JWH-073
PubChem records this structure as (1-Butyl-1H-indol-3-yl)-1-naphthalenylmethanone.
Also known as1-Butyl-3-(1-naphthoyl) indole · 1-Butyl-3-(1-naphthoyl)indole · 1-Butyl-3-(1-naphthoyl)-1H-indole
(1-butylindol-3-yl)-naphthalen-1-ylmethanone
- PubChem CID
- 10471670
- ChEMBL
- CHEMBL2380416
- Measurements
- 1
- InChIKey
- VCHHHSMPMLNVGS-UHFFFAOYSA-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.
What it is
1-butyl-3-(1-naphthoyl)indole is a DEA Schedule I controlled substance. Substances in the DEA Schedule I have no currently accepted medical use in the United States, a lack of accepted safety for use under medical supervision, and a high potential for abuse. It is a Cannabimimetic agents substance.
Recognized use
JWH-073 was designed and evaluated in basic scientific research to investigate structure activity relationships in the cannabinoid system.
Hazardous Substances Data Bank (HSDB)DEA; Office of Diversion control-Drug and Chemical Evaluation Section: JWH-073: 1-Butyl-3-(1-naphthoyl)indole (Synthetic Cannabinoid in Herbal Products) (March 2011). Available from, as of November 18, 2011: https://www.deadiversion.usdoj.gov/drugs_concern/spice/spice_jwh073.pdf
The popularity of these THC-like synthetic cannabinoids has significantly increased throughout the United States, and they are being abused for their psychoactive properties as reported by law enforcement, the medical community, and through scientific literature.
Hazardous Substances Data Bank (HSDB)DEA; Microgram Bulletin. March 2011. Washington, DC: Drug Enforcement Admin. Available from, as of November 18, 2011: https://www.justice.gov/dea/programs/forensicsci/microgram/mg2011/mg0311.pdf
How it acts
/Synthetic cannabinoid/ agonistic activity on the CB1 receptor is responsible for elevating mood and inducing a feeling of well-being. Some /synthetic cannabinoid/ users have reported effects similar to or even stronger than those obtained by smoking cannabis, such as physical relaxation, changes in perception, and mild euphoria.
Hazardous Substances Data Bank (HSDB)PMID 22007163Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3187647
... The butyl homolog of JWH-018, JWH-073 (naphthalen-1-yl-(1-butylindol-3-yl)methanone), which seems to bind more specifically to the CB1 receptor. The latter has been recently shown to act similarly to JWH-018, although it is less potent in inhibiting neurotransmission and slower in producing internalization of cannabinoid receptors.
Hazardous Substances Data Bank (HSDB)PMID 22007163Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3187647
Behavior carries the pharmacological classes and the acute-effect durations, with plasma half-life kept separate from duration of effect.
In the body
... The lack or low content of /JWH-018 and JWH-073/ in urine requires detailed identification of their metabolites, which are excreted with urine and are present in blood. Using gas and liquid chromatography-mass spectrometry, /investigators/ identified a series of metabolites in urine samples from humans and rats that were products of the following reactions: (a) mono- and dihydroxylation of the parent compounds with hydroxyl groups located at aromatic and aliphatic residues, (b) carboxylation, (c) N-dealkylation and (d) N-dealkylation and hydroxylation. The prevailing urinary metabolites in humans are monohydroxylated forms, while N-dealkylated and N-dealkyl monohydroxylated forms are fou…
Hazardous Substances Data Bank (HSDB)PMID 21481654Grigoryev A et al; J Chromatogr B Analyt Technol Biomed Life Sci 879 (15-16): 1126-36 (2011)
... This study evaluates nine human recombinant uridine diphosphate-glucuronosyltransferase (UGT) isoforms and human liver and intestinal microsomes for their ability to glucuronidate hydroxylated metabolites of 1-naphthalenyl-1(1-pentyl-1H-indol-3-yl)-methanone (JWH-018) and (1-butyl-1H-indol-3-yl)-1-naphthalenyl-methanone (JWH-073), the two most common synthetic cannabinoids found in K2 products. Conjugates were identified and characterized using liquid chromatography/tandem mass spectrometry, whereas kinetic parameters were quantified using high-performance liquid chromatography-UV-visible methods. UGT1A1, UGT1A3, UGT1A9, UGT1A10, and UGT2B7 were shown to be the major enzymes involved, sh…
