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
Ketamine was made in 1963 as a replacement for phencyclidine and was approved by the FDA in 1970 1. What it produces is not ordinary anesthesia: the record describes a cataleptic state — profound analgesia, unresponsiveness to command and amnesia, in a patient who may keep their eyes open, move their limbs involuntarily and breathe spontaneously — and it is this that the word dissociative names 2. The same passage that recommends it for patients at risk of hypotension or bronchospasm is matched by one recording what has limited it: vivid hallucinations, agitation and confusion, major abuse potential, and, with long-term use, inflammation of the bladder and urethra alongside a cholestatic liver injury that can resemble sclerosing cholangitis 2,3. A second indication appears here as emerging rather than settled — lower doses for depression, with trials launched on the strength of early reports 4. Its kinetics are fast and front-loaded: absorption is nearly complete but only 17% of a dose survives first-pass metabolism, distribution has a half-life of about two minutes, and the anesthetic phase of roughly forty-five minutes is ended as much by redistribution out of the brain as by conversion in the liver to norketamine, which is about a third as active 5,6,7. It is a Schedule III controlled substance 8.
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
Ketamine is a member of the class of cyclohexanones in which one of the hydrogens at position 2 is substituted by a 2-chlorophenyl group, while the other is substituted by a methylamino group. It has a role as an analgesic, a xenobiotic, an intravenous anaesthetic, a neurotoxin, a NMDA receptor antagonist and an environmental contaminant. It is a member of cyclohexanones, a secondary amino compound and a member of monochlorobenzenes. It is functionally related to a norketamine.
1cited by the summary above
Ketamine is an NMDA receptor antagonist with a potent anesthetic effect. It was developed in 1963 as a replacement for phencyclidine (PCP) by Calvin Stevens at Parke Davis Laboratories. It started being used for veterinary purposes in Belgium and in 1964 was proven that compared to PCP, it produced minor hallucinogenic effects and shorter psychotomimetic effects. It was FDA approved in 1970, and from there, it has been used as an anesthetic for children or patients undergoing minor surgeries but mainly for veterinary purposes.
Ketamine is a General Anesthetic. The physiologic effect of ketamine is by means of General Anesthesia.
3cited by the summary above
Ketamine is a parenterally administered, general anesthetic used largely for short term diagnostic and surgical procedures, but which has been limited in use because of its psychological side effects including vivid hallucinations, agitation and confusion. Ketamine also has major abuse potential and is used illicitly as a recreational drug. Long term ketamine use can cause inflammation and irritation to the urinary bladder and urethra, and similar changes have recently been described in the biliary tract, resulting in an acute or chronic cholestatic liver injury that can resemble sclerosing cholangitis.
Recognized use
Analgesics; Anesthetics, Dissociative; Excitatory Amino Acid Antagonists
Therapeutic Uses
Hazardous Substances Data Bank (HSDB)National Library of Medicine's Medical Subject Headings. Ketamine. Online file (MeSH, 2017). Available from, as of August 22, 2017: https://www.nlm.nih.gov/mesh/2017/mesh_browser/MBrowser.html
/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 August 22, 2017: https://clinicaltrials.gov/
2cited by the summary above
Ketamine has unique properties that make it useful for anesthetizing patients at risk for hypotension and bronchospasm and for certain pediatric procedures. However, significant side effects limit its routine use. Ketamine rapidly produces a hypnotic state quite distinct from that of other anesthetics. Patients have profound analgesia, unresponsiveness to commands, and amnesia, but may have their eyes open, move their limbs involuntarily, and breathe spontaneously. This cataleptic state has been termed dissociative anesthesia. The administration of ketamine has been shown to reduce the development of tolerance to long-term opioid use. Low-dose ketamine infusion for this purpose has been advo…
Therapeutic Uses
Hazardous Substances Data Bank (HSDB)Brunton, L. Chabner, B, Knollman, B. Goodman and Gillman's The Pharmaceutical Basis of Therapeutics, Twelth Edition, McGraw Hill Medical, New York, NY. 2011, p. 538
Ketamine has been studied in over 12,000 operative and diagnostic procedures, involving over 10,000 patients from 105 separate studies. During the course of these studies ketamine hydrochloride was administered as the sole agent, as induction for other general agents, or to supplement low-potency agents. Specific areas of application have included the following: 1. Debridement, painful dressings, and skin grafting in burn patients, as well as other superficial surgical procedures. 2. Neurodiagnostic procedures such as pneumonencephalograms, ventriculograms, myelograms, and lumbar punctures. ... 3. Diagnostic and operative procedures of the eye, ear, nose and mouth, including dental extractio…
Therapeutic Uses
Hazardous Substances Data Bank (HSDB)NIH; DailyMed. Current Medication Information for Ketamine hydrochloride- ketamine hydrochloride injection (Updated: May 2017). Available from, as of August 23, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=58487c78-a641-4278-acc0-343596ee8683
4cited by the summary above
Ketamine is indicated as an anesthetic agent for recommended diagnostic and surgical procedures. If skeletal muscle relaxation is needed, it should be combined with a muscle relaxant. If the surgical procedure involves visceral pain, it should be supplemented with an agent that obtunds visceral pain. Ketamine can be used for induction of anesthesia prior other general anesthetic agents and as a supplement of low potency agents. Reports have indicated a potential use of ketamine as a therapeutic tool for the management of depression when administered in lower doses. These reports have increased the interest for ketamine in this area and several clinical trials are launched for this indicatio…
Drug Indication
Ketamine hydrochloride, commonly known as ketamine, is a medication approved by the United States Food and Drug Administration (FDA) for use as a general anesthetic either on its own or in combination with other medications.
