Skip to content
PsychedeliaDokholyan Laboratory
Plate 375 of 545Verified

JWH-018

PubChem records this structure as Jwh 018.

Also known as1-Pentyl-3-(1-naphthoyl) indole · 1-Pentyl-3-(1-naphthoyl)indole · 1-pentyl-3-(1-naphthoyl)-indole

naphthalen-1-yl-(1-pentylindol-3-yl)methanone

PubChem CID
10382701
Measurements
11
InChIKey
JDNLPKCAXICMBW-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-pentyl-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 Hallucinogenic substances substance.

    Drug Enforcement Administration (DEA)

Recognized use

  • JWH-018 was developed and evaluated in basic scientific research to study structure activity relationships related to the cannabinoid receptors.

    Hazardous Substances Data Bank (HSDB)DEA; Office of Diversion control-Drug and Chemical Evaluation Section: JWH-018: 1-Pentyl-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_jwh018.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

  • ... JWH-018 is probably the most studied synthetic cannabinoid. It has been found in multiple preparations and has been shown to be a potent cannabinoid receptor (CB) agonist. CB1 is the principal receptor thought to be most highly responsible for the euphoria and psychoactive effects of THC. The CB2 receptor resides mostly in the immune system but has some effect on pain control and mood regulation. ...

    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

  • /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. The higher potency of action of these synthetic cannabinoids might be explained by in vitro experiments that have suggested that, while THC acts as a partial agonist on the CB1 receptor, JWH-018 acts as a full and potent agonist. Moreover, compared with THC, JWH-018 possesses approximately a fourfold higher affinity to the cannabinoid CB1 receptor and 10-fold higher…

    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 duration of effects in humans compared to THC seems to be shorter for JWH-018 (1-2 hours) and considerably longer for CP 47,497-C8 (5-6 hours), as reported in a self-experiment.

    Absorption, Distribution and Excretion

    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

  • ... The high pharmacological and addictive potency of JWH-018 highlights the importance of elucidating the metabolism of JWH-018, without which a meaningful insight into its pharmacokinetics and its toxicity would not be possible. In the present study, the cytochrome P450 phase I metabolites of JWH-018 were investigated, after in vitro incubation of the drug with human liver microsomes, followed by liquid chromatography-tandem mass spectrometry analysis. This revealed monohydroxylation of the naphthalene ring system, the indole moiety, and the alkyl side chain. In addition, observations were made of dihydroxylation of the naphthalene ring system, and the indole moiety, or as result of a comb…

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)Wintermeyer A et al; Analytical and Bioanalytical Chemistry 398 (5): 2141-2153 (2010)

  • ... 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…

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 21746969Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3186213

  • The aim of this study was to elucidate the metabolism of JWH-018. An ethanolic extract was prepared from an incense containing large amounts of JWH-018. After removal of the ethanol, the residue was given to Wistar rats by gastric intubation and urine was collected over 24 hours. For identification, the metabolites were isolated after enzymatic or acidic cleavage of conjugates by liquid-liquid extraction (LLE) or solid-phase extraction (C18) followed by acetylation. The metabolites were separated and identified by GC and MS in the electron ionization (EI) mode. The parent compound JWH-018 could be found in the urine extracts only in small amounts. Besides the parent compound, the N-dealkylat…

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)Kraemer T et al; Toxichem Krimtech 76 (2): 90 (2008) https://www.gtfch.org/cms/index.php/tk-76-2009?Itemid=270

  • ... It is worth nothing that unlike metabolites of most synthetic cannabinoids, JWH-018 hydroxylated metabolites retain in vitro and in vivo activity at CB1 receptors...

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 22007163Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3187647

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-018 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-018 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 — 11 measurements 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-018 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 JWH-018
Depiction served by PubChem for CID 10382701. Not redrawn here, so the picture and the identity come from the same record.
Formula
C24H23NOR
Molecular weight
341.45g/molR
Exact mass
341.1780DaR
cLogP
6.22R
TPSA
22.0ŲR
H-bond donors
0R
H-bond acceptors
2R
Rotatable bonds
6R
Aromatic rings
4R
Heavy atoms
26R
Fraction sp³
0.208R
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-073, 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

MeSH indexes no pharmacological class for this compound.

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. The high…
    Hazardous Substances Data Bank (HSDB)PMID 22007163Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3187647
  • ... JWH-018 (naphthalen-1-yl-(1-pentylindol-3-yl)methanone) was first synthesized during an analysis aiming at developing new cannabimimetic indole compounds with potential therapeutic effects comparable with those of THC. It belongs to the aminoalkylindole family and has been shown to have a binding affinity for the CB1 receptors in the…
    Hazardous Substances Data Bank (HSDB)PMID 22007163Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3187647
  • JWH-018 dose-dependently inhibits glutamate release in autaptic excitatory hippocampal neurons, probably acting on the CB1 receptor, an effect reversed by administration of the CB1 receptor antagonist rimonabant. In vivo studies showing that JWH-018 induces analgesia, catalepsy, hypomotility, and hypothermia, namely the tetrad of behavior…
    Hazardous Substances Data Bank (HSDB)PMID 22007163Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3187647
  • ... JWH-018 is probably the most studied synthetic cannabinoid. It has been found in multiple preparations and has been shown to be a potent cannabinoid receptor (CB) agonist. CB1 is the principal receptor thought to be most highly responsible for the euphoria and psychoactive effects of THC. The CB2 receptor resides mostly in the immune…
    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

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.

No diagnostic chapter is shown for this compound. Either PubChem records no MeSH pharmacological class for it, or the class it records is not one of the substance classes ICD-11 gives a chapter to. Inferring a chapter from the compound’s name or its binding profile would be a diagnosis this archive is in no position to make.