Hazardous Substances Data Bank (HSDB)PMID 21746969Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3186213
... Two subjects that consumed JWH-018 primarily excreted glucuronidated conjugates of 5-(3-(1-naphthoyl)-1H-indol-1-yl)-pentanoic acid (>30 ng/mL) and (1-(5-hydroxypentyl)-1H-indol-3-yl)(naphthalene-1-yl)-methanone (>50 ng/mL). Interestingly, oxidized metabolites of both JWH-018 and JWH-073 were detected in these specimens, suggesting either metabolic demethylation of JWH-018 to JWH-073 or a nonreported, previous JWH-073 exposure. Metabolic profiles generated from a subject who consumed a mixture of JWH-018 and JWH-073 were similar to profiles generated from subjects who presumably consumed JWH-018 exclusively. Oxidized metabolites of JWH-018 and JWH-073 were of the same pattern, but JWH-01…
Hazardous Substances Data Bank (HSDB)PMID 21506519Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3105467
... Results from four urine specimens collected after individuals reportedly self-administered either JWH-018 or a mixture of JWH-018 and JWH-073 showed the following: (1) all tested metabolites were excreted in high concentrations, (2) (omega)- and (omega-1)-hydroxyl metabolites were exclusively excreted as glucuronic acid conjugates, and (3) approximately 5%-80% of the (omega)-carboxyl metabolites was excreted as glucuronic acid conjugates. ...
Hazardous Substances Data Bank (HSDB)PMID 21740038Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3155992
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 JWH-073 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 JWH-073 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.
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.
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 — 1 measurement in this archive, equilibrium constants kept apart from functional readouts.
- Toxicology — 5 published passages, plus any assay in this archive bearing on toxicity.
- Legal — DEA Schedule I, 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 JWH-073 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.
- Formula
- C23H21NOR
- Molecular weight
- 327.43g/molR
- Exact mass
- 327.1623DaR
- cLogP
- 5.83R
- TPSA
- 22.0ŲR
- H-bond donors
- 0R
- H-bond acceptors
- 2R
- Rotatable bonds
- 5R
- Aromatic rings
- 4R
- Heavy atoms
- 25R
- Fraction sp³
- 0.174R
- Formal charge
- 0R
Computed with RDKit 2025.09.2 from the SMILES returned by PubChem. Audit run 26/09/2026.
Bemis–Murcko scaffold
O=C(c1cccc2ccccc12)c1c[nH]c2ccccc12
Shared with AM-2201, JWH-018, JWH-122, JWH-210. All families
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
—
No controlled human trial reporting a duration for this compound is cited here. The archive holds no other record of one either. A duration is not inferred from a chemical relative.
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.
No half-life is published for this compound in the sources this site reads.
Primary pharmacological drivers
ChEMBL holds no curated mechanism-of-action record for this compound. The measured affinities below are the evidence this archive has for what it binds.
Mechanism, as published
Quoted verbatim from the database named after each passage, never summarized.
/Synthetic cannabinoid/ agonistic activity on the CB1 receptor is responsible for elevating mood and inducing a feeling of well-being. Some /synthetic cannabinoid/ users have reported effects similar to or even stronger than those obtained by smoking cannabis, such as physical relaxation, changes in perception, and mild euphoria.
Hazardous Substances Data Bank (HSDB)PMID 22007163Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3187647 ... The butyl homolog of JWH-018, JWH-073 (naphthalen-1-yl-(1-butylindol-3-yl)methanone), which seems to bind more specifically to the CB1 receptor. The latter has been recently shown to act similarly to JWH-018, although it is less potent in inhibiting neurotransmission and slower in producing internalization of cannabinoid receptors.
Hazardous Substances Data Bank (HSDB)PMID 22007163Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3187647
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 Cannabinoid Receptor Agonists
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.