Drug Indication
8cited by the summary above
Ketamine, its salts, isomers, and salts of isomers (DEA Code Number: 7285) is a Schedule III controlled substance.
Use Classification
Hazardous Substances Data Bank (HSDB)21 CFR 1308.13(c) (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 III Controlled Substance: (A) The drug or other substance has a potential for abuse less than the drugs or other substances in schedules I and II. (B) The drug or other substance has a currently accepted medical use in treatment in the United States. (C) Abuse of the drug or other substance may lead to moderate or low physical dependence or high psychological dependence.
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
Ketamine is primarily used for the induction and maintenance of general anesthesia, usually in combination with some sedative drug. Other uses include sedation in intensive care, analgesia (particularly in emergency medicine), and treatment of bronchospasm. It is also a popular anesthetic in veterinary medicine. [Wikipedia] For use as the sole anesthetic agent for diagnostic and surgical procedures that do not require skeletal muscle relaxation.
Use Classification
How it acts
Ketamine interacts with N-methyl-D-aspartate (NMDA) receptors, opioid receptors, monoaminergic receptors, muscarinic receptors and voltage sensitive Ca ion channels. Unlike other general anaesthetic agents, ketamine does not interact with GABA receptors.
Long-term ketamine abuse is known to affect the lower urinary tract and produce symptoms of cystitis. However, the pathophysiology and causative mechanism of the changes in bladder function remain unclear. The present study aimed to investigate the existence of ketamine-induced cystitis in a rat model and characterize the underlining mechanisms. Rats were assigned to blank control, normal saline (NS), low-dose ketamine (LK, 5 mg/kg), and high-dose ketamine (HK, 50 mg/kg) groups. The two experimental groups received ketamine hydrochloride daily for 16 weeks. All rats were housed individually for assessment of urinary frequency and urine volume. Urinary biomarkers were measured at different ti…
Hazardous Substances Data Bank (HSDB)PMID 25091940Gu D et al; Mol Biol Rep 41 (11): 7313-22 (2014)
Behavior carries the pharmacological classes and the acute-effect durations, with plasma half-life kept separate from duration of effect.
In the body
5cited by the summary above
Ketamine absorption is very rapid and the bioavailability is around 93%. After the first pass metabolism, only 17% of the administered dose is absorbed. It distributes very rapidly and presents a distribution half-life of 1.95 min. The Cmax levels at peak reach 0.75 mcg/ml in plasma and 0.2 mcg/ml in cerebrospinal fluid.
Absorption, Distribution and Excretion
Pharmacokinetic studies have resulted in the recovery of 85-95% of the administered dose in urine mainly in the form of metabolites. Some other routes of elimination of ketamine are bile and feces. When administered intravenously the resultant recovery is distributed by 91% of the administered dose in urine and 3% in feces.
Absorption, Distribution and Excretion
The apparent volume of distribution of the central compartment and at steady-state are 371.3 ml/kg and 4060.3 ml/kg, respectively.
Absorption, Distribution and Excretion
The clearance rate of ketamine is high and of around 95 L/h/70kg.
Absorption, Distribution and Excretion
7cited by the summary above
Ketamine presents a mainly hepatic metabolism and its major metabolite is norketamine. The biotransformation of ketamine corresponds to N-dealkylation, hydroxylation of the cyclohexone ring, conjugation to glucuronic acid and dehydration of the hydroxylated metabolites for the formation of cyclohexene derivatives.
Metabolism/Metabolites
Ketamine is hepatically metabolized to norketamine, which has reduced CNS activity; norketamine is further metabolized and excreted in urine and bile.
