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PsychedeliaDokholyan Laboratory
Plate 385 of 545Verified

LSD

PubChem records this structure as (+)-Lysergic acid diethylamide.

Also known as(+)-Lysergic acid diethylamide · Lysergide · LYSERGIC ACID DIETHYLAMIDE · D-Lsd · N,N-Diethyllysergamide · Lysergsaeurediaethylamid · N,N-Diethyl-D-lysergamide · Lysergaure diethylamid

(6aR,9R)-N,N-diethyl-7-methyl-6,6a,8,9-tetrahydro-4H-indolo[4,3-fg]quinoline-9-carboxamide

PubChem CID
5761
Measurements
170
InChIKey
VAYOSLLFUXYJDT-RDTXWAMCSA-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.

Synthesized summary

written by this site — every other word below is quoted

LSD is an ergoline alkaloid, formally the condensation of lysergic acid with diethylamine, and the sources file it at once as a hallucinogen, a serotonergic agonist and a dopamine agonist 1. It was not sought: it was made while working from ergot toward circulatory and respiratory stimulants, and the effect on animals led instead to a model of psychosis 2. That double life runs through the whole record, which carries it both as a laboratory reagent — a serotonin antagonist used in biochemical research — and as an experimental adjunct in the study and treatment of mental disorders 3. Two therapeutic passages here are recent and specific rather than general: a placebo-controlled fMRI study of LSD with music-listening in psychedelic psychotherapy 4, and a twelve-month follow-up of LSD-assisted psychotherapy for anxiety in life-threatening illness, in which no lasting adverse reactions were reported and the measured reduction in anxiety was sustained 5. Taken orally, effects appear within about half an hour and continue for eight to twelve hours or more, dose-dependently 6. Almost none of the dose leaves intact — roughly one percent unchanged in twenty-four-hour urine — the rest being hydroxylated and glucuronidated in the liver to inactive metabolites 7,8. It is Schedule I 9. One passage is an open question rather than a finding, and is noted because it is the only one of its kind here: the record carries an unresolved debate over chronic flashbacks, observing that explanations in terms of LSD physically remaining in the body have been discounted experimentally 10.

Drawn only from the passages printed below, so every claim above can be checked against material on this page. The numbers are those passages. Synthesized by Claude Opus 5 (claude-opus-5), via Claude Code on 2026-08-27.

What it is

  • Prismatic crystals (from benzene). Tasteless and odorless. A hallucinogen.

    CAMEO Chemicals

  • 1cited by the summary above

    Lysergic acid diethylamide is an ergoline alkaloid arising from formal condensation of lysergic acid with diethylamine. It has a role as a hallucinogen, a serotonergic agonist and a dopamine agonist. It is a monocarboxylic acid amide, an organic heterotetracyclic compound and an ergoline alkaloid. It is functionally related to a lysergamide.

    ChEBI

  • Lysergic acid diethylamide 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)

  • 10cited by the summary above

    Debate continues over the nature and causes of chronic flashbacks. Explanations in terms of LSD physically remaining in the body for months or years after consumption have been discounted by experimental evidence. Some say HPPD is a manifestation of post-traumatic stress disorder, not related to the direct action of LSD on brain chemistry, and varies according to the susceptibility of the individual to the disorder. Many emotionally intense experiences can lead to flashbacks when a person is reminded acutely of the original experience. However, not all published case reports of chronic flashbacks appear to describe an anxious hyper-vigilant state reminiscent of post-traumatic stress disorder…

    DrugBank

Recognized use

  • /CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations;…

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)NIH/NLM; ClinicalTrials.Gov. Available from, as of October 2, 2017: https://clinicaltrials.gov/

  • 4cited by the summary above

    /EXPL THER/ Psychedelic drugs such as lysergic acid diethylamide (LSD) were used extensively in psychiatry in the past and their therapeutic potential is beginning to be re-examined today. Psychedelic psychotherapy typically involves a patient lying with their eyes-closed during peak drug effects, while listening to music and being supervised by trained psychotherapists. In this context, music is considered to be a key element in the therapeutic model; working in synergy with the drug to evoke therapeutically meaningful thoughts, emotions and imagery. The underlying mechanisms involved in this process have, however, never been formally investigated. Here we studied the interaction between LS…

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)PMID 27084302Kaelen M et al; Eur Neuropsychopharmacol 26 (7): 1099-109 (2016)

  • 5cited by the summary above

    /EXPL THER/ A recently published study showed the safety and efficacy of LSD-assisted psychotherapy in patients with anxiety associated with life-threatening diseases. Participants of this study were included in a prospective follow-up. 12 months after finishing LSD psychotherapy, 10 participants were tested for anxiety (STAI) and participated in a semi-structured interview. A Qualitative Content Analysis (QCA) was carried out on the interviews to elaborate about LSD effects and lasting psychological changes. None of the participants reported lasting adverse reactions. The significant benefits as measured with the STAI were sustained over a 12-month period. In the QCA participants consistent…

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)PMID 25389218Gasser P et al; J Psychopharmacol 29 (1): 57-68 (2015)

  • For more Therapeutic Uses (Complete) data for LSD (7 total), please visit the HSDB record page.

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)

  • 2cited by the summary above

    Lysergic acid diethylamide (LSD) is a classical hallucinogen originally synthesized by Albert Hoffman. He accidentally concocted the drug while making experimental substances from ergots to create circulatory and respiratory stimulants. The most pronounced effect on the animals allowed him to create a model for psychosis and study the induced temporary psychotic-like states. During the psychotic state, he also noted permitted recall and produced improved insight.

    Drug Indication

    StatPearls

  • 9cited by the summary above

    Lysergic acid diethylamide (DEA Code Number: 7315) is a Schedule I controlled substance.

    Use Classification

    Hazardous Substances Data Bank (HSDB)21 CFR 1308.11(d) (USDEA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of October 19, 2017: https://www.ecfr.gov

  • Schedule I Controlled Substance: (A) The drug or other substance has a high potential for abuse; (B) The drug or other substance has no currently accepted medical use in treatment in the United States; and (C) There is a lack of accepted safety for use of the drug or other substance under medical supervision.

    Use Classification

    Hazardous Substances Data Bank (HSDB)US Department of Justice/Office of Diversion Control; Schedule of Controlled Substances. Available from, as of October 19, 2017: https://www.deadiversion.usdoj.gov/21cfr/21usc/812.htm

  • 3cited by the summary above

    In biochemical research as antagonist to serotonin. Has been used experimentally as adjunct in study and treatment of mental disorders

    Use Classification

    Hazardous Substances Data Bank (HSDB)O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 1049

  • For more Uses (Complete) data for LSD (6 total), please visit the HSDB record page.

    Use Classification

    Hazardous Substances Data Bank (HSDB)

How it acts

  • The goal of the present study was to better delineate the mechanisms of action of the prototypical hallucinogen LSD. LSD (0.03, 0.1 and 0.3 mg/kg, s.c.) produced locomotor hyperactivity, disruption of /prepulse inhibition (PPI)/ and a number of behaviors indicative of 5-HT activation such as wet-dog shakes, back muscle contractions and forepaw treading. These various behavioral effects of LSD were studied in both Sprague-Dawley and Wistar rats, although with the exception of back muscle contractions which were more prominent in Sprague-Dawley rats, no major strain differences were detected. The PPI disruption induced by LSD (0.1 mg/kg) in Sprague-Dawley rats was completely reversed by pretre…

    Hazardous Substances Data Bank (HSDB)PMID 11557170Ouagazzal A et al; Neuropsychopharmacology 25 (4): 565-75 (2001)

  • ... By genetically expressing /5-HT(2A) receptor (2AR)/ only in cortex, /investigators/show that 2AR-regulated pathways on cortical neurons are sufficient to mediate the signaling pattern and behavioral response to hallucinogens. Hallucinogenic and nonhallucinogenic 2AR agonists both regulate signaling in the same 2AR-expressing cortical neurons. However, the signaling and behavioral responses to the hallucinogens are distinct. While lisuride and LSD both act at 2AR expressed by cortex neurons to regulate phospholipase C, LSD responses also involve pertussis toxin-sensitive heterotrimeric G(i/o) proteins and Src. ...

