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PsychedeliaDokholyan Laboratory
Plate 314 of 545Verified

DOB

PubChem records this structure as 2,5-Dimethoxy-4-bromoamphetamine.

Also known as2,5-Dimethoxy-4-bromoamphetamine · DOB-4 · 4-DOB · Brolamfetamine · 4-Bromo-2,5-dimethoxyamphetamine · Brolanfetamina · Brolamfetamine [INN] · bromoamphetamine

1-(4-bromo-2,5-dimethoxyphenyl)propan-2-amine

PubChem CID
62065
Measurements
60
InChIKey
FXMWUTGUCAKGQL-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

  • 4-bromo-2,5-dimethoxy-amphetamine 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)

  • RN given refers to (alpha)-isomer; a serotonin agonist that interferes with Meth A tumor growth in mice by selective vasoconstrictive action

    Medical Subject Headings (MeSH)

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 DOB 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 DOB 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 — 60 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — nothing published for DOB. 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 DOB 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 DOB
Depiction served by PubChem for CID 62065. Not redrawn here, so the picture and the identity come from the same record.
Formula
C11H16BrNO2R
Molecular weight
274.16g/molR
Exact mass
273.0364DaR
cLogP
2.36R
TPSA
44.5ŲR
H-bond donors
1R
H-bond acceptors
3R
Rotatable bonds
4R
Aromatic rings
1R
Heavy atoms
15R
Fraction sp³
0.455R
Formal charge
0R

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

Bemis–Murcko scaffold

c1ccccc1

Shared with 2-Bromomescaline, 2-TOET, 2-TOM, 2,3,4,5-Tetramethoxyamphetamine, 2,4-dimethoxyamphetamine, 2,5-Dimethoxy-4-(2-fluoroethyl)amphetamine and 129 more. 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 does hold onset and duration ranges for it, inherited from an earlier build, but their source column is empty and so they cannot be shown. 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.

Filed under Hallucinogens

  • 6C49Disorders due to use of hallucinogens

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

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, HTR1Ecerebellum — 1.0 nTPM, from HTR1E, HTR2A, HTR2Bhippocampal formation — 6.1 nTPM, from HTR1A, HTR2A, HTR2Camygdala — 3.5 nTPM, from HTR2A, HTR2C, HTR1Ahypothalamus — 12.6 nTPM, from HTR2C, HTR2A, HTR1Athalamus — no resolved target expressed herebasal ganglia — 28.2 nTPM, from HTR2C, HTR1D, HTR2Amedulla 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 — 4.6 nTPM, from HTR2B, HTR2A, HTR1Asmooth muscle — 15.7 nTPM, from HTR2B, HTR2A, HTR1Elung — 0.8 nTPM, from HTR2B, HTR2A, HTR1Bliver — 3.3 nTPM, from HTR2B, HTR2Akidney — 3.1 nTPM, from HTR2B, HTR1B, HTR2Astomach — 4.7 nTPM, from HTR1B, HTR2B, HTR1Eduodenum — 8.0 nTPM, from HTR1D, HTR2B, HTR2Asmall intestine — 7.1 nTPM, from HTR1D, HTR2B, HTR2Acolon — 8.5 nTPM, from HTR2B, HTR2A, HTR1Dadrenal gland — 17.2 nTPM, from HTR2B, HTR1B, HTR2Athyroid gland — 3.2 nTPM, from HTR2B, HTR1E, HTR2Apancreas — 0.2 nTPM, from HTR2B, HTR1D, HTR1Eurinary bladder — 2.0 nTPM, from HTR2B, HTR1B, HTR2Askeletal muscle — 0.3 nTPM, from HTR2A, HTR2Bspleen — 0.4 nTPM, from HTR2Bsalivary gland — 0.4 nTPM, from HTR2B, HTR1B, HTR2A
028 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. cerebellum

    1.0 nTPM

  9. retina

    0.7 nTPM

  10. pituitary gland

    0.4 nTPM

Peripheral & autonomic

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

  1. adrenal gland

    17.2 nTPM

  2. smooth muscle

    15.7 nTPM

  3. colon

    8.5 nTPM

  4. duodenum

    8.0 nTPM

  5. small intestine

    7.1 nTPM

  6. stomach 1

    4.7 nTPM

  7. heart muscle

    4.6 nTPM

  8. liver

    3.3 nTPM

  9. thyroid gland

    3.2 nTPM

  10. kidney

    3.1 nTPM

  11. urinary bladder

    2.0 nTPM

  12. lung

    0.8 nTPM

  13. salivary gland

    0.4 nTPM

  14. spleen

    0.4 nTPM

  15. skeletal muscle

    0.3 nTPM

  16. pancreas

    0.2 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, Serotonin (5-HT) 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 10 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.