Metabolism/Metabolites
Hazardous Substances Data Bank (HSDB)Brunton, L. Chabner, B, Knollman, B. Goodman and Gillman's The Pharmaceutical Basis of Therapeutics, Twelth Edition, McGraw Hill Medical, New York, NY. 2011, p. 539
6cited by the summary above
The biotransformation of ketamine includes N-dealkylation (metabolite I), hydroxylation of the cyclohexone ring (metabolites III and IV), conjugation with glucuronic acid and dehydration of the hydroxylated metabolites to form the cyclohexene derivative (metabolite II). Following intravenous administration, the ketamine concentration has an initial slope (alpha phase) lasting about 45 minutes with a half-life of 10 to 15 minutes. This first phase corresponds clinically to the anesthetic effect of the drug. The anesthetic action is terminated by a combination of redistribution from the CNS to slower equilibrating peripheral tissues and by hepatic biotransformation to metabolite I. This metabo…
Metabolism/Metabolites
Hazardous Substances Data Bank (HSDB)NIH; DailyMed. Current Medication Information for Ketamine hydrochloride- ketamine hydrochloride injection (Updated: May 2017). Available from, as of August 23, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=58487c78-a641-4278-acc0-343596ee8683
The pharmacokinetics of ketamine-HCl in the cat was described by a 2-compartment open model. The n-dealkylated amine metabolite of ketamine-HCl was detected in plasma of all cats and peak levels which were 0.27 to 0.38 times ketamine-HCl level were reached between 5 and 20 min after injection.
Metabolism/Metabolites
Hazardous Substances Data Bank (HSDB)Heavner JE, Bloedow DC; Vet Anesth 6 (2): 16 (1979)
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 Ketamine 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 Ketamine 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.
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.
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 — 29 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 — listed by the DEA among its drugs of concern, with no schedule stated in the record held here.
- 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 Ketamine 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.
- Formula
- C13H16ClNOR
- Molecular weight
- 237.73g/molR
- Exact mass
- 237.0920DaR
- cLogP
- 2.90R
- TPSA
- 29.1ŲR
- H-bond donors
- 1R
- H-bond acceptors
- 2R
- Rotatable bonds
- 2R
- Aromatic rings
- 1R
- Heavy atoms
- 16R
- Fraction sp³
- 0.462R
- Formal charge
- 0R
Computed with RDKit 2025.09.2 from the SMILES returned by PubChem. Audit run 26/09/2026.
Bemis–Murcko scaffold
O=C1CCCCC1c1ccccc1
Shared with 2-Fluorodeschloroketamine, Blixeprodil, Bromoketamine, Deoxymethoxetamine, Deschloroketamine, Eticyclidone and 9 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.
1.5–5 h
“The half-life of ketamine in humans is between 1.5 and 5 h”
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.
Long-term ketamine abuse is known to affect the lower urinary tract and produce symptoms of cystitis. However, the pathophysiology and causative mechanism of the changes in bladder function remain unclear. The present study aimed to investigate the existence of ketamine-induced cystitis in a rat model and characterize the underlining mech…
Hazardous Substances Data Bank (HSDB)PMID 25091940Gu D et al; Mol Biol Rep 41 (11): 7313-22 (2014) Recreational abuse of ketamine has been associated with the emergence of a new bladder pain syndrome, ketamine-induced cystitis, characterized by chronic inflammation and urothelial ulceration. We investigated the direct effects of ketamine on normal human urothelium maintained in organ culture or as finite cell lines in vitro. Exposure o…
Hazardous Substances Data Bank (HSDB)PMID 27001627Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4861758 Several lines of evidence indicate that ketamine has a rapid antidepressant-like effect in rodents and humans, but underlying mechanisms are unclear. In the present study, we investigated the effect of ketamine on serotonin (5-HT) release in the rat prefrontal cortex by in vivo microdialysis. A subcutaneous administration of ketamine (5 a…
Hazardous Substances Data Bank (HSDB)PMID 24852262Nishitani N et al; Int J Neuropsychopharmacol 17 (8): 1321-6 (2014) Ketamine interacts with N-methyl-D-aspartate (NMDA) receptors, opioid receptors, monoaminergic receptors, muscarinic receptors and voltage sensitive Ca ion channels. Unlike other general anaesthetic agents, ketamine does not interact with GABA receptors.