    Hazardous Substances Data Bank (HSDB)PMID 17270739Gonzalez-Maeso J et al; Neuron 53 (3): 439-52 (2007)

Behavior carries the pharmacological classes and the acute-effect durations, with plasma half-life kept separate from duration of effect.

In the body

  • /LSD/ is converted metabolized in the liver via hydroxylation and glucuronidation, and excreted predominantly as a pharmacologically inactive compound.

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017, p. 1117

  • 6cited by the summary above

    When taken orally, the effects become apparent within about 30 minutes and may continue for 8 to 12 hours or more. The duration and intensity of effects are dose-dependent.

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)European Monitoring Centre for Drugs and Drug Addiction (EMCDDA); Drug Profiles: Lysergide (LSD). Available from, as of November 6, 2017: https://www.emcdda.europa.eu/drug-profiles

  • 8cited by the summary above

    Following a dose of 160 ug to 13 subjects, plasma concentrations varied considerably up to 9 ug/L. Only about 1 % is excreted unchanged in the urine in 24 hours.

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)European Monitoring Centre for Drugs and Drug Addiction (EMCDDA); Drug Profiles: Lysergide (LSD). Available from, as of November 6, 2017: https://www.emcdda.europa.eu/drug-profiles

  • The qualitative and quantitative aspects of the metabolism and elimination of (14)C-LSD in the rat, guinea pig and rhesus monkey have been investigated. Rats given an i.p. dose (1 mg/kg) excreted 73% of the (14)C in the feces, 16% in the urine and 3.4% in the expired air as (14)CO2 in 96 hr. Guinea pigs similarly dosed, excreted 40% in the feces, 28% (urine) and 18% (expired (14)CO2) in 96 hr. Rhesus monkeys (0.15 mg/kg i.m.) eliminated 39% of the (14)C in the urine and 23% in the feces in 96 hr. Extensive biliary excretion of (14)C-LSD occurred in both the rat and guinea pig. Bile duct-cannulated rats excreted 68% of an i.v. dose (1.33 mg/kg) in the bile in 5 hr and the guinea pig 52% in 6…

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)PMID 117811Siddik ZH et al.; Biochem Pharmacol 28 (20): 3093-101 (1979)

  • Three case reports are presented, including autopsy findings and toxicological screening results, which were tested positive for the potent hallucinogenic drug lysergic acid diethylamide (LSD). LSD and its main metabolites were quantified in brain tissue and femoral blood, and furthermore hematoma and urine when available. LSD, its main metabolite 2-oxo-3-hydroxy-LSD (oxo-HO-LSD), and iso-LSD were quantified in biological samples according to a previously published procedure involving liquid-liquid extraction and ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS). ...

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 28803722Mardal M et al; Forensic Sci Int 278: e14-e18 (2017)

  • 7cited by the summary above

    Following a dose of 160 ug to 13 subjects ... in humans, LSD is extensively transformed in the liver by hydroxylation and glucuronide conjugation to inactive metabolites. ...A major metabolite found in urine is 2-oxylysergide.

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)European Monitoring Centre for Drugs and Drug Addiction (EMCDDA); Drug Profiles: Lysergide (LSD). Available from, as of November 6, 2017: https://www.emcdda.europa.eu/drug-profiles

  • The metabolism of lysergic acid diethylamide (LSD) to 2-oxo-3-hydroxy lysergic acid diethylamide (O-H-LSD) was investigated in liver microsomes and cyropreserved hepatocytes from humans. Previous studies have demonstrated that O-H-LSD is present in human urine at concentrations 16-43 times greater than LSD, the parent compound. Additionally, these studies have determined that O-H-LSD is not generated during the specimen extraction and analytical processes or due to parent compound degradation in aqueous urine samples. However, these studies have not been conclusive in demonstrating that O-H-LSD is uniquely produced during in vivo metabolism. Phase I drug metabolism was investigated by incuba…

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 11043658Klette KL et al; J Anal Toxicol 24 (7): 550-6 (2000)

  • The qualitative and quantitative aspects of the metabolism and elimination of (14)C-LSD in the rat, guinea pig and rhesus monkey have been investigated. ...(14)C-LSD is almost completely metabolized by all three species and little unchanged drug is excreted. The metabolites identified were 13- and 14-hydroxy-LSD and their glucuronic acid conjugates, 2-oxo-LSD, de-ethyl LSD and a naphthostyril derivative. There occur, however, important species differences in the nature and amounts of the various metabolites. In the rat and guinea pig the major metabolites were the glucuronic acid conjugates of 13- and 14-hydroxy-LSD which were found in both urine and bile. The guinea pig excreted significant…

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 117811Siddik ZH et al.; Biochem Pharmacol 28 (20): 3093-101 (1979)

History, discovery and cultural use

Written by this site · every claim referenced

Albert Hofmann found that lysergic acid diethylamide had powerful psychoactive effects about a decade before the 1957 report that brought psilocybin mushrooms to Western attention 1. What followed is often called the golden era of psychedelic research: between the 1940s and the 1960s more than a thousand clinical papers described treatment of some 40,000 patients 1. Hofmann later co-wrote the standard ethnobotanical survey of hallucinogenic plants with Richard Evans Schultes 2.

  1. 1Stroud 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.
  2. 2Schultes 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.

Ref 1 read directly at NBK587225, which gives the decade-before-1957 dating and the golden-era figures. Ref 2 is cited only for its own authorship, which is on its title page. Nothing above is quoted from LSD’s own database records; those appear as quotations elsewhere on this plate.

Histories of this field

Scholarship on psychedelics generally, not on LSD 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 — 170 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — 13 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 LSD 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 LSD
Depiction served by PubChem for CID 5761. Not redrawn here, so the picture and the identity come from the same record.
Formula
C20H25N3OR
Molecular weight
323.44g/molR
Exact mass
323.1998DaR
cLogP
2.91R
TPSA
39.3ŲR
H-bond donors
1R
H-bond acceptors
2R
Rotatable bonds
3R
Aromatic rings
2R
Heavy atoms
24R
Fraction sp³
0.450R
Formal charge
0R

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

Bemis–Murcko scaffold

C1=C2c3cccc4[nH]cc(c34)C[C@H]2NCC1

Shared with 1B-LSD, 1DD-LSD, 1H-LSD, 1P-AL-LAD, 1P-ETH-LAD, 1P-LSD and 23 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

8.2 ± 2.1 h at 100 µg; 11.6 ± 1.7 h at 200 µg

100 and 200 µg, oral

“The subjective effects lasted (mean ± standard deviation) 8.2 ± 2.1 and 11.6 ± 1.7 h for the 100- and 200-µg LSD doses, respectively”
Dolder PC et al., Clinical pharmacokinetics 2017. PMID 28197931

6.7 h to 11 h across 25–200 µg

“The average duration of subjective effects increased from 6.7 to 11 h with increasing doses of 25-200 µg”
Holze F et al., Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 2021. PMID 33059356

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.