- Mood 2
- matched on “anxiety”, “mood” · in PMID 22007163; Toxicology: Hazardous Substances Data Bank (HSDB)
- Perception 2
- matched on “hallucinat” · in PMID 22007163; Toxicology: Hazardous Substances Data Bank (HSDB)
- Thought content 1
- matched on “paranoi” · in PMID 22007163
- Psychomotor activity 2
- matched on “agitat” · in PMID 22007163; Toxicology: Hazardous Substances Data Bank (HSDB)
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.
Brain
basal ganglia: drawn as the caudate nucleus, putamen and globus pallidus.
Measured but not drawn — this anatomogram has no outline for them: pituitary gland 17.3, midbrain 2.1, spinal cord 1.7, retina 1.1.
Body
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.
cerebral cortex
18.6 nTPM- CB1CNR18.1 pX18.6
cerebellum
18.3 nTPM- CB1CNR18.1 pX18.3
pituitary gland
17.3 nTPM- CB1CNR18.1 pX17.3
basal ganglia
15.1 nTPM- CB1CNR18.1 pX15.1
amygdala
13.3 nTPM- CB1CNR18.1 pX13.3
hippocampal formation
13.2 nTPM- CB1CNR18.1 pX13.2
hypothalamus
9.0 nTPM- CB1CNR18.1 pX9.0
midbrain
2.1 nTPM- CB1CNR18.1 pX2.1
spinal cord
1.7 nTPM- CB1CNR18.1 pX1.7
retina
1.1 nTPM- CB1CNR18.1 pX1.1
Peripheral & autonomic
Tissues outside the CNS expressing the same targets — where a compound's bodily effects become possible.
colon
10.0 nTPM- CB1CNR18.1 pX10.0
small intestine
8.1 nTPM- CB1CNR18.1 pX8.1
adrenal gland
4.6 nTPM- CB1CNR18.1 pX4.6
thyroid gland
3.9 nTPM- CB1CNR18.1 pX3.9
stomach 1
3.4 nTPM- CB1CNR18.1 pX3.4
urinary bladder
3.4 nTPM- CB1CNR18.1 pX3.4
lung
2.8 nTPM- CB1CNR18.1 pX2.8
smooth muscle
2.3 nTPM- CB1CNR18.1 pX2.3
skeletal muscle
1.8 nTPM- CB1CNR18.1 pX1.8
salivary gland
1.8 nTPM- CB1CNR18.1 pX1.8
spleen
1.4 nTPM- CB1CNR18.1 pX1.4
pancreas
1.2 nTPM- CB1CNR18.1 pX1.2
heart muscle
0.8 nTPM- CB1CNR18.1 pX0.8
kidney
0.6 nTPM- CB1CNR18.1 pX0.6
duodenum
0.6 nTPM- CB1CNR18.1 pX0.6
liver
0.1 nTPM- CB1CNR18.1 pX0.1
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.
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 1 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.
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 JWH-073 in this archive.
As published
Quoted verbatim from the database named after each passage, never summarized — a summary of a toxicology statement is a new claim.