5-HT2A — Ki 10.00 pX5-HT2 — Ki 9.10 pX5-HT2C — Ki 8.89 pX5-HT2B — Ki 8.54 pXSerotonin (5-HT) receptor — Kd 7.35 pX5-HT1E — Ki 6.25 pX5-HT1B — Ki 6.08 pX5-HT1D — Ki 6.00 pX5-HT1 — Ki 5.48 pX5-HT1A — Ki 5.42 pX5-HT2A5-HT25-HT2C5-HT2BSerotonin (5-HT)…5-HT1E5-HT1B5-HT1D5-HT15-HT1A579
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 DOB in this archive.

Published toxicology

— None. The toxicology databases this site reads — HSDB, RTECS and LiverTox, by way of PubChem — hold no record for DOB. 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 59

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

TargetClassTypeValue (nM)pXOrganismAssay
5-HT2ASerotonin receptorsKi0.10010.00Rattus norvegicusCHEMBL839446
5-HT2ASerotonin receptorsKi0.2909.54UNDEFINEDPMID 18847250
5-HT2ASerotonin receptorsKi0.6009.22HUMANPMID 9933142
5-HT2Serotonin receptorsKi0.7909.10Rattus norvegicusCHEMBL617528
5-HT2ASerotonin receptorsKi0.8009.10Rattus norvegicusCHEMBL4009955
5-HT2ASerotonin receptorsKi1.009.00RATPMID 7984267
5-HT2ASerotonin receptorsKi1.178.93HUMANPMID 15322733
5-HT2CSerotonin receptorsKi1.308.89HUMANPMID 9933142
5-HT2ASerotonin receptorsKi1.518.82HUMANPMID 10498829
5-HT2ASerotonin receptorsKi1.908.72UNDEFINEDPMID 18847250
5-HT2ASerotonin receptorsKi2.208.66Rattus norvegicusCHEMBL617926
5-HT2ASerotonin receptorsKi2.208.66Rattus norvegicusCHEMBL621533
5-HT2CSerotonin receptorsKi2.808.55Rattus norvegicusCHEMBL621508
5-HT2CSerotonin receptorsKi2.808.55Rattus norvegicusCHEMBL621525
5-HT2BSerotonin receptorsKi2.888.54HUMANPMID 10498829
5-HT2CSerotonin receptorsKi3.018.52RATPMID 7984267
5-HT2ASerotonin receptorsKi3.308.48HUMANPMID 10611640
5-HT2CSerotonin receptorsKi6.318.20HUMANPMID 15322733
5-HT2CSerotonin receptorsKi7.768.11HUMANPMID 10498829
5-HT2CSerotonin receptorsKi10.008.00RATPMID 9928251
5-HT2CSerotonin receptorsKi10.008.00RATPMID 10611640
5-HT2BSerotonin receptorsKi21.807.66RATPMID 9933142
5-HT2ASerotonin receptorsKi22.007.66Rattus norvegicusCHEMBL621546
5-HT2ASerotonin receptorsKi22.007.66Rattus norvegicusCHEMBL980602
5-HT2ASerotonin receptorsKi26.237.58HUMANPDSP
5-HT2BSerotonin receptorsKi26.907.57HUMANPMID 9933142
5-HT2ASerotonin receptorsKi32.007.49Rattus norvegicusCHEMBL621531
5-HT2Serotonin receptorsKi41.007.39Rattus norvegicusCHEMBL617444
5-HT2Serotonin receptorsKi41.007.39Rattus norvegicusCHEMBL617529
5-HT2Serotonin receptorsKi41.007.39Rattus norvegicusCHEMBL617438
5-HT2ASerotonin receptorsKi41.007.39Homo sapiensCHEMBL617383
5-HT2ASerotonin receptorsKi41.007.39RATPDSP
5-HT2ASerotonin receptorsKi41.007.39Rattus norvegicusCHEMBL4009954
5-HT2ASerotonin receptorsKi41.007.39UNDEFINEDPMID 18847250
5-HT2ASerotonin receptorsKi41.007.39Rattus norvegicusCHEMBL621544
5-HT2BSerotonin receptorsKi43.657.36HUMANPMID 15322733
Serotonin (5-HT) receptorSerotonin receptorsKd44.677.35Rattus norvegicusCHEMBL619176
Serotonin (5-HT) receptorSerotonin receptorsKd44.677.35Rattus norvegicusCHEMBL619177
Serotonin (5-HT) receptorSerotonin receptorsKd44.677.35Rattus norvegicusCHEMBL3279114
5-HT2CSerotonin receptorsKi60.257.22RATPMID 7984267
5-HT2CSerotonin receptorsKi69.007.16PIGPDSP
5-HT2CSerotonin receptorsKi69.007.16PIGPDSP
5-HT2CSerotonin receptorsKi70.007.15Rattus norvegicusCHEMBL616834
5-HT2CSerotonin receptorsKi70.007.15Rattus norvegicusCHEMBL621526
5-HT2ASerotonin receptorsKi81.007.09HUMANPMID 10611640
5-HT2ASerotonin receptorsKi85.117.07RATPMID 7984267
5-HT2CSerotonin receptorsKi1526.82RATPMID 9928251
5-HT2CSerotonin receptorsKi1526.82RATPMID 10611640
5-HT1ESerotonin receptorsKi5566.25HUMANPMID 2664084
5-HT1BSerotonin receptorsKi8316.08RATPDSP
5-HT1BSerotonin receptorsKi8316.08RATPDSP
5-HT1DSerotonin receptorsKi1,0006.00BOVINEPMID 2664084
5-HT1DSerotonin receptorsKi1,4485.84COWPDSP
5-HT1DSerotonin receptorsKi1,8005.74RATPDSP
5-HT1Serotonin receptorsKi3,3405.48Rattus norvegicusCHEMBL615400
5-HT1DSerotonin receptorsKi3,4005.47RATPDSP
5-HT1ASerotonin receptorsKi3,7705.42RATPDSP
5-HT1ASerotonin receptorsKi3,7705.42RATPDSP
5-HT1ASerotonin receptorsKi6,3275.20HUMANPDSP

