.89RATPMID 10991998
CB1Cannabinoid receptorsKi1706.77RATPMID 10991998
UncheckedUnclassifiedKi3026.52— organism not recordedCHEMBL3252948
CB1Cannabinoid receptorsKi1,6005.80RATPMID 10991998
L-lactate dehydrogenase A chainEnzymesKi14,0004.85Homo sapiensCHEMBL4842434

Functional readouts 8

IC₅₀, EC₅₀, AC₅₀ and potency. Assay-dependent, and not interchangeable with a binding constant.

TargetClassTypeValue (nM)pXOrganismAssay
Cannabinoid receptorCannabinoid receptorsIC505.808.24Rattus norvegicusCHEMBL660013
CB1Cannabinoid receptorsIC505.808.24Rattus norvegicusCHEMBL658880
Transient receptor potential cation channel subfamily M member 8Ion channelsIC501606.80Homo sapiensCHEMBL5253448
Cannabinoid receptorCannabinoid receptorsIC502186.66Rattus norvegicusCHEMBL660019
AutotaxinUnclassifiedEC504606.34Homo sapiensCHEMBL5533697
HemozoinUnclassifiedIC5011,3004.95Plasmodium falciparumCHEMBL5054968
Nuclear receptor subfamily 1 group I member 2Nuclear receptorsEC5012,6004.90Homo sapiensCHEMBL3531878
UncheckedUnclassifiedPotency35,4814.45— organism not recordedCHEMBL3215169
P
PubChem
C
ChEMBL
R
Computed here with RDKit
D
Derived here from the stored measurement

IX · Trials

Registered clinical trials

Studies filed with ClinicalTrials.gov that name this compound as an intervention. A registered trial is a protocol, not a result — status and enrollment are printed beside every row, and withdrawn studies are counted rather than hidden.

242T

Registered studies

68T

Open or ongoing

238T

With a phase recorded

By phase

A study may carry two phase codes at once, so these count studies bearing each phase and do not sum to the total.

  • Early phase 131
  • Phase 183
  • Phase 283
  • Phase 323
  • Phase 413
  • Not applicable30

By status

The registry’s own status for each record. Withdrawn and terminated studies are counted here rather than hidden — a stopped trial is part of what is known.

  • Completed131
  • Recruiting42
  • Terminated15
  • Unknown status15
  • Not yet recruiting13
  • Active, not recruiting13
  • Withdrawn12
  • Suspended1

The 25 most recently started, of 242

Newest first by start date. Each identifier opens the registry record it came from; the title is the sponsor’s own, quoted.

  • NCT05432284Not yet recruiting · Phase 1

    Behavioral Pharmacology of THC and Beta-Myrcene

    Enrollment
    32Testimated
    Started
    2027-07
    Sponsor
    Johns Hopkins University

    Conditions Cannabis Use

    Matched “THC” in the study’s intervention “THC”

  • NCT07570953Not yet recruiting · Phase 2 / Phase 3

    A Study Of Synthetic THC And Sleep

    Enrollment
    72Testimated
    Started
    2026-11
    Sponsor
    Mayo Clinic

    Conditions Obstructive Sleep Apnea

    Matched “Dronabinol” in the study’s intervention “Dronabinol”

  • NCT07694466Not yet recruiting · Early phase 1

    Lung Health and Breath Biomarkers: Acute Effects of Inhaled Cannabis

    Enrollment
    12Testimated
    Started
    2026-10-01
    Sponsor
    Hannah Harris

    Conditions Cannabis Use · Tobacco · Biomarkers

    Matched “THC” in the study’s intervention “Cannabis (THC)”

  • NCT07148206Not yet recruiting · Phase 3

    Dronabinol and Epidiolex to Manage Uncontrolled Residual Symptoms of Buprenorphine Initiation Trial

    Enrollment
    40Testimated
    Started
    2026-10
    Sponsor
    Montefiore Medical Center