DrugBank Ketamine is a rapid-acting general anesthetic producing an anesthetic state characterized by profound analgesia, normal pharyngeal-laryngeal reflexes, normal or slightly enhanced skeletal muscle tone, cardiovascular and respiratory stimulation, and occasionally a transient and minimal respiratory depression. The anesthetic state produced…
DrugBank
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 Anesthetics, Dissociative
- 6C4DDisorders due to use of dissociative drugs including ketamine and phencyclidine [PCP]
Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR): Phencyclidine-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.
- Mood 2
- matched on “depression” · in Pharmacology: Pharmacodynamics; Toxicology: Hazardous Substances Data Bank (HSDB)
- Perception 4
- matched on “hallucinat”, “hallucinogen”, “perceptu” · in Toxicology: Hazardous Substances Data Bank (HSDB); PMID 26361209; PMID 25142291; PMID 24223927
- Cognition 4
- matched on “concentrat”, “confus”, “disorient” · in PMID 27001627; Pharmacology: Pharmacodynamics; Toxicology: Hazardous Substances Data Bank (HSDB); PMID 25142291
- Thought content 1
- matched on “delusion” · in PMID 26361209
- Psychomotor activity 2
- matched on “sedat” · in Toxicology: StatPearls; PMID 25142291
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
basal ganglia: drawn as the caudate nucleus, putamen and globus pallidus.
Measured but not drawn — this anatomogram has no outline for them: retina 0.9, midbrain 0.6, pituitary gland 0.3, spinal cord 0.2.
Body
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.
cerebellum
4.4 nTPMbasal ganglia
3.8 nTPMcerebral cortex
2.7 nTPMhypothalamus
2.6 nTPMamygdala
1.9 nTPMretina
0.9 nTPMhippocampal formation
0.9 nTPMmidbrain
0.6 nTPMpituitary gland
0.3 nTPMspinal cord
0.2 nTPM
Peripheral & autonomic
Tissues outside the CNS expressing the same targets — where a compound's bodily effects become possible.
skeletal muscle
1.0 nTPMadrenal gland
0.8 nTPMthyroid gland
0.4 nTPMspleen
0.4 nTPMstomach 1
0.3 nTPMsalivary gland
0.3 nTPMsmooth muscle
0.2 nTPM- MOROPRM14.9 pX0.2
lung
0.2 nTPMliver
0.2 nTPM- MOROPRM14.9 pX0.2
kidney
0.2 nTPM- MOROPRM14.9 pX0.2
duodenum
0.2 nTPMsmall intestine
0.2 nTPMcolon
0.2 nTPMpancreas
0.2 nTPMheart muscle
0.1 nTPMurinary bladder
0.1 nTPM- MOROPRM14.9 pX0.1
Each row joins two published measurements and nothing else: the affinity this archive holds for the compound at that target, and the transcript level the Human Protein Atlas reports for that target’s gene in that region. Bars scale with expression only. Expression is not activation — a receptor transcribed in a region is a receptor available to be bound there, which is a weaker and more defensible claim than saying the region is affected.
1 of this compound’s targets could not be resolved to a gene and are absent from both columns: NMDA.
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 4 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.
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 Ketamine 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 Mouse ip 400 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. 2190
LD50 Mouse iv 77 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. 2190
LD50 Mouse ip 224 +/- 4 mg/kg
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. 982
LD50 Rat ip 229 +/- 5 mg/kg
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. 982
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: Ketamine is a cyclohexanone derivative used as an anesthetic agent in human and veterinary procedures. Ketamine hydrochloride injection, USP is indicated as the sole anesthetic agent for diagnostic and surgical procedures that do not require skeletal muscle relaxation. HUMAN STUDIES: Ketamine is a unique anesthetic because it has both hypnotic and analgesic effects and also potential hallucino…
Ketamine is potentially fatal in alcohol-intoxicated patients. It has been used recreationally as a drug of abuse. The street name for ketamine is "K" or "Special K." Illicit use of ketamine includes snorting or inhalation, and it is ingestable in food or drinks. The recreational use of ketamine can lead to toxicity. Ketamine overdose induces varying dose-dependent symptoms, notably altering consciousness and manifes…
Ketamine has several clinically useful properties, including analgesia and less cardiorespiratory depressant effects than other anaesthetic agents, it also causes some stimulation of the cardiocascular system. Ketamine has been reported to produce general as well as local anaesthesia. It interacts with N-methyl-D-aspartate (NMDA) receptors, opioid receptors, monoaminergic receptors, muscarinic receptors and voltage s…