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.

Affect0Mood3Perception2Cognition0Thought process0Thought content1Psychomotor activity2Insight and judgment0
This measures the literature, not the compound. Each spoke counts how many of the 9 records this archive holds for this compound say something under that domain — 3 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 “anxiety”, “euphoria”, “mood” · in Pharmacology: Mechanism of Action; PMID 22007163; Toxicology: Hazardous Substances Data Bank (HSDB)
Perception 2
matched on “hallucinat” · in Toxicology: Hazardous Substances Data Bank (HSDB); PMID 22007163
Thought content 1
matched on “paranoi” · in PMID 22007163
Psychomotor activity 2
matched on “agitat” · in Toxicology: Hazardous Substances Data Bank (HSDB); PMID 22007163

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

cerebral cortex — 18.6 nTPM, from CNR1cerebellum — 18.3 nTPM, from CNR1hippocampal formation — 13.2 nTPM, from CNR1amygdala — 13.3 nTPM, from CNR1hypothalamus — 9.0 nTPM, from CNR1thalamus — no resolved target expressed herebasal ganglia — 15.1 nTPM, from CNR1medulla oblongata — no resolved target expressed here

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

heart — 0.8 nTPM, from CNR1smooth muscle — 2.3 nTPM, from CNR1lung — 2.8 nTPM, from CNR1, CNR2liver — 0.1 nTPM, from CNR1, CNR2kidney — 0.6 nTPM, from CNR1stomach — 3.4 nTPM, from CNR1, CNR2duodenum — 0.6 nTPM, from CNR1, CNR2small intestine — 8.1 nTPM, from CNR1, CNR2colon — 10.0 nTPM, from CNR1, CNR2adrenal gland — 4.6 nTPM, from CNR1thyroid gland — 3.9 nTPM, from CNR1, CNR2pancreas — 1.2 nTPM, from CNR1urinary bladder — 3.4 nTPM, from CNR1, CNR2skeletal muscle — 1.8 nTPM, from CNR1, CNR2spleen — 8.4 nTPM, from CNR2, CNR1salivary gland — 1.8 nTPM, from CNR1, CNR2
019 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. cerebral cortex

    18.6 nTPM

  2. cerebellum

    18.3 nTPM

  3. pituitary gland

    17.3 nTPM

  4. basal ganglia

    15.1 nTPM

  5. amygdala

    13.3 nTPM

  6. hippocampal formation

    13.2 nTPM

  7. hypothalamus

    9.0 nTPM

  8. midbrain

    2.1 nTPM

  9. spinal cord

    1.7 nTPM

  10. retina

    1.1 nTPM

Peripheral & autonomic

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

  1. colon

    10.0 nTPM

  2. spleen

    8.4 nTPM

  3. small intestine

    8.1 nTPM

  4. adrenal gland

    4.6 nTPM

  5. thyroid gland

    3.9 nTPM

  6. stomach 1

    3.4 nTPM

  7. urinary bladder

    3.4 nTPM

  8. lung

    2.8 nTPM

  9. smooth muscle

    2.3 nTPM

  10. skeletal muscle

    1.8 nTPM

  11. salivary gland

    1.8 nTPM

  12. pancreas

    1.2 nTPM

  13. heart muscle

    0.8 nTPM

  14. kidney

    0.6 nTPM

  15. duodenum

    0.6 nTPM

  16. liver

    0.1 nTPM

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.

1 of this compound’s targets could not be resolved to a gene and are absent from both columns: Cannabinoid receptor.

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 3 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.

CB1 — Ki 8.89 pXCB2 — Ki 8.54 pXCannabinoid receptor — Ki 8.54 pXCB1CB2Cannabinoid rece…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 JWH-018 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/ ... 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

  • /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/ 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

  • For more Human Toxicity Excerpts (Complete) data for 1-pentyl-3-(1-naphthoyl) indole (15 total), please visit the HSDB record page.

    Hazardous Substances Data Bank (HSDB)

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 9

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

TargetClassTypeValue (nM)pXOrganismAssay
CB1Cannabinoid receptorsKi1.308.89Mus musculusCHEMBL3541169
CB2Cannabinoid receptorsKi2.908.54Homo sapiensCHEMBL1026911
Cannabinoid receptorCannabinoid receptorsKi2.908.54Rattus norvegicusCHEMBL4360730
CB2Cannabinoid receptorsKi2.908.54Homo sapiensCHEMBL3239857
Cannabinoid receptorCannabinoid receptorsKi3.408.47Rattus norvegicusCHEMBL4360722
Cannabinoid receptorCannabinoid receptorsKd3.408.47Rattus norvegicusCHEMBL4360721
CB1Cannabinoid receptorsKi4.308.37Homo sapiensCHEMBL4432232
Cannabinoid receptorCannabinoid receptorsKd6.508.19Rattus norvegicusCHEMBL4360717
CB1Cannabinoid receptorsKi9.508.02Homo sapiensCHEMBL3239858

Functional readouts 2

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

TargetClassTypeValue (nM)pXOrganismAssay
Cannabinoid receptorCannabinoid receptorsEC5036.007.44Rattus norvegicusCHEMBL4360757
UncheckedUnclassifiedEC5069.007.16— organism not recordedCHEMBL4360731
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-018 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-018 · 1-Pentyl-3-(1-naphthoyl) indole · 1-Pentyl-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-018 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

    Beyond THC: The New Generation of Cannabinoid Designer Drugs

    Fattore L, Fratta W · Frontiers in behavioral neuroscience 2011

    • · Mechanism of Action
    • · Human Toxicity Excerpts

    PMID 22007163