    Conditions Opioid Use Disorder

    Matched “Dronabinol” in the study’s intervention “Dronabinol Capsules”

  • NCT07231965Not yet recruiting · Phase 2 / Phase 3

    Synthetic THC And Blood Pressure

    Enrollment
    50Testimated
    Started
    2026-10
    Sponsor
    Mayo Clinic

    Conditions Blood Pressure

    Matched “Dronabinol” in the study’s intervention “Dronabinol”

  • NCT07815691Not yet recruiting · Phase 2

    Endocannabinoids in Reward

    Enrollment
    78Testimated
    Started
    2026-09-15
    Sponsor
    Medical University of South Carolina

    Conditions Cannabis Use Disorder

    Matched “Dronabinol” in the study’s intervention “Dronabinol”

  • NCT07214155Recruiting · Phase 1

    Effects of Various Cannabis Strains on Perceptual, Subjective and Objective Use Outcomes

    Enrollment
    70Testimated
    Started
    2026-09-15
    Sponsor
    Johns Hopkins University

    Conditions Cannabis Intoxication

    Matched “THC” in the study’s intervention “0 mg THC (placebo)”

  • NCT07783295Not yet recruiting · Phase 2

    Full-Spectrum Cannabis Extract for Chronic Pain and Bone Health Biomarkers in Women

    Enrollment
    80Testimated
    Started
    2026-09-01
    Sponsor
    Associação Pan-Americana Multidisciplinar de Endocanabinologia

    Conditions Chronic Pain · Fibromyalgia · Osteoporosis · Orofacial Pain

    Matched “THC” in the study’s intervention “Full-Spectrum Cannabis Extract 5:1 (CBD:THC)”

  • NCT06222268Not yet recruiting · Phase 1 / Phase 2

    Wayne State Warriors Marijuana Clinical Research Program: Cannabinoid Adjunct to Prolonged Exposure & Recovery

    Enrollment
    280Testimated
    Started
    2026-09
    Sponsor
    Leslie Lundahl

    Conditions PTSD · Post Traumatic Stress Disorder · Suicide · Cannabis Use

    Matched “Delta-9-tetrahydrocannabinol” in the study’s intervention “Delta-9-tetrahydrocannabinol (THC) only”

  • NCT05067387Recruiting · Phase 1

    Evaluation of Oral THC and CBD in Men and Women

    Enrollment
    22Testimated
    Started
    2026-08-13
    Sponsor
    University of California, Los Angeles

    Conditions Drug Abuse · Intoxication by Drug · Impairment

    Matched “THC” in the study’s intervention “THC”

  • NCT07635563Recruiting · Phase 2

    DReAMzz- Dronabinol and Acetazolamide Medication for Sleep Apnea (ZZ). Dose Confirmation Crossover Study for IHL-42X in Subjects With Obstructive Sleep Apnea.

    Enrollment
    120Testimated
    Started
    2026-07-21
    Sponsor
    Incannex Healthcare Ltd

    Conditions Obstructive Sleep Apnea (OSA)

    Matched “Dronabinol” in the study’s intervention “IHL-42X: 2.5 mg dronabinol + 125 mg acetazolamide”

  • NCT06758596Not yet recruiting · Early phase 1

    Research Investigating Drug Effects-2 (RiDE-2)

    Enrollment
    144Testimated
    Started
    2026-07-15
    Sponsor
    University of Illinois at Chicago

    Conditions Cannabis Use · Substance Use Disorder (SUD) · Healthy

    Matched “THC” in the study’s intervention “THC”

  • NCT07296874Not yet recruiting · Phase 2

    Acute Effects of Cannabis on Cognition and Affect

    Enrollment
    90Testimated
    Started
    2026-07
    Sponsor
    Washington State University

    Conditions Cannabis Use

    Matched “THC” in the study’s intervention “THC 20mg”

  • NCT07656350Recruiting · Not applicable

    Challenging the Endocannabinoid System in Sleep Restricted Healthy Volunteers to Modulate Physiological Arousal (CANISLEEP) Study