Hepatotoxicity
Short term use of ketamine for anesthesia has been associated with rare instances of serum enzyme elevations, but not with clinically apparent liver injury. With chronic or intermittent use, however, unusual biliary and hepatic complications have been described. In a manner similar to its effects on the urinary tract, ketamine can also cause abnormalities in the biliary system with dilation and irregularity of the in…
Human Toxicity Excerpts
/HUMAN EXPOSURE STUDIES/ Ketamine, the NMDA glutamate receptor antagonist drug, is increasingly employed as an experimental model of psychosis in healthy volunteers. At subanesthetic doses, it safely and reversibly causes delusion-like ideas, amotivation and perceptual disruptions reminiscent of the aberrant salience experiences that characterize first-episode psychosis. However, auditory verbal hallucinations, a hal…
Hazardous Substances Data Bank (HSDB)PMID 26361209Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4684980
/HUMAN EXPOSURE STUDIES/ /The study objective was/ to assess the psychiatric side effects of ketamine when administered in subanesthetic doses to hospitalized patients. It is hypothesized that such effects occur frequently. In this retrospective study, the medical records of 50 patients hospitalized on medical and surgical units at our facility who had continuous intravenous infusions of ketamine for pain or mild sed…
Hazardous Substances Data Bank (HSDB)PMID 25142291Rasmussen KG; Acta Neuropsychiatr 26 (4): 230-3 (2014)
/HUMAN EXPOSURE STUDIES/ Recurrent interactions between neurons in the visual cortex are crucial for the integration of image elements into coherent objects, such as in figure-ground segregation of textured images. Blocking N-methyl-D-aspartate (NMDA) receptors in monkeys can abolish neural signals related to figure-ground segregation and feature integration. However, it is unknown whether this also affects perceptua…
Hazardous Substances Data Bank (HSDB)PMID 24223927Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3815103
/HUMAN EXPOSURE STUDIES/ Evidence suggests that some aspects of schizophrenia can be induced in healthy volunteers through acute administration of the non-competitive NMDA-receptor antagonist, ketamine. In probabilistic inference tasks, patients with schizophrenia have been shown to 'jump to conclusions' (JTC) when asked to make a decision. We aimed to test whether healthy participants receiving ketamine would adopt…
Hazardous Substances Data Bank (HSDB)PMID 22389244Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3546628
For more Human Toxicity Excerpts (Complete) data for Ketamine (29 total), please visit the HSDB record page.
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 21
Ki and Kd — a concentration at equilibrium. Directly comparable across rows at the same target.
| Target | Class | Type | Value (nM) | pX | Organism | Assay |
|---|---|---|---|---|---|---|
| NMDA | Glutamate receptors | Ki | 180 | 6.74 | Rattus norvegicus | CHEMBL4687770 |
| NMDA | Glutamate receptors | Ki | 180 | 6.74 | Rattus norvegicus | CHEMBL4687805 |
| NMDA | Glutamate receptors | Ki | 180 | 6.74 | Rattus norvegicus | CHEMBL4687798 |
| NMDA | Glutamate receptors | Ki | 180 | 6.74 | Rattus norvegicus | CHEMBL4687796 |
| NMDA | Glutamate receptors | Ki | 180 | 6.74 | Rattus norvegicus | CHEMBL4687795 |
| NMDA | Glutamate receptors | Ki | 180 | 6.74 | Rattus norvegicus | CHEMBL4687771 |
| NMDA | Glutamate receptors | Ki | 324 | 6.49 | RAT | PMID 31152702 |
| NMDA | Glutamate receptors | Ki | 324 | 6.49 | RAT | PMID 27314670 |
| NMDA | Glutamate receptors | Ki | 324 | 6.49 | RAT | PMID 28513099 |
| NMDA | Glutamate receptors | Ki | 324 | 6.49 | RAT | PMID 27314670 |
| NMDA | Glutamate receptors | Ki | 324 | 6.49 | RAT | PMID 27520396 |
| NMDA | Glutamate receptors | Ki | 420 | 6.38 | Homo sapiens | CHEMBL761030 |
| NMDA | Glutamate receptors | Ki | 659 | 6.18 | HUMAN | PMID 23527166 |
| NMDA | Glutamate receptors | Ki | 661 | 6.18 | RAT | PDSP |
| Unchecked | Unclassified | Ki | 684 | 6.16 | — organism not recorded | CHEMBL1909154 |
| NMDA | Glutamate receptors | Ki | 1,190 | 5.92 | RAT | PMID 7566488 |
| NMDA | Glutamate receptors | Ki | 1,900 | 5.72 | Homo sapiens | CHEMBL4401966 |
| NMDA | Glutamate receptors | Ki | 2,507 | 5.60 | RAT | PMID 7566488 |
| MOR | Opioid receptors | Ki | 11,482 | 4.94 | Homo sapiens | PMID 42332075 |
| KOR | Opioid receptors | Ki | 15,849 | 4.80 | Homo sapiens | PMID 42332075 |
| DOR | Opioid receptors | Ki | 131,826 | 3.88 | Homo sapiens | PMID 42332075 |
Functional readouts 8
IC₅₀, EC₅₀, AC₅₀ and potency. Assay-dependent, and not interchangeable with a binding constant.