2.6 h (2.2–3.4 h)

“The plasma half-life was 2.6 h (2.2-3.4 h)”
Dolder PC et al., Clinical pharmacokinetics 2017. PMID 28197931

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.

  • The goal of the present study was to better delineate the mechanisms of action of the prototypical hallucinogen LSD. LSD (0.03, 0.1 and 0.3 mg/kg, s.c.) produced locomotor hyperactivity, disruption of /prepulse inhibition (PPI)/ and a number of behaviors indicative of 5-HT activation such as wet-dog shakes, back muscle contractions and fo…
    Hazardous Substances Data Bank (HSDB)PMID 11557170Ouagazzal A et al; Neuropsychopharmacology 25 (4): 565-75 (2001)
  • ... By genetically expressing /5-HT(2A) receptor (2AR)/ only in cortex, /investigators/show that 2AR-regulated pathways on cortical neurons are sufficient to mediate the signaling pattern and behavioral response to hallucinogens. Hallucinogenic and nonhallucinogenic 2AR agonists both regulate signaling in the same 2AR-expressing cortical…
    Hazardous Substances Data Bank (HSDB)PMID 17270739Gonzalez-Maeso J et al; Neuron 53 (3): 439-52 (2007)
  • Lysergic acid diethylamide (LSD) produces altered mood and hallucinations in humans and binds with high affinity to serotonin-2A (5-HT(2A)) receptors. Although LSD interacts with other receptors, the activation of 5-HT(2A) receptors is thought to mediate the hallucinogenic properties of LSD. The goal of this study was to identify the brai…
    Hazardous Substances Data Bank (HSDB)PMID 12220572Gresch PJ; Neuroscience 114 (3): 707-13 (2002)
  • ... The indoleamine hallucinogen D-lysergic acid diethylamide (LSD, which binds to 5-HT1A, 1B, 1D, 1E, 1F, 2A, 2C, 5, 6, 7, dopamine D1 and D2, and alpha1 and alpha2 adrenergic receptors), but not their non-hallucinogenic congeners, inhibited N-methyl-D-aspartate (NMDA)-induced inward current and NMDA receptor-mediated synaptic responses…
    Hazardous Substances Data Bank (HSDB)PMID 10510170Arvanov VL et al; Eur J Neurosci 11 (9): 3064-72 (1999)

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.

Affect0Mood4Perception9Cognition3Thought process0Thought content0Psychomotor activity1Insight and judgment0
This measures the literature, not the compound. Each spoke counts how many of the 23 records this archive holds for this compound say something under that domain — 9 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 4
matched on “depressed”, “elation”, “mood” · in PMID 12220572; PMID 10510170; PMID 4162426; PMID 28940312
Perception 9
matched on “hallucinat”, “hallucinogen”, “perceptu”, “synesthes” · in PMID 11557170; PMID 17270739; PMID 12220572; PMID 10510170; Toxicology: Hazardous Substances Data Bank (HSDB); Toxicology: StatPearls; Toxicology: Toxin and Toxin Target Database (T3DB); PMID 4162426; PMID 28940312
Cognition 3
matched on “cognitiv”, “concentrat” · in PMID 10510170; PMID 14209776; Toxicology: Hazardous Substances Data Bank (HSDB)
Psychomotor activity 1
matched on “hyperactiv” · in PMID 11557170

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, ADRB1, HTR1Acerebellum — 5.8 nTPM, from ADRA2A, HTR5A, DRD4hippocampal formation — 6.1 nTPM, from HTR1A, ADRB1, HTR2Aamygdala — 3.7 nTPM, from ADRB1, HTR2A, DRD2hypothalamus — 12.6 nTPM, from HTR2C, DRD2, ADRA2Athalamus — no resolved target expressed herebasal ganglia — 62.0 nTPM, from DRD2, HTR2C, DRD1medulla 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 56.6, midbrain 23.4, retina 10.8, spinal cord 2.2.

Body

heart — 20.3 nTPM, from ADRB1, ADRA1A, ADRB2smooth muscle — 15.7 nTPM, from HTR2B, ADRB2, ADRA1Alung — 18.4 nTPM, from ADRB2, ADRB1, ADRA2Aliver — 56.2 nTPM, from ADRA1A, ADRB2, HTR2Bkidney — 6.3 nTPM, from ADRA2A, HTR2B, ADRB2stomach — 7.1 nTPM, from ADRB2, HTR1B, HTR2Bduodenum — 9.4 nTPM, from ADRA2A, HTR1D, HTR4small intestine — 8.5 nTPM, from HTR4, HTR1D, HTR2Bcolon — 8.5 nTPM, from HTR2B, ADRA2A, ADRB2adrenal gland — 17.2 nTPM, from HTR2B, SLC6A2, DRD2thyroid gland — 8.7 nTPM, from ADRA2A, HTR2B, ADRB2pancreas — 28.8 nTPM, from ADRA2A, DRD4, ADRB1urinary bladder — 14.8 nTPM, from ADRA2A, ADRB2, HTR7skeletal muscle — 10.9 nTPM, from ADRB2, ADRB1, ADRA2Aspleen — 13.1 nTPM, from ADRA2A, ADRA1A, ADRB2salivary gland — 11.3 nTPM, from DRD2, ADRB2, ADRA2A
062 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

    62.0 nTPM

  2. pituitary gland

    56.6 nTPM

  3. midbrain

    23.4 nTPM

  4. cerebral cortex

    18.2 nTPM

  5. hypothalamus

    12.6 nTPM

  6. retina

    10.8 nTPM

  7. hippocampal formation

    6.1 nTPM

  8. cerebellum

    5.8 nTPM

  9. amygdala

    3.7 nTPM

  10. spinal cord

    2.2 nTPM

Peripheral & autonomic

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

  1. liver

    56.2 nTPM

  2. pancreas

    28.8 nTPM

  3. heart muscle

    20.3 nTPM

  4. lung

    18.4 nTPM

  5. adrenal gland

    17.2 nTPM

  6. smooth muscle

    15.7 nTPM

  7. urinary bladder

    14.8 nTPM

  8. spleen

    13.1 nTPM

  9. salivary gland

    11.3 nTPM

  10. skeletal muscle

    10.9 nTPM

  11. duodenum

    9.4 nTPM

  12. thyroid gland

    8.7 nTPM

  13. small intestine

    8.5 nTPM

  14. colon

    8.5 nTPM

  15. stomach 1

    7.1 nTPM

  16. kidney

    6.3 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.

2 of this compound’s targets could not be resolved to a gene and are absent from both columns: 5-HT2, 5-HT5B.

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

5-HT1A — Ki 9.51 pX5-HT7 — Ki 9.40 pX5-HT2A — Ki 9.32 pX5-HT2B — Ki 9.01 pX5-HT2C — Ki 8.96 pX5-HT6 — Ki 8.90 pX5-HT2 — Ki 8.60 pX5-HT5B — Ki 8.49 pX5-HT1B — Ki 8.41 pX5-HT1D — Ki 8.41 pX5-HT5A — Ki 8.05 pX5-HT1E — Ki 7.03 pX5-HT4 — Ki 6.00 pXD2 — Ki 7.70 pXD3 — Ki 7.57 pXD1 — Ki 7.52 pXD4 — Ki 7.25 pXD5 — Ki 6.47 pXAlpha2A — Ki 7.92 pXBeta1 — Ki 6.85 pXAlpha1A — Ki 6.17 pXBeta2 — Ki 6.13 pXNET — Ki 5.25 pX5-HT1A5-HT75-HT2A5-HT2B5-HT2C5-HT65-HT25-HT5B5-HT1B5-HT1D5-HT5A5-HT1E5-HT4D2D3D1D4D5Alpha2ABeta1Alpha1ABeta2NET579
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 LSD in this archive.