Functional readouts 1

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

TargetClassTypeValue (nM)pXOrganismAssay
5-HT2ASerotonin receptorsEC5072.007.14Rattus norvegicusCHEMBL617114
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 DOB 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 2,5-Dimethoxy-4-bromoamphetamine · Brolamfetamine · 4-Bromo-2,5-dimethoxyamphetamine. 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 DOB 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

    Agonist high and low affinity state ratios predict drug intrinsic activity and a revised ternary complex mechanism at serotonin 5-HT(2A) and 5-HT(2C) receptors

    Egan C, Grinde E, Dupre A et al. · Synapse (New York, N.Y.) 2000

    • · 4 measurements at 2 targets (Ki), strongest 5-HT2A at 8.48 pX

    PMID 10611640

  2. 02

    Comparisons of hallucinogenic phenylisopropylamine binding affinities at cloned human 5-HT2A, -HT(2B) and 5-HT2C receptors

    Nelson DL, Lucaites VL, Wainscott DB et al. · Naunyn-Schmiedeberg's archives of pharmacology 1999

    • · 4 measurements at 3 targets (Ki), strongest 5-HT2A at 9.22 pX

    PMID 9933142

  3. 03

    Molecular biology of 5-HT receptors

    Boess FG, Martin IL · Neuropharmacology 1994

    • · 4 measurements at 2 targets (Ki), strongest 5-HT2A at 9.00 pX

    PMID 7984267

  4. 04

    Potential modes of interaction of 9-aminomethyl-9,10-dihydroanthracene (AMDA) derivatives with the 5-HT2A receptor: a ligand structure-affinity relationship, receptor mutagenesis and receptor modeling investigation

    Runyon SP, Mosier PD, Roth BL et al. · Journal of medicinal chemistry 2008

    • · 3 measurements at 1 target (Ki), strongest 5-HT2A at 9.54 pX

    PMID 18847250

  5. 05

    Pharmacological characterisation of the agonist radioligand binding site of 5-HT(2A), 5-HT(2B) and 5-HT(2C) receptors

    Knight AR, Misra A, Quirk K et al. · Naunyn-Schmiedeberg's archives of pharmacology 2004

    • · 3 measurements at 3 targets (Ki), strongest 5-HT2A at 8.93 pX

    PMID 15322733

  6. 06

    Functional characterization of agonists at recombinant human 5-HT2A, 5-HT2B and 5-HT2C receptors in CHO-K1 cells

    Porter RH, Benwell KR, Lamb H et al. · British journal of pharmacology 1999

    • · 3 measurements at 3 targets (Ki), strongest 5-HT2A at 8.82 pX

    PMID 10498829

  7. 07

    Pharmacological characterization of the constitutively activated state of the serotonin 5-HT2C receptor

    Herrick-Davis K, Grinde E, Gauthier C et al. · Annals of the New York Academy of Sciences 1998

    • · 2 measurements at 1 target (Ki), strongest 5-HT2C at 8.00 pX

    PMID 9928251

  8. 08

    Detection of a novel serotonin receptor subtype (5-HT1E) in human brain: interaction with a GTP-binding protein

    Leonhardt S, Herrick-Davis K, Titeler M · Journal of neurochemistry 1989

    • · 2 measurements at 2 targets (Ki), strongest 5-HT1E at 6.25 pX

    PMID 2664084