| Target | Class | Type | Value (nM) | pX | Organism | Assay |
|---|---|---|---|---|---|---|
| NMDA | Glutamate receptors | IC50 | 610 | 6.21 | Rattus norvegicus | CHEMBL753124 |
| NMDA | Glutamate receptors | IC50 | 610 | 6.21 | Rattus norvegicus | CHEMBL749326 |
| NMDA | Glutamate receptors | IC50 | 700 | 6.15 | Rattus norvegicus | CHEMBL4401965 |
| Unchecked | Unclassified | IC50 | 1,010 | 6.00 | — organism not recorded | CHEMBL1909154 |
| NMDA | Glutamate receptors | IC50 | 10,000 | 5.00 | Rattus norvegicus | CHEMBL4687772 |
| MOR | Opioid receptors | EC50 | 11,749 | 4.93 | Homo sapiens | PMID 42332075 |
| KOR | Opioid receptors | EC50 | 33,884 | 4.47 | Homo sapiens | PMID 42332075 |
| DOR | Opioid receptors | EC50 | 229,087 | 3.64 | Homo sapiens | PMID 42332075 |
- 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.
812T
Registered studies
137T
Open or ongoing
773T
With a phase recorded
The registry returned more studies than this fetch retrieved, so the counts above are a floor rather than a total. Follow the registry link below for the full set.
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 138
- Phase 1103
- Phase 2188
- Phase 3111
- Phase 4226
- Not applicable177
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.
- Completed432
- Unknown status121
- Recruiting76
- Terminated73
- Withdrawn39
- Not yet recruiting35
- Active, not recruiting21
- Suspended10
- Enrolling by invitation5
The 25 most recently started, of 812
Newest first by start date. Each identifier opens the registry record it came from; the title is the sponsor’s own, quoted.
- NCT07728851Not yet recruiting · Phase 2
Nebulized Ketamine for Severe Asthma Attacks in Children
- Enrollment
- 60Testimated
- Started
- 2027-01-01
- Sponsor
- Sultan Qaboos University
Conditions Asthma Acute · Exacerbation of Allergic Asthma
Matched “Ketamine” in the study’s intervention “Ketamine (1 mg/kg)”
- NCT06419985Suspended · Phase 2
Ketamine HCl Prolonged Release Oral Tablets for CRPS
- Enrollment
- 65Testimated
- Started
- 2027-01
- Sponsor
- University of Southern California
Conditions Complex Regional Pain Syndromes
Matched “Ketamine” in the study’s intervention “80mg/day Ketamine HCl Prolonged Release”
- NCT07768618Not yet recruiting · Phase 2
Electrophysiologic Mechanisms of Ketamine Antidepressant Response
- Enrollment
- 37Testimated
- Started
- 2026-12
- Sponsor
- Emory University
Conditions Epilepsy · Depressive Symptoms
Matched “Ketamine” in the study’s intervention “Ketamine”
- NCT07139106Not yet recruiting · Phase 4
Understanding the Role of the Kappa Opioid Receptor in Ketamine's Attenuation of Suicidal Thoughts
- Enrollment
- 12Testimated
- Started
- 2026-10-01
- Sponsor
- New York State Psychiatric Institute
Conditions Major Depressive Disorder (MDD)
Matched “Ketamine” in the study’s intervention “Ketamine hydrochloride infusion”
- NCT07683988Not yet recruiting · Phase 1
Oral and Sublingual Ketamine
- Enrollment
- 10Testimated
- Started
- 2026-10-01
- Sponsor
- Western University, Canada
Conditions Major Depression Severe
Matched “Ketamine” in the study’s intervention “75 mg of oral ketamine”
- NCT07839338Not yet recruiting · Phase 3
A Study Comparing Oral Ketamine With Oral Midazolam for the Treatment of Major Depressive Episodes
- Enrollment
- 220Testimated
- Started
- 2026-10
- Sponsor
- Jawaharlal Institute of Postgraduate Medical Education & Research
Conditions Major Depressive Episode
Matched “Ketamine” in the study’s intervention “Oral ketamine”
- NCT07648771Not yet recruiting
Outcomes Registry After Ketamine Infusions for Chronic Pain: A Longitudinal Evaluation
- Enrollment
- 800Testimated
- Started
- 2026-10
- Sponsor
- Stanford University
Conditions Chronic Pain · Ketamine