Lethal-dose values — animal studies

These are not human doses. An LD50 is the dose killing half of a group of animals of one species by one route, and it is a poor predictor of human risk for these compounds. Each value is printed whole, with the species and route it was measured in, because a lethal dose separated from those two facts is worse than no figure at all. Nothing here supports inferring a safe dose for anyone.

  • LD50 Guinea pig sc 16 mg/kg

    Hazardous Substances Data Bank (HSDB)Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 1276

  • LD50 Rabbit iv 300 mg/kg

    Hazardous Substances Data Bank (HSDB)Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 1276

  • LD50 Mouse iv 46 mg/kg

    Hazardous Substances Data Bank (HSDB)Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 1276

  • LD50 Mouse ip 50 mg/kg

    Hazardous Substances Data Bank (HSDB)Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 1276

  • LD50 Rat iv 16 mg/kg

    Hazardous Substances Data Bank (HSDB)Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 1276

As published

Quoted verbatim from the database named after each passage, never summarized — a summary of a toxicology statement is a new claim.

Toxicity Summary

  • IDENTIFICATION AND USE: LSD is a colorless, odorless and tasteless solid. It is a Schedule I controlled substance. It is used in biochemical research as antagonist to serotonin. LSD has been used experimentally as adjunct in study and treatment of mental disorders. HUMAN STUDIES: LSD has significant cardiovascular effects owing to its sympathomimetic actions. Tachycardia, hypertension, arrhythmias, shock, and respira…

    Hazardous Substances Data Bank (HSDB)

  • There is no evidence of organ damage or neuropsychological deficits, even at very high doses. Rarely, non-medical use may result in clinically distressing and persistent perceptual hallucinations, although they have not been observed in clinical research. The biggest concern is that dangerous and erratic behavior will result from intense subjective experiences with LSD.

    StatPearls

  • LSD preferentially inhibits serotonergic cell firing by acting as an agonist at the 5-HT1A receptors in the raphe nuclei, locus coeruleus, and cortex. It also acts as a partial agonist on the postsynaptic 5-HT1A site and has high affinity for the other 5-HT1 subtypes 5-HT1B, 5-HT1D, and 5-HT1E. LSD's hallucinogenic effects are caused by its ability to act as a partial agonist at the 5-HT2A receptor, especially on neo…

    Toxin and Toxin Target Database (T3DB)

Human Toxicity Excerpts

  • /HUMAN EXPOSURE STUDIES/ In human volunteers, 198 trials were made to determine the threshold dose for recognition of lysergic acid diethylamide (LSD-25) and the effect upon this of chlorpromazine and phenoxybenzamine. The threshold dose of LSD was determined to be 20 ug or 0.260 to 0.295 ug/kg. Chlorpromazine, in a dose of 25 mg., given 30 min beforehand or phenoxybenzamine, in a 10 mg. dose, given at the same time…

    Hazardous Substances Data Bank (HSDB)PMID 14477403Murphree HB; Clin Pharmacol Ther 3: 314-20 (1962)

  • /HUMAN EXPOSURE STUDIES/ Thirty-six LSD doses of 0.08-0.73 ug/kg (6-40 ug total dose) were administered orally to humans either just prior to sleep or 1 hr after onset of sleep. All night EEGs and EOGs were recorded on control nights, on nights when LSD was administered, and frequently on nights following those in which the drug was given ...On 21 nights following administration of LSD a prolongation of either the fi…

    Hazardous Substances Data Bank (HSDB)PMID 4162426Muzio JN et al; Electroencephalogr Clin Neurophysiol 21 (4): 313-24 (1966)

  • /HUMAN EXPOSURE STUDIES/ It has been proposed that the thalamocortical system is an important site of action of hallucinogenic drugs and an essential component of the neural correlates of consciousness. Hallucinogenic drugs such as LSD can be used to induce profoundly altered states of consciousness, and it is thus of interest to test the effects of these drugs on this system. 100 ug LSD was administrated orally to 2…

    Hazardous Substances Data Bank (HSDB)PMID 28940312Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5698745

  • /HUMAN EXPOSURE STUDIES/ Recent evidence shows that the serotonin 2A receptor (5-hydroxytryptamine2A receptor, 5-HT2AR) is critically involved in the formation of visual hallucinations and cognitive impairments in lysergic acid diethylamide (LSD)-induced states and neuropsychiatric diseases. However, the interaction between 5-HT2AR activation, cognitive impairments and visual hallucinations is still poorly understood…

    Hazardous Substances Data Bank (HSDB)Schmidt A et al; Psychol Med 2: 1-13 (2017)

  • For more Human Toxicity Excerpts (Complete) data for LSD (48 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 169

