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PsychedeliaDokholyan Laboratory
Plate 541 of 545Verified

WIN 55212-2

PubChem records this structure as Win 55212-2.

Also known asWI5 · WIN-2

[(11R)-2-methyl-11-(morpholin-4-ylmethyl)-9-oxa-1-azatricyclo[6.3.1.04,12]dodeca-2,4(12),5,7-tetraen-3-yl]-naphthalen-1-ylmethanone

PubChem CID
5311501
Measurements
28
InChIKey
HQVHOQAKMCMIIM-HXUWFJFHSA-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

  • WIN 55212-2 is a organic heterotricyclic compound that is 5-methyl-3-(morpholin-4-ylmethyl)-2,3-dihydro[1,4]oxazino[2,3,4-hi]indole substituted at position 6 by a 1-naphthylcarbonyl group. It has a role as an analgesic, a neuroprotective agent and an apoptosis inhibitor. It is an organic heterotricyclic compound, a member of morpholines, a naphthyl ketone and a synthetic cannabinoid.

    ChEBI

  • (5-methyl-3-(morpholinomethyl)-2,3-dihydro-[1,4]oxazino[2,3,4-hi]indol-6-yl)(naphthalen-1-yl)methanone 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.

    Drug Enforcement Administration (DEA)

  • WIN 55,212-2 is a chemical described as an aminoalkylindole derivative, which produces effects similar to those of cannabinoids such as tetrahydrocannabinol (THC) but has an entirely different chemical structure. It is a potent cannabinoid receptor agonist that has been found to be a potent analgesic in a rat model of neuropathic pain. It activates p42 and p44 MAP kinase via receptor-mediated signaling.

    DrugBank

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 WIN 55212-2 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 WIN 55212-2 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 — 28 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — nothing published for WIN 55212-2. An absent record is an absence of study, not evidence of safety.
  • 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 WIN 55212-2 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 WIN 55212-2
Depiction served by PubChem for CID 5311501. Not redrawn here, so the picture and the identity come from the same record.
Formula
C27H26N2O3R
Molecular weight
426.52g/molR
Exact mass
426.1943DaR
cLogP
4.60R
TPSA
43.7ŲR
H-bond donors
0R
H-bond acceptors
5R
Rotatable bonds
4R
Aromatic rings
4R
Heavy atoms
32R
Fraction sp³
0.296R
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)c1cn2c3c(cccc13)OC[C@H]2CN1CCOCC1

No other compound in this archive shares it. 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.

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.

None of the 0 records this archive holds for this compound uses a term from any of the clinical domains. That is a statement about the literature recorded here, not about the compound.

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.

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

CB1 — Ki 9.85 pXCB2 — Ki 9.54 pXCB1CB2579
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 WIN 55212-2 in this archive.

Published toxicology

— None. The toxicology databases this site reads — HSDB, RTECS and LiverTox, by way of PubChem — hold no record for WIN 55212-2. They index compounds that have been studied for decades, so most of this archive has no entry. An absent record is an absence of study, not evidence of safety.

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 28

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

TargetClassTypeValue (nM)pXOrganismAssay
CB1Cannabinoid receptorsKi0.1409.85RATPMID 11160626
CB2Cannabinoid receptorsKi0.2909.54HUMANPMID 11160626
CB1Cannabinoid receptorsKi0.4109.39MOUSEPMID 11160626
CB2Cannabinoid receptorsKi0.4109.39HUMANPMID 12065738
CB2Cannabinoid receptorsKi0.5609.25MOUSEPMID 11160626
CB2Cannabinoid receptorsKi1.208.92RATPMID 10336536
CB2Cannabinoid receptorsKi1.308.89RATPMID 11160626
CB2Cannabinoid receptorsKi2.108.68HUMANPMID 17942307
CB1Cannabinoid receptorsKi4.408.36RATPMID 10336536
CB2Cannabinoid receptorsKi9.108.04HUMANPMID 16392793
CB2Cannabinoid receptorsKi9.468.02MOUSEPMID 10688601
CB1Cannabinoid receptorsKi9.878.01HUMANPMID 11160626
CB2Cannabinoid receptorsKi10.407.98RATPMID 10688601
CB1Cannabinoid receptorsKi11.007.96RATPMID 10991998
CB1Cannabinoid receptorsKi11.707.93HUMANPMID 12065738
CB1Cannabinoid receptorsKi14.007.85RATPMID 10991998
CB1Cannabinoid receptorsKi21.007.68HUMANPMID 17942307
CB1Cannabinoid receptorsKi24.007.62RATPMID 11408610
CB2Cannabinoid receptorsKi24.607.61HUMANPMID 16392793
CB1Cannabinoid receptorsKi25.707.59NewtPMID 10854287
CB1Cannabinoid receptorsKi29.007.54RATPMID 10991998
CB1Cannabinoid receptorsKi42.007.38RATPMID 10991998
CB1Cannabinoid receptorsKi58.607.23theromyzon TessulatumPMID 9125406
CB1Cannabinoid receptorsKi62.407.20Hirudo medicinalisPMID 9125406
CB1Cannabinoid receptorsKi63.307.20Zebra FinchPMID 11259544
CB1Cannabinoid receptorsKi1306.89RATPMID 10991998
CB1Cannabinoid receptorsKi1706.77RATPMID 10991998
CB1Cannabinoid receptorsKi2506.60RATPMID 10991998
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 WIN 55212-2 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 WIN 55212-2. 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 WIN 55212-2 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 7.96 pX