Matched “Ketamine” in the study’s intervention “Ketamine (Ketalar)”
- NCT07369024Recruiting · Phase 2
Sub-dissociative Dose Ketamine in Treatment of Vaso-occlusive Pain Event in Children and Young Adults
- Enrollment
- 120Testimated
- Started
- 2026-09-10
- Sponsor
- Mohsen Saidinejad
Conditions Sickle Cell Disease · Vaso-Occlusive Pain Episode in Sickle Cell Disease · Ketamine Infusion · Pain Management · Vaso-Occlusive Crises
Matched “Ketamine” in the study’s intervention “Sub-dissociative Ketamine Infusion”
- NCT07099534Not yet recruiting · Phase 2
Ketamine Infusion for Symptomatic Improvement in Severe Borderline Personality Disorder
- Enrollment
- 38Testimated
- Started
- 2026-09-01
- Sponsor
- University Hospital, Toulouse
Conditions Infusion of Ketamine in Severe Borderline Personality Disorder · Borderline Personality Disorder (BPD)
Matched “Ketamine” in the study’s intervention “IV Ketamine (0.5 mg/kg) Infusion - Two Doses Administered 24 Hours Apart for Severe Borderline Personality Disorder”
- NCT07112456Not yet recruiting · Phase 2
Nebulized Ketamine Plus Standard Care vs. Standard Care Alone in Moderate to Severe Asthma Exacerbations
- Enrollment
- 100Testimated
- Started
- 2026-09-01
- Sponsor
- Oman Medical Speciality Board
Conditions Asthma Acute · Asthma Attack · Asthma Exacerbations
Matched “Ketamine” in the study’s intervention “Nebulized ketamine (0.5 mg/kg in normal saline to a total volume of 5ml) plus standard asthma excaerbationcare”
- NCT07801703Not yet recruiting · Phase 2 / Phase 3
Behavioural Activation Therapy and Ketamine for Treatment-Resistant Depression
- Enrollment
- 60Testimated
- Started
- 2026-09
- Sponsor
- The Royal's Institute of Mental Health Research
Conditions Treatment Resistant Depression · Major Depressive Disorder (MDD)
Matched “Ketamine” in the study’s intervention “Ketamine (0.5 mg/kg)”
- NCT06378528Suspended · Early phase 1
Ketamine-assisted Psychotherapy for Adolescent PTSD (KAP)
- Enrollment
- 5Testimated
- Started
- 2026-09
- Sponsor
- University of Wisconsin, Madison
Conditions Posttraumatic Stress Disorder
Matched “Ketamine” in the study’s intervention “Ketamine”
- NCT07563296Recruiting · Phase 2
KALM-B: Ketamine-assisted Psychotherapy (KAP) to Lessen Morbidity After Burn Injury
- Enrollment
- 12Testimated
- Started
- 2026-08-24
- Sponsor
- Irma Fleming
Conditions PTSD and Trauma-related Symptoms
Matched “Ketamine” in the study’s intervention “Ketamine-assisted Psychotherapy Session #1”
- NCT07739641Not yet recruiting · Not applicable
A COMPARATIVE STUDY BETWEEN OPIOID-FREE GENERAL ANAESTHESIA AND OPIOID-BASED GENERAL ANAESTHESIA ON THE QUALITY OF RECOVERY IN PATIENTS UNDERGOING ELECTIVE LAPAROSCOPIC HYSTRECTOMY: A Randomized Trial
- Enrollment
- 66Testimated
- Started
- 2026-08-22
- Sponsor
- Ain Shams University
Conditions Post Operative Recovery · Post Operative Nausea and Vomiting (PONV) · Post Operative Analgesia
Matched “Ketamine” in the study’s intervention “Opioid-Free Anaesthesia (Dexmedetomidine, Ketamine, and Lidocaine)”
- NCT07746115Completed · Not applicable
Testing Two Doses of Nebulized Ketamine for Postoperative Sore Throat
- Enrollment
- 195Tactual
- Started
- 2026-08-15
- Sponsor
- Aswan University Hospital
Conditions Postoperative Sore Throat
Matched “Ketamine” in the study’s intervention “Ketamine 50 MG/ML”
- NCT07680140Recruiting · Phase 4
Biomarker-Guided Antidepressant Selection
- Enrollment
- 27Testimated
- Started
- 2026-08-10
- Sponsor
- Weill Medical College of Cornell University
Conditions Depression - Major Depressive Disorder · Treatment-resistant Depression (TRD) · rTMS · Ketamine · fMRI
Matched “Ketamine” in the study’s intervention “Ketamine”
- NCT07670052Not yet recruiting · Phase 4
Intraperitoneal Ketamine Versus Fentanyl as Adjuvants to Bupivacaine in Laparoscopic Cholecystectomy