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

TargetClassTypeValue (nM)pXOrganismAssay
5-HT1ASerotonin receptorsKi0.3109.51BOVINEPDSP
5-HT7Serotonin receptorsKi0.3989.40GUINEA PIGPMID 10051134
5-HT1ASerotonin receptorsKi0.4309.37RATPDSP
5-HT2ASerotonin receptorsKi0.4759.32HUMANPMID 24488404
5-HT1ASerotonin receptorsKi0.6409.19HUMANPDSP
5-HT2ASerotonin receptorsKi0.7109.15HUMANPMID 24488404
5-HT2ASerotonin receptorsKi0.7209.14HUMANPMID 24488404
5-HT2ASerotonin receptorsKi0.7599.12HUMANPMID 15322733
5-HT2ASerotonin receptorsKi0.9509.02HUMANPDSP
5-HT2BSerotonin receptorsKi0.9779.01HUMANPMID 15322733
5-HT2ASerotonin receptorsKi0.9809.01RATPDSP
5-HT1ASerotonin receptorsKi1.098.96HUMANPMID 7984267
5-HT2CSerotonin receptorsKi1.108.96HUMANPMID 15322733
5-HT1ASerotonin receptorsKi1.108.96Homo sapiensCHEMBL616134
5-HT1ASerotonin receptorsKi1.108.96Homo sapiensCHEMBL615775
5-HT1ASerotonin receptorsKi1.108.96HUMANPMID 12213075
5-HT1ASerotonin receptorsKi1.208.92RATPDSP
5-HT6Serotonin receptorsKi1.268.90RATPMID 7696602
5-HT2ASerotonin receptorsKi1.358.87RATPDSP
5-HT1ASerotonin receptorsKi1.508.82HUMANPMID 28720478
UncheckedUnclassifiedKi1.508.82— organism not recordedCHEMBL1013930
5-HT2ASerotonin receptorsKi1.808.74RATPDSP
5-HT6Serotonin receptorsKi1.868.73RATPMID 9225298
5-HT7Serotonin receptorsKi2.008.70Rattus norvegicusCHEMBL620750
5-HT1ASerotonin receptorsKi2.058.69RATPDSP
5-HT2ASerotonin receptorsKi2.118.68RATPDSP
5-HT6Serotonin receptorsKi2.298.64HUMANPMID 14645659
5-HT2ASerotonin receptorsKi2.408.62RATPDSP
5-HT2ASerotonin receptorsKi2.408.62RATPDSP
5-HT2ASerotonin receptorsKi2.408.62RATPDSP
5-HT2Serotonin receptorsKi2.508.60Rattus norvegicusCHEMBL617138
5-HT2ASerotonin receptorsKi2.508.60RATPDSP
5-HT2ASerotonin receptorsKi2.568.59HUMANPDSP
5-HT1ASerotonin receptorsKi2.578.59PIGPDSP
5-HT1ASerotonin receptorsKi2.578.59PIGPDSP
5-HT6Serotonin receptorsKi2.638.58RATPMID 14645659
5-HT2ASerotonin receptorsKi2.708.57HUMANPMID 10611640
5-HT2ASerotonin receptorsKi2.778.56RATPDSP
5-HT1ASerotonin receptorsKi2.788.56HUMANPMID 24488404
5-HT2CSerotonin receptorsKi2.808.55RATPMID 10611640
5-HT6Serotonin receptorsKi2.828.55MOUSEPMID 14645659
5-HT2ASerotonin receptorsKi2.918.54RATPDSP
5-HT2CSerotonin receptorsKi2.918.54HUMANPMID 24488404
5-HT2ASerotonin receptorsKi2.928.53RATPDSP
5-HT1ASerotonin receptorsKi3.008.52HUMANPMID 26318099
5-HT5BSerotonin receptorsKi3.208.49RATPMID 8224165
5-HT5BSerotonin receptorsKi3.238.49RATPMID 7984267
5-HT2ASerotonin receptorsKi3.508.46Rattus norvegicusCHEMBL617926
5-HT2ASerotonin receptorsKi3.508.46RATPMID 2795135
5-HT2ASerotonin receptorsKi3.508.46Rattus norvegicusCHEMBL871423
5-HT2ASerotonin receptorsKi3.508.46Rattus norvegicusCHEMBL872922
5-HT2ASerotonin receptorsKi3.508.46RATPMID 12213075
5-HT2BSerotonin receptorsKi3.728.43HUMANPMID 23519215
5-HT2ASerotonin receptorsKi3.808.42BOVINEPDSP
5-HT2CSerotonin receptorsKi3.808.42Rattus norvegicusCHEMBL616833
5-HT2CSerotonin receptorsKi3.808.42PIGPDSP
5-HT1ASerotonin receptorsKi3.908.41RATPDSP
5-HT1BSerotonin receptorsKi3.908.41RATPMID 12213075
5-HT1DSerotonin receptorsKi3.908.41Homo sapiensCHEMBL617312
5-HT1ASerotonin receptorsKi4.108.39RATPDSP
5-HT2ASerotonin receptorsKi4.208.38HUMANPMID 26318099
5-HT2ASerotonin receptorsKi4.408.36Rattus norvegicusCHEMBL621536
5-HT2ASerotonin receptorsKi4.408.36Rattus norvegicusCHEMBL618896
5-HT2ASerotonin receptorsKi4.768.32RATPDSP
5-HT1ASerotonin receptorsKi4.928.31HUMANPDSP
5-HT2CSerotonin receptorsKi5.008.30PIGPDSP
5-HT2CSerotonin receptorsKi5.018.30PIGPDSP
5-HT1ASerotonin receptorsKi5.108.29Rattus norvegicusCHEMBL616418
5-HT1ASerotonin receptorsKi5.108.29Rattus norvegicusCHEMBL616090
5-HT2ASerotonin receptorsKi5.208.28HUMANPMID 10611640
5-HT2ASerotonin receptorsKi5.308.28HUMANPMID 28720478
5-HT2CSerotonin receptorsKi5.508.26RATPMID 12213075
5-HT2CSerotonin receptorsKi5.508.26Rattus norvegicusCHEMBL621525
5-HT2CSerotonin receptorsKi5.508.26Rattus norvegicusCHEMBL621513
5-HT2CSerotonin receptorsKi5.508.26Rattus norvegicusCHEMBL871424
5-HT2CSerotonin receptorsKi6.208.21MOUSEPDSP
5-HT2CSerotonin receptorsKi6.318.20PIGPDSP
5-HT1DSerotonin receptorsKi6.318.20CALFPDSP
5-HT2ASerotonin receptorsKi6.318.20Rattus norvegicusCHEMBL615616
5-HT7Serotonin receptorsKi6.318.20Homo sapiensCHEMBL618164
5-HT1BSerotonin receptorsKi6.608.18RATPDSP
5-HT7Serotonin receptorsKi6.608.18Homo sapiensCHEMBL619865
5-HT7Serotonin receptorsKi6.608.18RATPMID 12213075
5-HT6Serotonin receptorsKi6.908.16RATPMID 12213075
5-HT6Serotonin receptorsKi6.908.16Homo sapiensCHEMBL620810
5-HT2CSerotonin receptorsKi7.008.15RATPMID 10611640
5-HT2ASerotonin receptorsKi7.078.15RATPMID 7984267
5-HT1DSerotonin receptorsKi7.088.15CALFPDSP
5-HT1DSerotonin receptorsKi7.088.15COWPDSP
5-HT1ASerotonin receptorsKi7.308.14HUMANPMID 20126400
5-HT1DSerotonin receptorsKi7.708.11RATPDSP
5-HT2CSerotonin receptorsKi7.908.10PIGPDSP
5-HT2CSerotonin receptorsKi7.908.10PIGPDSP
5-HT2CSerotonin receptorsKi7.948.10PIGPDSP
5-HT2CSerotonin receptorsKi7.948.10PIGPDSP
5-HT2CSerotonin receptorsKi7.948.10PIGPDSP
5-HT7Serotonin receptorsKi7.948.10RATPMID 10051134
5-HT2BSerotonin receptorsKi8.918.05HUMANPMID 10498829
5-HT5ASerotonin receptorsKi9.008.05RATPMID 12213075
5-HT5ASerotonin receptorsKi9.008.05Homo sapiensCHEMBL618087
5-HT7Serotonin receptorsKi9.508.02RATPMID 8397408
5-HT7Serotonin receptorsKi9.508.02MammalianPMID 7696602
5-HT7Serotonin receptorsKi9.548.02RATPMID 7984267
5-HT7Serotonin receptorsKi9.558.02Rattus norvegicusCHEMBL620766
5-HT1DSerotonin receptorsKi10.008.00RATPDSP
5-HT7Serotonin receptorsKi10.008.00RATPMID 9149537
5-HT2BSerotonin receptorsKi11.007.96BOVINEPMID 2795135
5-HT2CSerotonin receptorsKi11.707.93PIGPDSP
5-HT2CSerotonin receptorsKi11.707.93PIGPDSP
5-HT2CSerotonin receptorsKi11.707.93PIGPDSP
Alpha2AAdrenergic receptorsKi12.007.92HUMANPMID 26318099
5-HT2ASerotonin receptorsKi12.027.92RATPMID 7984267
5-HT1DSerotonin receptorsKi12.587.90DogPMID 7984267
5-HT2CSerotonin receptorsKi12.607.90PIGPDSP
5-HT2ASerotonin receptorsKi13.007.89RATPDSP
5-HT1DSerotonin receptorsKi14.007.85HUMANPDSP
5-HT2CSerotonin receptorsKi14.007.85HUMANPMID 28720478
5-HT2CSerotonin receptorsKi15.007.82HUMANPMID 26318099
5-HT7Serotonin receptorsKi15.487.81GUINEA PIGPMID 7647964
5-HT7Serotonin receptorsKi15.857.80GUINEA PIGPMID 9149537
5-HT6Serotonin receptorsKi16.597.78RATPMID 9225298
D2Dopamine receptorsKi20.007.70CALFPMID 995128
5-HT2ASerotonin receptorsKi21.387.67HUMANPMID 10498829
5-HT1DSerotonin receptorsKi24.007.62BOVINEPDSP
D2Dopamine receptorsKi25.007.60HUMANPMID 26318099
D3Dopamine receptorsKi27.007.57RATPMID 12213075
D3Dopamine receptorsKi27.007.57Homo sapiensCHEMBL673836
D3Dopamine receptorsKi27.107.57HUMANPMID 24488404
5-HT1DSerotonin receptorsKi28.977.54COWPDSP
5-HT2BSerotonin receptorsKi30.007.52Homo sapiensCHEMBL617645
5-HT2BSerotonin receptorsKi30.007.52RATPMID 12213075
D1Dopamine receptorsKi30.007.52CALFPMID 995128
5-HT7Serotonin receptorsKi30.907.51GUINEA PIGPMID 7647964
D2Dopamine receptorsKi38.807.41HUMANPMID 24488404
5-HT1BSerotonin receptorsKi39.007.41RATPDSP
5-HT2CSerotonin receptorsKi45.717.34HUMANPMID 10498829
D4Dopamine receptorsKi56.007.25Homo sapiensCHEMBL671609
D4Dopamine receptorsKi56.007.25RATPMID 12213075
5-HT1ESerotonin receptorsKi93.007.03Homo sapiensCHEMBL616716
5-HT1ESerotonin receptorsKi93.007.03RATPMID 12213075
D3Dopamine receptorsKi96.007.02HUMANPMID 26318099
D2Dopamine receptorsKi1206.92Homo sapiensCHEMBL670786
D2Dopamine receptorsKi1206.92RATPMID 12213075
Beta1Adrenergic receptorsKi1406.85Homo sapiensCHEMBL647767
Beta1Adrenergic receptorsKi1406.85RATPMID 12213075
5-HT1BSerotonin receptorsKi1516.82RATPDSP
5-HT1BSerotonin receptorsKi1516.82RATPDSP
5-HT1BSerotonin receptorsKi1706.77RATPDSP
D1Dopamine receptorsKi1806.74RATPMID 12213075
D1Dopamine receptorsKi1806.74Mus musculusCHEMBL668649
5-HT7Serotonin receptorsKi2006.70RATPMID 7984267
D1Dopamine receptorsKi2736.56HUMANPMID 24488404
D1Dopamine receptorsKi3106.51HUMANPMID 26318099
D4Dopamine receptorsKi3306.48HUMANPMID 24488404
D5Dopamine receptorsKi3406.47Homo sapiensCHEMBL675958
D5Dopamine receptorsKi3406.47RATPMID 12213075
5-HT2ASerotonin receptorsKi5286.28RATPDSP
Alpha1AAdrenergic receptorsKi6706.17HUMANPMID 26318099
Beta2Adrenergic receptorsKi7406.13Homo sapiensCHEMBL652495
Beta2Adrenergic receptorsKi7406.13RATPMID 12213075
5-HT4Serotonin receptorsKi1,0006.00RATPMID 7796807
H1UnclassifiedKi1,1005.96HUMANPMID 26318099
H1UnclassifiedKi1,3005.89RATPMID 282646
H1UnclassifiedKi1,5405.81RATPMID 12213075
H1UnclassifiedKi1,5405.81Homo sapiensCHEMBL694564
5-HT2ASerotonin receptorsKi4,0835.39RATPDSP
5-HT2ASerotonin receptorsKi5,0005.30BOVINEPDSP
5-HT2ASerotonin receptorsKi5,3005.28RATPDSP
NETMonoamine transportersKi5,6005.25HUMANPMID 24488404