    Enrollment
    60Testimated
    Started
    2026-06-02
    Sponsor
    King's College London

    Conditions Healthy Volunteer

    Matched “THC” in the study’s intervention “THC”

  • NCT07603518Recruiting · Phase 1

    The Pharmacokinetics of a Hemp-Based Topical Product

    Enrollment
    20Testimated
    Started
    2026-05-26
    Sponsor
    Johns Hopkins University

    Conditions Cannabis

    Matched “THC” in the study’s intervention “THC”

  • NCT07422311Not yet recruiting · Phase 2 / Phase 3

    To Evaluate the Efficacy, Safety, and Tolerability of Dronabinol Oral Solution for Agitation in Patients With Alzheimer's Disease

    Enrollment
    140Testimated
    Started
    2026-05-01
    Sponsor
    Benuvia Therapeutics Inc.

    Conditions Agitation in Dementia

    Matched “Dronabinol” in the study’s intervention “Dronabinol Oral Solution”

  • NCT07225777Terminated · Phase 2

    Sex Differences in Neurobehavioral Response to THC

    Enrollment
    5Tactual
    Started
    2026-04-27
    Sponsor
    Medical University of South Carolina

    Conditions Cannabis Use Disorder

    Matched “Dronabinol” in the study’s intervention “Dronabinol”

  • NCT06834997Withdrawn · Phase 2

    Dronabinol As an Adjunct for Reducing Pain (DARP)-Texas Children's Hospital

    Enrollment
    0Tactual
    Started
    2026-04-01
    Sponsor
    Baylor College of Medicine

    Conditions Endometriosis · Endometriosis Related Pain · Endometriosis, Pain

    Matched “Dronabinol” in the study’s intervention “Dronabinol Capsules”

  • NCT07471347Not yet recruiting · Not applicable

    Exploring The Effect Of Cannabidiol On Cannabis Tolerance Using A Novel Vaporiser Device In Heavy Users (Stage 1)

    Enrollment
    10Testimated
    Started
    2026-03
    Sponsor
    King's College London

    Conditions Cannabis Intoxication

    Matched “Delta-9-tetrahydrocannabinol” in the study’s intervention “delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD)”

  • NCT06878417Recruiting · Not applicable

    Cannabinoids for Osteoarthritis Pain Effectiveness Trial

    Enrollment
    100Testimated
    Started
    2026-01-29
    Sponsor
    University Health Network, Toronto

    Conditions Osteoarthritis of Knee · Osteoarthritis Hip

    Matched “THC” in the study’s intervention “THC”

  • NCT07401628Completed · Not applicable

    In-Vehicle Real-Time Cannabis Influenced Driving Detection

    Enrollment
    45Tactual
    Started
    2026-01-05
    Sponsor
    University of Bern

    Conditions Driving Under the Influence · Cannabis-impaired Driving

    Matched “THC” in the study’s intervention “Cannabis (THC)”

  • NCT05052541Recruiting · Phase 3

    Safety and Efficacy of Oral Cannabis in Chronic Spine Pain

    Enrollment
    157Testimated
    Started
    2026-01
    Sponsor
    University of Colorado, Denver

    Conditions Back Pain · Neck Pain

    Matched “THC” in the study’s intervention “THC/CBD”

  • NCT07176208Recruiting · Phase 1

    Clinical Study to Evaluate the Effects of Oral Delta-9-tetrahydrocannabinol (Δ9-THC) With and Without Alcohol on Perception and Driving Performance in Healthy Adults

    Enrollment
    48Testimated
    Started
    2025-12-29
    Sponsor
    Food and Drug Administration (FDA)

    Conditions Cannabis, Drug Effects · Driving Performance

    Matched “Dronabinol” in the study’s intervention “5 mg Dronabinol (Marinol®) + Placebo Beverage”

