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PsychedeliaDokholyan Laboratory
Plate 492 of 545Verified

Quipazine

Also known as2-Piperazin-1-ylquinoline · 2-(1-Piperazinyl)quinoline · Quipazina · Quipazinum · 2-Piperazin-1-yl-quinoline · 2-(piperazin-1-yl)quinoline · Quipazine [INN] · 1-(2-Quinolinyl)piperazine

2-piperazin-1-ylquinoline

PubChem CID
5011
Measurements
56
InChIKey
XRXDAJYKGWNHTQ-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.

— No descriptive record. PubChem holds no attributed passage about Quipazine under any heading this site reads, and ChEMBL curates no mechanism for it. That is the common case for the research chemicals in this archive: they have structures and binding measurements, and nobody has written a monograph. The measurements are still on the plates that follow.

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 Quipazine 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 Quipazine 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 — 56 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — nothing published for Quipazine. An absent record is an absence of study, not evidence of safety.
  • 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 Quipazine 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 quipazine
Depiction served by PubChem for CID 5011. Not redrawn here, so the picture and the identity come from the same record.
Formula
C13H15N3R
Molecular weight
213.28g/molR
Exact mass
213.1266DaR
cLogP
1.64R
TPSA
28.2ŲR
H-bond donors
1R
H-bond acceptors
3R
Rotatable bonds
1R
Aromatic rings
2R
Heavy atoms
16R
Fraction sp³
0.308R
Formal charge
0R

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

Bemis–Murcko scaffold

c1ccc2nc(N3CCNCC3)ccc2c1

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 — 18.2 nTPM, from HTR2A, HTR1A, HTR6cerebellum — 0.2 nTPM, from SLC6A4, HTR2A, HTR1Bhippocampal formation — 6.1 nTPM, from HTR1A, HTR2A, HTR2Camygdala — 3.5 nTPM, from HTR2A, HTR2C, HTR1Ahypothalamus — 12.6 nTPM, from HTR2C, HTR2A, HTR7thalamus — no resolved target expressed herebasal ganglia — 28.2 nTPM, from HTR2C, HTR6, HTR1Dmedulla 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: midbrain 2.2, spinal cord 1.0, retina 0.7, pituitary gland 0.4.

Body

heart — 0.9 nTPM, from SLC6A4, HTR2A, HTR1Asmooth muscle — 2.4 nTPM, from HTR2A, HTR3A, HTR7lung — 27.2 nTPM, from SLC6A4, HTR2A, HTR1Bliver — 0.4 nTPM, from HTR7, HTR2Akidney — 0.3 nTPM, from HTR1B, SLC6A4, HTR3Astomach — 4.7 nTPM, from HTR1B, HTR3A, SLC6A4duodenum — 9.7 nTPM, from SLC6A4, HTR1D, HTR3Asmall intestine — 38.0 nTPM, from SLC6A4, HTR1D, HTR3Acolon — 2.0 nTPM, from HTR3A, HTR7, HTR2Aadrenal gland — 0.5 nTPM, from HTR1B, HTR3A, HTR2Athyroid gland — 0.4 nTPM, from SLC6A4, HTR2A, HTR1Bpancreas — 2.7 nTPM, from HTR3A, SLC6A4, HTR1Durinary bladder — 2.1 nTPM, from HTR7, HTR1B, HTR2Askeletal muscle — 0.9 nTPM, from HTR7, HTR2Aspleen — 1.0 nTPM, from HTR7, HTR3A, SLC6A4salivary gland — 4.8 nTPM, from HTR3A, SLC6A4, HTR1B
038 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. basal ganglia