Functional readouts 1

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

TargetClassTypeValue (nM)pXOrganismAssay
5-HT2ASerotonin receptorsEC509.808.01Rattus 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.

35T

Registered studies

11T

Open or ongoing

32T

With a phase recorded

By phase

A study may carry two phase codes at once, so these count studies bearing each phase and do not sum to the total.

  • Early phase 18
  • Phase 113
  • Phase 28
  • Not applicable4

By status

The registry’s own status for each record. Withdrawn and terminated studies are counted here rather than hidden — a stopped trial is part of what is known.

  • Completed23
  • Recruiting6
  • Not yet recruiting3
  • Active, not recruiting2
  • Unknown status1

The 25 most recently started, of 35

Newest first by start date. Each identifier opens the registry record it came from; the title is the sponsor’s own, quoted.

  • NCT07503002Not yet recruiting · Phase 1

    Shortened LSD Intervention for Major Depressive Disorder

    Enrollment
    10Testimated
    Started
    2026-10-01
    Sponsor
    Johns Hopkins University

    Conditions Major Depression Moderate · Major Depression Severe · Major Depression

    Matched “LSD” in the study’s intervention “LSD”

  • NCT07490405Not yet recruiting

    Long-term Efficacy and Safety of LSD Versus TIPS for Cirrhotic Portal Hypertension Bleeding and Hypersplenism

    Enrollment
    140Testimated
    Started
    2026-06-01
    Sponsor
    Northern Jiangsu People's Hospital

    Conditions Liver Cirrhosis

    Matched “LSD” in the study’s intervention “LSD”

  • NCT07309471Recruiting · Not applicable

    Pharmacokinetics of Didehydro-LSD (DDH-LSD) Compared With LSD

    Enrollment
    24Testimated
    Started
    2026-03-06
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions LSD Reaction

    Matched “LSD” in the study’s intervention “DDH-LSD”

  • NCT05474989Recruiting · Phase 2

    LSD Treatment for Persons With Alcohol Use Disorder

    Enrollment
    128Testimated
    Started
    2026-01-27
    Sponsor
    Felix Mueller

    Conditions Alcohol Use Disorder (AUD)

    Matched “LSD” in the study’s intervention “LSD”

  • NCT07189299Not yet recruiting · Not applicable

    Microdosing LSD in Women With Premenstrual Disorders

    Enrollment
    150Testimated
    Started
    2025-10-01
    Sponsor
    Friederike Holze

    Conditions PMS · PMDD

    Matched “LSD” in the study’s intervention “LSD 10 μg every Day”

  • NCT07061886Completed · Early phase 1

    Drug Effects on Mood and Behavior - Expectancy

    Enrollment
    42Tactual
    Started
    2025-06-26
    Sponsor
    University of Chicago

    Conditions LSD

    Matched “LSD” in the study’s intervention “LSD”

  • NCT07017478Completed · Early phase 1

    Mood Effects of Serotonin Agonists: Depression

    Enrollment
    41Tactual
    Started
    2025-06-09
    Sponsor
    University of Chicago

    Conditions LSD · Major Depressive Disorder · Depression

    Matched “LSD” in the study’s intervention “LSD”

  • NCT05477459Recruiting · Phase 2

    LSD to Improve Cluster Headache Impact Trial

    Enrollment
    65Testimated
    Started
    2025-04-16
    Sponsor
    Radboud University Medical Center

    Conditions Chronic Cluster Headache

    Matched “LSD” in the study’s intervention “LSD tartrate”

  • NCT06899334Recruiting · Phase 1

    Direct Comparison of Altered States of Consciousness Induced by LSD, Psilocybin, and DMT in Healthy Participants

    Enrollment
    24Testimated
    Started
    2025-04-01
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions Healthy

    Matched “LSD” in the study’s intervention “LSD”

  • NCT06557239Completed

    Salivary Oxytocin as a Biomarker in Psychedelic Assisted Psychotherapy

    Enrollment
    10Tactual
    Started
    2024-08-05
    Sponsor
    Tatiana Aboulafia Brakha

    Conditions Depression, Anxiety

    Matched “(+)-Lysergic acid diethylamide” in the study’s intervention “Lysergic Acid Diethylamide (LSD)”