  • NCT06261489Recruiting · Phase 2

    Cannabis (THC vs. CBD) in Multiple Sclerosis

    Enrollment
    30Testimated
    Started
    2025-12-05
    Sponsor
    University of Calgary

    Conditions Multiple Sclerosis

    Matched “THC” in the study’s intervention “THC”

  • NCT06859710Recruiting · Phase 1

    THC and CBD: A Controlled Human Study Probing a Harm Reduction Strategy

    Enrollment
    30Testimated
    Started
    2025-11-05
    Sponsor
    University of California, Los Angeles

    Conditions Abuse, Drug · Pain

    Matched “THC” in the study’s intervention “THC”

Records from ClinicalTrials.gov (U.S. National Library of Medicine, NIH), API v2. A study is listed against a compound only when a verified name for that compound appears as a whole word in one of the study's own intervention names. A short code must appear as written, and a name the registry uses for something else (Aleph, a vaccine maker) is not matched. Title matches are not accepted. The matched name and the intervention text it matched are shown with every row.

Searched as Tetrahydrocannabinol · Delta-9-tetrahydrocannabinol · Dronabinol. Run this search at the registry — it returns the unfiltered result, including studies this page rejected as belonging to a different molecule.

A registered trial is a protocol somebody filed with the registry. It is not a result, and nothing on this plate says whether Tetrahydrocannabinol (THC) worked.

XI · Literature

Sources behind this dossier

The papers this compound's values were read from, ranked by what each contributed. Not a review of the field.

Every paper below is one some value on this page came from — a binding constant, a passage of pharmacology or toxicology, or a measured duration. Each entry says what this archive took from it. Nothing else is claimed about any of them: the title is the study’s own account of itself, and a summary written here would be an assertion with no source behind it.

  1. 01

    Cannabinoid agonist signal transduction in rat brain: comparison of cannabinoid agonists in receptor binding, G-protein activation, and adenylyl cyclase inhibition

    Breivogel CS, Childers SR · The Journal of pharmacology and experimental therapeutics 2000

    • · 7 measurements at 1 target (Ki), strongest CB1 at 7.49 pX

    PMID 10991998

  2. 02

    Determining the magnitude and duration of acute Δ(9)-tetrahydrocannabinol (Δ(9)-THC)-induced driving and cognitive impairment: A systematic and meta-analytic review

    McCartney D, Arkell TR, Irwin C et al. · Neuroscience and biobehavioral reviews 2021

    • · ~5 h to recovery of driving-related cognitive skills

    PMID 33497784

  3. 03

    Cannabidiol (CBD) content in vaporized cannabis does not prevent tetrahydrocannabinol (THC)-induced impairment of driving and cognition

    Arkell TR, Lintzeris N, Kevin RC et al. · Psychopharmacology 2019

    • · 4 timed observations on the simulation plate

    PMID 31044290

  4. 04

    Controlled vaporized cannabis, with and without alcohol: subjective effects and oral fluid-blood cannabinoid relationships

    Hartman RL, Brown TL, Milavetz G et al. · Drug testing and analysis 2016

    • · Duration of acute subjective effects

    PMID 26257143

  5. 05
  6. 06

    Δ9-Tetrahydrocannabinol-mediated epigenetic modifications elicit myeloid-derived suppressor cell activation via STAT3/S100A8

    Sido JM, Yang X, Nagarkatti PS et al. · Journal of leukocyte biology 2015

    • · Mechanism of Action

    PMID 25713087

  7. 07

    The subjective psychoactive effects of oral dronabinol studied in a randomized, controlled crossover clinical trial for pain

    Issa MA, Narang S, Jamison RN et al. · The Clinical journal of pain 2014

    • · Human Toxicity Excerpts

    PMID 24281276

  8. 08

    Synaptic targets of Δ9-tetrahydrocannabinol in the central nervous system

    Hoffman AF, Lupica CR · Cold Spring Harbor perspectives in medicine 2013

    • · Mechanism of Action

    PMID 23209160