    PMID 10991998

  2. 02

    In vitro and in vivo pharmacological characterization of JTE-907, a novel selective ligand for cannabinoid CB2 receptor

    Iwamura H, Suzuki H, Ueda Y et al. · The Journal of pharmacology and experimental therapeutics 2001

    • · 6 measurements at 2 targets (Ki), strongest CB1 at 9.85 pX

    PMID 11160626

  3. 03

    New 1,8-naphthyridine and quinoline derivatives as CB2 selective agonists

    Manera C, Cascio MG, Benetti V et al. · Bioorganic & medicinal chemistry letters 2007

    • · 2 measurements at 2 targets (Ki), strongest CB2 at 8.68 pX

    PMID 17942307

  4. 04

    Novel 4-oxo-1,4-dihydroquinoline-3-carboxamide derivatives as new CB2 cannabinoid receptors agonists: synthesis, pharmacological properties and molecular modeling

    Stern E, Muccioli GG, Millet R et al. · Journal of medicinal chemistry 2006

    • · 2 measurements at 1 target (Ki), strongest CB2 at 8.04 pX

    PMID 16392793

  5. 05

    Characterization of the diarylether sulfonylester (-)-(R)-3-(2-hydroxymethylindanyl-4-oxy)phenyl-4,4,4-trifluoro-1-sulfonate (BAY 38-7271) as a potent cannabinoid receptor agonist with neuroprotective properties

    Mauler F, Mittendorf J, Horváth E et al. · The Journal of pharmacology and experimental therapeutics 2002

    • · 2 measurements at 2 targets (Ki), strongest CB2 at 9.39 pX

    PMID 12065738

  6. 06

    Cloning and pharmacological characterization of the rat CB(2) cannabinoid receptor

    Griffin G, Tao Q, Abood ME · The Journal of pharmacology and experimental therapeutics 2000

    • · 2 measurements at 1 target (Ki), strongest CB2 at 8.02 pX

    PMID 10688601

  7. 07

    Synthesis and characterization of potent and selective agonists of the neuronal cannabinoid receptor (CB1)

    Hillard CJ, Manna S, Greenberg MJ et al. · The Journal of pharmacology and experimental therapeutics 1999

    • · 2 measurements at 2 targets (Ki), strongest CB2 at 8.92 pX

    PMID 10336536

  8. 08

    Identification and characterization of the leech CNS cannabinoid receptor: coupling to nitric oxide release

    Stefano GB, Salzet B, Salzet M · Brain research 1997

    • · 2 measurements at 1 target (Ki), strongest CB1 at 7.23 pX

    PMID 9125406

  9. 09

    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 7.62 pX

    PMID 11408610

  10. 10

    Zebra finch CB1 cannabinoid receptor: pharmacology and in vivo and in vitro effects of activation

    Soderstrom K, Johnson F · The Journal of pharmacology and experimental therapeutics 2001

    • · 1 measurement at 1 target (Ki), strongest CB1 at 7.20 pX

    PMID 11259544

  11. 11

    Behaviroal, pharmacological, and molecular characterization of an amphibian cannabinoid receptor

    Soderstrom K, Leid M, Moore FL et al. · Journal of neurochemistry 2000

    • · 1 measurement at 1 target (Ki), strongest CB1 at 7.59 pX

    PMID 10854287