  • NCT05883540Recruiting · Phase 2

    Lysergic Acid Diethylamide (LSD) in Palliative Care

    Enrollment
    60Testimated
    Started
    2024-06-09
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions Palliative Care · Pain · Anxiety · Depression · Demoralization · Psychological Distress and 4 more

    Matched “(+)-Lysergic acid diethylamide” in the study’s intervention “Lysergic Acid Diethylamide Tartrate”

  • NCT05976698Completed · Not applicable

    LSD-Perceptual-Choice-Study

    Enrollment
    30Tactual
    Started
    2024-02-26
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions LSD Reaction

    Matched “LSD” in the study’s intervention “LSD 10 μg”

  • NCT05964647Completed · Phase 1

    Effect of Ketanserin, Olanzapine, and Lorazepam After LSD Administration on the Acute Response to LSD in Healthy Subjects

    Enrollment
    20Tactual
    Started
    2024-02-01
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions Healthy

    Matched “LSD” in the study’s intervention “LSD (150 µg) + ketanserin (40 mg)”

  • NCT05953038Active, not recruiting · Early phase 1

    LSD Occupancy of the Serotonin 2A Receptor in the Human Brain

    Enrollment
    40Testimated
    Started
    2023-11-08
    Sponsor
    Rigshospitalet, Denmark

    Conditions Basic Science

    Matched “(+)-Lysergic acid diethylamide” in the study’s intervention “Lysergic Acid Diethylamide Tartrate”

  • NCT05670184Unknown status · Phase 1 / Phase 2

    The Effect of LSD on Neural Synchrony, Prosocial Behavior, and Relationship Quality

    Enrollment
    60Testimated
    Started
    2023-01-01
    Sponsor
    Maastricht University

    Conditions Prosocial Behavior

    Matched “LSD” in the study’s intervention “LSD”

  • NCT05175430Completed · Phase 1

    Effects of SERT Inhibition on the Subjective Response to LSD in Healthy Subjects

    Enrollment
    24Tactual
    Started
    2022-10-24
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions Healthy

    Matched “(+)-Lysergic acid diethylamide” in the study’s intervention “Lysergic Acid Diethylamide”

  • NCT05177419Completed · Phase 1

    Effects of LSD on Neuroplasticity in Healthy Subjects

    Enrollment
    45Tactual
    Started
    2022-05-02
    Sponsor
    University of Fribourg

    Conditions Healthy

    Matched “(+)-Lysergic acid diethylamide” in the study’s intervention “Lysergic Acid Diethylamide”

  • NCT04865653Completed · Phase 1

    LSD Base and LSD Tartrate Bioequivalence and Bioavailability in Healthy Subjects

    Enrollment
    20Tactual
    Started
    2022-03-17
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions Healthy

    Matched “(+)-Lysergic acid diethylamide” in the study’s intervention “Lysergic Acid Diethylamide Base oral drinking solution”

  • NCT04516902Completed · Phase 1

    Effects of MDMA Co-administration on the Response to LSD in Healthy Subjects

    Enrollment
    24Tactual
    Started
    2021-01-01
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions Healthy

    Matched “(+)-Lysergic acid diethylamide” in the study’s intervention “Lysergic Acid Diethylamide”

  • NCT04558294Completed · Phase 1

    Effect of Ketanserin After LSD Administration

    Enrollment
    24Tactual
    Started
    2020-10-16
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions Healthy

    Matched “(+)-Lysergic acid diethylamide” in the study’s intervention “Lysergic Acid Diethylamide”

  • NCT07164287Active, not recruiting

    Retrospective Observational Study of Intensity Effects in Psychedelic-assisted Treatment

    Enrollment
    376Testimated
    Started
    2020-06-01
    Sponsor
    University Hospital, Geneva

    Conditions Major Depressive Disorder (MDD) · Anxiety Disorders · Substance Use Disorder (SUD) · PTSD - Post Traumatic Stress Disorder

    Matched “(+)-Lysergic acid diethylamide” in the study’s intervention “Lysergic Acid Diethylamide (LSD) or psilocybin”

  • NCT04227756Completed · Phase 1

    Comparative Acute Effects of LSD, Psilocybin and Mescaline

    Enrollment
    32Tactual
    Started
    2020-05-19
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions Healthy

    Matched “LSD” in the study’s intervention “LSD”

  • NCT03866252Completed · Phase 2

    LSD Therapy for Persons Suffering From Major Depression

    Enrollment
    60Tactual
    Started
    2019-11-01
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions Major Depressive Disorder

    Matched “LSD” in the study’s intervention “LSD”

  • NCT03604744Completed · Early phase 1

    Direct Comparison of Altered States of Consciousness Induced by LSD and Psilocybin

    Enrollment
    28Tactual
    Started
    2019-03-27
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions Healthy

    Matched “LSD” in the study’s intervention “LSD”

  • NCT03781128Recruiting · Phase 2

    Lysergic Acid Diethylamide (LSD) as Treatment for Cluster Headache

    Enrollment
    30Testimated
    Started
    2019-01-02
    Sponsor
    University Hospital, Basel, Switzerland

    Conditions Cluster Headache

    Matched “(+)-Lysergic acid diethylamide” in the study’s intervention “Lysergic Acid Diethylamide”

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 (+)-Lysergic acid diethylamide · LYSERGIC ACID DIETHYLAMIDE · N,N-Diethyllysergamide. Run this search at the registry — it returns the unfiltered result, including studies this page rejected as belonging to a different molecule.

A registered trial is a protocol somebody filed with the registry. It is not a result, and nothing on this plate says whether LSD 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

    Lysergamides of isomeric 2,4-dimethylazetidines map the binding orientation of the diethylamide moiety in the potent hallucinogenic agent N,N-diethyllysergamide (LSD)

    Nichols DE, Frescas S, Marona-Lewicka D et al. · Journal of medicinal chemistry 2002

    • · 17 measurements at 17 targets (Ki), strongest 5-HT1A at 8.96 pX

    PMID 12213075

  2. 02

    Mefloquine and psychotomimetics share neurotransmitter receptor and transporter interactions in vitro

    Janowsky A, Eshleman AJ, Johnson RA et al. · Psychopharmacology 2014

    • · 10 measurements at 8 targets (Ki), strongest 5-HT2A at 9.32 pX

    PMID 24488404

  3. 03

    Receptor interaction profiles of novel N-2-methoxybenzyl (NBOMe) derivatives of 2,5-dimethoxy-substituted phenethylamines (2C drugs)

    Rickli A, Luethi D, Reinisch J et al. · Neuropharmacology 2015

    • · 9 measurements at 9 targets (Ki), strongest 5-HT1A at 8.52 pX

    PMID 26318099

  4. 04

    Molecular biology of 5-HT receptors

    Boess FG, Martin IL · Neuropharmacology 1994

    • · 7 measurements at 5 targets (Ki), strongest 5-HT1A at 8.96 pX

    PMID 7984267

  5. 05

    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 8.57 pX

    PMID 10611640

  6. 06

    Monoamine receptor interaction profiles of 4-thio-substituted phenethylamines (2C-T drugs)

    Luethi D, Trachsel D, Hoener MC et al. · Neuropharmacology 2018

    • · 3 measurements at 3 targets (Ki), strongest 5-HT1A at 8.82 pX

    PMID 28720478

  7. 07

    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 9.12 pX

    PMID 15322733

  8. 08

    Differences in the central nervous system distribution and pharmacology of the mouse 5-hydroxytryptamine-6 receptor compared with rat and human receptors investigated by radioligand binding, site-directed mutagenesis, and molecular modeling