Human Toxicity Excerpts
/SIGNS AND SYMPTOMS/ Although gastrointestinal effects, such as nausea, vomiting, and retching, are the most common after consumption of /synthetic cannabinoids/, cardiovascular effects, such as extremely elevated heart rate and blood pressure, chest pain, and cardiac ischemia are among the most dangerous consequences. Occasional inappropriate laughter, injected conjunctiva, xerostomia, and nystagmus have been descri…
Hazardous Substances Data Bank (HSDB)PMID 22007163Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3187647
/SIGNS AND SYMPTOMS/ In general, the desired effects of /synthetic cannabinoids/ include a sense of empathy and well-being. However, there is an increasing number of clinical reports describing patients presenting for emergency medical care after smoking /synthetic cannabinoid/ products, the most common symptoms being nausea, anxiety, agitation/panic attacks, tachycardia, paranoid ideation, and hallucinations. /Synth…
Hazardous Substances Data Bank (HSDB)PMID 22007163Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3187647
/SIGNS AND SYMPTOMS/ Symptoms described with synthetic marijuana use are elevated heart rate, elevated blood pressure, palpitations, diaphoresis, tremulousness, anxiety, and agitation. Other physical findings may include mydriasis, although this finding is not consistent with intoxication. Psychosis with auditory and visual hallucinations is mentioned in rare circumstances, most commonly with individuals who have und…
Hazardous Substances Data Bank (HSDB)Dan Quan et al; Emergency Medicine Reports 32 (20): 237-247 (2011) https://xa.yimg.com/kq/groups/14639670/1131750640/name/Legal+Drug+of+Abuse+2011.pdf
/SIGNS AND SYMPTOMS/ ... Accidental overdosing with a risk of severe psychiatric complications may be more likely to occur because the type and amount of cannabinoid may vary considerably from batch to batch even within the same product. In general, there may be a risk of the appearance of a full CB receptor agonist leading to life-threatening conditions if overdosed (unlike THC, which acts only as a partial agonist)…
Hazardous Substances Data Bank (HSDB)EMCDDA; European Monitoring Centre for Drugs and Drug Addiction; Thematic Papers: Understanding the Spice Phenomenon (November 2009). Available from, as of November 21, 2011: https://www.emcdda.europa.eu/publications/thematic-papers/spice
For more Human Toxicity Excerpts (Complete) data for 1-Butyl-3-(1-naphthoyl) indole (9 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 1
Ki and Kd — a concentration at equilibrium. Directly comparable across rows at the same target.
| Target | Class | Type | Value (nM) | pX | Organism | Assay |
|---|---|---|---|---|---|---|
| CB1 | Cannabinoid receptors | Ki | 8.90 | 8.05 | RAT | PMID 11408610 |
- 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.
— No registered study names JWH-073 as an intervention. That is an absence of registered research, not evidence about the compound. Most of this archive has never been the subject of a registered trial.
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 JWH-073 · 1-Butyl-3-(1-naphthoyl) indole · 1-Butyl-3-(1-naphthoyl)indole. Run this search at the registry.
A registered trial is a protocol somebody filed with the registry. It is not a result, and nothing on this plate says whether JWH-073 worked.
X · Legal
Controlled-substance status
United States federal scheduling, read from the DEA records this archive holds and shown with the passage each was read from. Not legal advice, and not necessarily current.
- DEA class
- Synthetic Cannabinoids
- Added
- February 2010
As the DEA states it
Quoted whole. The badge above is a reading of these passages and adds nothing to them.
JWH-073 (Class: Synthetic Cannabinoids, Added Date: 02-2010)
Schedule I - Substances in the DEA Schedule I have no currently accepted medical use in the United States, a lack of accepted safety for use under medical supervision, and a high potential for abuse.
Other regulatory records
Registers outside the DEA that hold an entry for JWH-073 — chemical-safety and national inventories, each naming itself. They are not scheduling decisions.
Schedule I shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. Each drug or substance has been assigned the DEA Controlled Substances Code Number set forth opposite it. ... Temporary listing of substances subject to emergency scheduling. Any material, compound, mixture or preparation which contains any quantity of the following substances. 1-Butyl-3-(1-naphthoyl)indole, its optical, positional, and geometric isomers, salts and salts of isomers (DEA Code Number: 7173) are included on this list.
Hazardous Substances Data Bank (HSDB)21 CFR 1380.11(g) (USFDA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of November 14, 2011: https://www.ecfr.gov
United States federal status only. State law differs, and so does the law of every other country — none of it is represented here. Scheduling changes, and this reflects the DEA records held by PubChem descriptive sections when the monograph was last harvested, not necessarily today. This is a record of what a database publishes, not legal advice.
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.
- 01
Evidence for a new G protein-coupled cannabinoid receptor in mouse brain
Breivogel CS, Griffin G, Di Marzo V et al. · Molecular pharmacology 2001
- · 1 measurement at 1 target (Ki), strongest CB1 at 8.05 pX
- 02
Beyond THC: The New Generation of Cannabinoid Designer Drugs
Fattore L, Fratta W · Frontiers in behavioral neuroscience 2011
- · Mechanism of Action
- · Human Toxicity Excerpts