    28.2 nTPM

  2. cerebral cortex

    18.2 nTPM

  3. hypothalamus

    12.6 nTPM

  4. hippocampal formation

    6.1 nTPM

  5. amygdala

    3.5 nTPM

  6. midbrain

    2.2 nTPM

  7. spinal cord

    1.0 nTPM

  8. retina

    0.7 nTPM

  9. pituitary gland

    0.4 nTPM

  10. cerebellum

    0.2 nTPM

Peripheral & autonomic

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

  1. small intestine

    38.0 nTPM

  2. lung

    27.2 nTPM

  3. duodenum

    9.7 nTPM

  4. salivary gland

    4.8 nTPM

  5. stomach 1

    4.7 nTPM

  6. pancreas

    2.7 nTPM

  7. smooth muscle

    2.4 nTPM

  8. urinary bladder

    2.1 nTPM

  9. colon

    2.0 nTPM

  10. spleen

    1.0 nTPM

  11. heart muscle

    0.9 nTPM

  12. skeletal muscle

    0.9 nTPM

  13. adrenal gland

    0.5 nTPM

  14. thyroid gland

    0.4 nTPM

  15. liver

    0.4 nTPM

  16. kidney

    0.3 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.

3 of this compound’s targets could not be resolved to a gene and are absent from both columns: 5-HT1, 5-HT2, 5-HT3.

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

5-HT3A — Ki 9.02 pX5-HT3 — Ki 9.00 pX5-HT2 — Ki 7.77 pX5-HT2A — Ki 6.89 pX5-HT2C — Ki 6.72 pX5-HT1B — Ki 6.70 pX5-HT1 — Ki 6.64 pX5-HT1A — Ki 5.80 pX5-HT7 — Ki 5.52 pX5-HT6 — Ki 5.44 pX5-HT1D — IC50 5.43 pXSERT — Ki 7.52 pX5-HT3A5-HT35-HT25-HT2A5-HT2C5-HT1B5-HT15-HT1A5-HT75-HT65-HT1DSERT579
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 Quipazine in this archive.

Published toxicology

— None. The toxicology databases this site reads — HSDB, RTECS and LiverTox, by way of PubChem — hold no record for Quipazine. 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 38

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

TargetClassTypeValue (nM)pXOrganismAssay
5-HT3ASerotonin receptorsKi0.9609.02Rattus norvegicusCHEMBL1037804
5-HT3ASerotonin receptorsKi0.9609.02Rattus norvegicusCHEMBL1006686
5-HT3Serotonin receptorsKi1.009.00Rattus norvegicusCHEMBL619416
5-HT3Serotonin receptorsKi1.208.92Rattus norvegicusCHEMBL620632
5-HT3Serotonin receptorsKi1.418.85Rattus norvegicusCHEMBL619415
5-HT3Serotonin receptorsKi1.808.74Rattus norvegicusCHEMBL618919
5-HT3Serotonin receptorsKi1.808.74Rattus norvegicusCHEMBL619785
5-HT3Serotonin receptorsKi1.808.74Homo sapiensCHEMBL619771
5-HT3Serotonin receptorsKi1.828.74Rattus norvegicusCHEMBL619425
5-HT3Serotonin receptorsKi3.028.52Rattus norvegicusCHEMBL619645
5-HT3Serotonin receptorsKi3.048.52Rattus norvegicusCHEMBL619789
5-HT3Serotonin receptorsKi6.318.20Rattus norvegicusCHEMBL619427
5-HT2Serotonin receptorsKi17.007.77Rattus norvegicusCHEMBL617413
SERTMonoamine transportersKi30.007.52Homo sapiensCHEMBL1949348
SERTMonoamine transportersKi31.007.51Rattus norvegicusCHEMBL806136
SERTMonoamine transportersKi31.007.51Rattus norvegicusCHEMBL805335
SERTMonoamine transportersKi43.007.37Rattus norvegicusCHEMBL812555
5-HT2ASerotonin receptorsKi1306.89Rattus norvegicusCHEMBL617930
5-HT2CSerotonin receptorsKi1906.72Rattus norvegicusCHEMBL621511
5-HT1BSerotonin receptorsKi2006.70Rattus norvegicusCHEMBL616795
5-HT2CSerotonin receptorsKi2006.70Homo sapiensCHEMBL616819
5-HT1BSerotonin receptorsKi2086.68Rattus norvegicusCHEMBL616782
5-HT1Serotonin receptorsKi2306.64Rattus norvegicusCHEMBL615400
5-HT2Serotonin receptorsKi2306.64Rattus norvegicusCHEMBL617444
5-HT2Serotonin receptorsKi2306.64Rattus norvegicusCHEMBL872918
UncheckedUnclassifiedKi2306.64— organism not recordedCHEMBL615402
5-HT2CSerotonin receptorsKi3166.50Rattus norvegicusCHEMBL617499
5-HT1BSerotonin receptorsKi3206.49Rattus norvegicusCHEMBL616773
5-HT2Serotonin receptorsKi6456.19Rattus norvegicusCHEMBL617447
5-HT2ASerotonin receptorsKi7946.10Rattus norvegicusCHEMBL1039634
5-HT2ASerotonin receptorsKi7946.10Rattus norvegicusCHEMBL1006688
5-HT2ASerotonin receptorsKi7946.10Rattus norvegicusCHEMBL617332
5-HT1ASerotonin receptorsKi1,5855.80Rattus norvegicusCHEMBL616159
5-HT2ASerotonin receptorsKi1,8005.74Rattus norvegicusCHEMBL621541
5-HT1ASerotonin receptorsKd1,9955.70Homo sapiensCHEMBL1061237
5-HT7Serotonin receptorsKi3,0335.52Homo sapiensCHEMBL619855
5-HT1ASerotonin receptorsKi3,3005.48Rattus norvegicusCHEMBL615963
5-HT6Serotonin receptorsKi3,6005.44Homo sapiensCHEMBL618118