    Hirst WD, Abrahamsen B, Blaney FE et al. · Molecular pharmacology 2003

    • · 3 measurements at 1 target (Ki), strongest 5-HT6 at 8.64 pX

    PMID 14645659

  9. 09

    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-HT2B at 8.05 pX

    PMID 10498829

  10. 10

    [3H]-Mesulergine labels 5-HT7 sites in rat brain and guinea-pig ileum but not rat jejunum

    Hemedah M, Coupar IM, Mitchelson FJ · British journal of pharmacology 1999

    • · 2 measurements at 1 target (Ki), strongest 5-HT7 at 9.40 pX

    PMID 10051134

  11. 11

    Functional and radioligand binding characterization of rat 5-HT6 receptors stably expressed in HEK293 cells

    Boess FG, Monsma FJ Jr, Carolo C et al. · Neuropharmacology 1997

    • · 2 measurements at 1 target (Ki), strongest 5-HT6 at 8.73 pX

    PMID 9225298

  12. 12

    The 5-HT7 receptor: orphan found

    Eglen RM, Jasper JR, Chang DJ et al. · Trends in pharmacological sciences 1997

    • · 2 measurements at 1 target (Ki), strongest 5-HT7 at 8.00 pX

    PMID 9149537

  13. 13

    Characterization and distribution of putative 5-ht7 receptors in guinea-pig brain

    To ZP, Bonhaus DW, Eglen RM et al. · British journal of pharmacology 1995

    • · 2 measurements at 1 target (Ki), strongest 5-HT7 at 7.81 pX

    PMID 7647964

  14. 14

    5-HT6 receptors positively coupled to adenylyl cyclase in striatal neurones in culture

    Sebben M, Ansanay H, Bockaert J et al. · Neuroreport 1994

    • · 2 measurements at 2 targets (Ki), strongest 5-HT6 at 8.90 pX

    PMID 7696602

  15. 15

    Differentiation of 5-hydroxytryptamine2 receptor subtypes using 125I-R-(-)2,5-dimethoxy-4-iodo-phenylisopropylamine and 3H-ketanserin

    McKenna DJ, Peroutka SJ · The Journal of neuroscience : the official journal of the Society for Neuroscience 1989

    • · 2 measurements at 2 targets (Ki), strongest 5-HT2A at 8.46 pX

    PMID 2795135

  16. 16

    Properties of [3H]haloperidol and [3H]dopamine binding associated with dopamine receptors in calf brain membranes

    Burt DR, Creese I, Snyder SH · Molecular pharmacology 1976

    • · 2 measurements at 2 targets (Ki), strongest D2 at 7.70 pX

    PMID 995128

  17. 17

    Structural features for functional selectivity at serotonin receptors

    Wacker D, Wang C, Katritch V et al. · Science (New York, N.Y.) 2013

    • · 1 measurement at 1 target (Ki), strongest 5-HT2B at 8.43 pX

    PMID 23519215

  18. 18

    Psychedelics and the human receptorome

    Ray TS · PloS one 2010

    • · 1 measurement at 1 target (Ki), strongest 5-HT1A at 8.14 pX

    PMID 20126400

  19. 19

    The 5-HT4 receptor: molecular cloning and pharmacological characterization of two splice variants

    Gerald C, Adham N, Kao HT et al. · The EMBO journal 1995

    • · 1 measurement at 1 target (Ki), strongest 5-HT4 at 6.00 pX

    PMID 7796807

  20. 20

    Cloning and characterization of the rat 5-HT5B receptor. Evidence that the 5-HT5B receptor couples to a G protein in mammalian cell membranes

    Wisden W, Parker EM, Mahle CD et al. · FEBS letters 1993

    • · 1 measurement at 1 target (Ki), strongest 5-HT5B at 8.49 pX

    PMID 8224165

  21. 21

    Molecular cloning, characterization, and localization of a high-affinity serotonin receptor (5-HT7) activating cAMP formation

    Ruat M, Traiffort E, Leurs R et al. · Proceedings of the National Academy of Sciences of the United States of America 1993

    • · 1 measurement at 1 target (Ki), strongest 5-HT7 at 8.02 pX

    PMID 8397408

  22. 22

    Histamine H1 receptors identified in mammalian brain membranes with [3H]mepyramine

    Tran VT, Chang RS, Snyder SH · Proceedings of the National Academy of Sciences of the United States of America 1978

    • · 1 measurement at 1 target (Ki), strongest H1 at 5.89 pX

    PMID 282646

  23. 23

    Comparative acute effects of mescaline, lysergic acid diethylamide, and psilocybin in a randomized, double-blind, placebo-controlled cross-over study in healthy participants

    Ley L, Holze F, Arikci D et al. · Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 2023

    • · 2 timed observations on the simulation plate

    PMID 37231080

  24. 24

    Acute dose-dependent effects of lysergic acid diethylamide in a double-blind placebo-controlled study in healthy subjects

    Holze F, Vizeli P, Ley L et al. · Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 2021

    • · 6.7 h to 11 h across 25–200 µg

    PMID 33059356

  25. 25

    Increased thalamic resting-state connectivity as a core driver of LSD-induced hallucinations

    Müller F, Lenz C, Dolder P et al. · Acta psychiatrica Scandinavica 2017

    • · Human Toxicity Excerpts

    PMID 28940312

  26. 26

    Pharmacokinetics and Pharmacodynamics of Lysergic Acid Diethylamide in Healthy Subjects

    Dolder PC, Schmid Y, Steuer AE et al. · Clinical pharmacokinetics 2017

    • · Duration of acute subjective effects
    • · Plasma elimination half-life

    PMID 28197931

  27. 27

    Hallucinogens recruit specific cortical 5-HT(2A) receptor-mediated signaling pathways to affect behavior

    González-Maeso J, Weisstaub NV, Zhou M et al. · Neuron 2007

    • · Mechanism of Action

    PMID 17270739

  28. 28

    Lysergic acid diethylamide-induced Fos expression in rat brain: role of serotonin-2A receptors

    Gresch PJ, Strickland LV, Sanders-Bush E · Neuroscience 2002

    • · Mechanism of Action

    PMID 12220572

  29. 29

    Effect of LSD on prepulse inhibition and spontaneous behavior in the rat. A pharmacological analysis and comparison between two rat strains

    Ouagazzal A, Grottick AJ, Moreau J et al. · Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 2001

    • · Mechanism of Action

    PMID 11557170

  30. 30

    LSD and DOB: interaction with 5-HT2A receptors to inhibit NMDA receptor-mediated transmission in the rat prefrontal cortex

    Arvanov VL, Liang X, Russo A et al. · The European journal of neuroscience 1999

    • · Mechanism of Action

    PMID 10510170

  31. 31

    Alterations in the nocturnal sleep cycle resulting from LSD

    Muzio JN, Roffwarg HP, Kaufman E · Electroencephalography and clinical neurophysiology 1966

    • · Human Toxicity Excerpts

    PMID 4162426

  32. 32

    PERSISTENCE OF LYSERGIC ACID DIETHYLAMIDE IN THE PLASMA OF HUMAN SUBJECTS

    AGHAJANIAN GK, BING OH · Clinical pharmacology and therapeutics 1964

    • · Biological Half-Life

    PMID 14209776

  33. 33

    Quantitative studies in humans on the antagonism of lysergic acid diethylamide by chlorpromazine and phenoxybenzamine

    MURPHREE HB · Clinical pharmacology and therapeutics 1962

    • · Human Toxicity Excerpts

    PMID 14477403