Functional readouts 18

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

TargetClassTypeValue (nM)pXOrganismAssay
5-HT3Serotonin receptorsIC500.4479.35Rattus norvegicusCHEMBL618142
5-HT3Serotonin receptorsIC500.4479.35Homo sapiensCHEMBL618141
5-HT3Serotonin receptorsIC503.808.42Rattus norvegicusCHEMBL617709
5-HT3Serotonin receptorsIC506.208.21Rattus norvegicusCHEMBL617698
5-HT2CSerotonin receptorsIC5061.667.21Homo sapiensCHEMBL617855
5-HT2CSerotonin receptorsIC5061.667.21Homo sapiensCHEMBL617854
5-HT1BSerotonin receptorsIC503806.42Rattus norvegicusCHEMBL616754
5-HT2CSerotonin receptorsIC504706.33Rattus norvegicusCHEMBL617838
5-HT2ASerotonin receptorsIC501,4005.85Rattus norvegicusCHEMBL617458
5-HT1ASerotonin receptorsIC501,4455.84Homo sapiensCHEMBL615580
5-HT1ASerotonin receptorsIC501,4455.84Homo sapiensCHEMBL615579
5-HT1ASerotonin receptorsIC502,7005.57Rattus norvegicusCHEMBL615926
5-HT2ASerotonin receptorsIC503,4675.46Bos taurusCHEMBL617198
5-HT2ASerotonin receptorsIC503,4675.46Bos taurusCHEMBL873476
5-HT1DSerotonin receptorsIC503,7155.43Sus scrofaCHEMBL617559
5-HT1DSerotonin receptorsIC503,7155.43Sus scrofaCHEMBL617560
5-HT1BSerotonin receptorsIC507,0795.15Rattus norvegicusCHEMBL873475
5-HT1BSerotonin receptorsIC507,0795.15Rattus norvegicusCHEMBL616188
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 Quipazine 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 quipazine · 2-Piperazin-1-ylquinoline · 2-(1-Piperazinyl)quinoline. 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 Quipazine 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.

No reference is recorded against any value for this compound. Its measurements come from ChEMBL assay records that carry an assay identifier but no publication, so there is no paper to cite here — an absence in the upstream record, not a judgment about the evidence. The assay identifiers in Every measurement resolve to the records the values were read from.