- Enrollment
- 84Testimated
- Started
- 2026-08-01
- Sponsor
- Assiut University
Conditions Postoperative Pain
Matched “Ketamine” in the study’s intervention “Ketamine”
- NCT07410078Recruiting · Not applicable
Comparative Assessment of Oral Premedication Regimens in Pediatric Ambulatory Surgery
- Enrollment
- 135Testimated
- Started
- 2026-07-26
- Sponsor
- Diskapi Yildirim Beyazit Education and Research Hospital
Conditions Pediatric Anesthesia · Premedication
Matched “Ketamine” in the study’s intervention “Oral Midazolam plus Ketamine Premedication”
- NCT07614581Not yet recruiting
Intra-Sessional Autonomic Arc Detection in Ketamine-Assisted Therapy for PTSD: A Signal Characterisation Pilot Study
- Enrollment
- 5Testimated
- Started
- 2026-07-15
- Sponsor
- Adriaan Dirk van der Wart
Conditions Post-Traumatic Stress Disorder
Matched “Ketamine” in the study’s intervention “Ketamine-assisted therapy (independently arranged)”
- NCT07708740Recruiting · Not applicable
Two Intravenous Doses of Ketamine in Reducing the Oculocardiac Reflex in Adult Patients Undergoing Ophthalmic Surgery
- Enrollment
- 40Testimated
- Started
- 2026-07-01
- Sponsor
- Cairo University
Conditions Ketamine · Oculocardiac Reflex · Ophthalmic Surgery
Matched “Ketamine” in the study’s intervention “0.5 mg/kg intravenous ketamine”
- NCT07691372Not yet recruiting · Phase 1
Pharmacokinetics and Safety of Single-Dose Wafermine™ (Ketamine Sublingual Wafer) in Healthy Subjects
- Enrollment
- 14Testimated
- Started
- 2026-06-09
- Sponsor
- iX Biopharma Ltd.
Conditions Healthy Adult Participants
Matched “Ketamine” in the study’s intervention “Wafermine™ (ketamine sublingual wafer)”
- NCT07636070Not yet recruiting · Not applicable
Multimodal Opioid-Free Anesthesia in RIRS
- Enrollment
- 60Testimated
- Started
- 2026-06-01
- Sponsor
- murat sahin
Conditions Kidney Stone · Retrograde Intrarenal Surgery (RIRS) · Postoperative Pain
Matched “Ketamine” in the study’s intervention “Dexmedetomidine-Ketamine Opioid-Free Anesthesia”
- NCT06062628Recruiting · Early phase 1
Ketamine in Severe Traumatic Brain Injury
- Enrollment
- 10Testimated
- Started
- 2026-06-01
- Sponsor
- University of Texas Southwestern Medical Center
Conditions Traumatic Brain Injury · Traumatic Encephalopathy
Matched “Ketamine” in the study’s intervention “Ketamine Hydrochloride”
- NCT07639359Recruiting · Phase 2
Subanesthetic Ketamine Infusions for Depressive Symptoms in Intensive Care Unit Patients
- Enrollment
- 50Testimated
- Started
- 2026-05-14
- Sponsor
- Hospital Italiano de Buenos Aires
Conditions Critical Illness · Depressive Symptoms
Matched “Ketamine” in the study’s intervention “Ketamine (0.5 mg/kg)”
- NCT06781697Recruiting · Phase 3
InTRavenous kEtAmine and immerSive virtUal Reality to Treat dEpression
- Enrollment
- 31Testimated
- Started
- 2026-05-03
- Sponsor
- Sunnybrook Health Sciences Centre
Conditions Treatment Resistant Depression
Matched “Ketamine” in the study’s intervention “Ketamine”
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 Ketamine · dl-Ketamine · (+-)-Ketamine. 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 Ketamine worked.
X · Legal
Controlled-substance status
United States federal scheduling, read from the DEA records this archive holds and shown with the passage each was read from. Not legal advice, and not necessarily current.
- DEA class
- Depressants and Tranquilizers
- Added
- October 1998
As the DEA states it
Quoted whole. The badge above is a reading of these passages and adds nothing to them.
Ketamine (Class: Depressants and Tranquilizers, Added Date: 10-1998)
Other regulatory records
Registers outside the DEA that hold an entry for Ketamine — chemical-safety and national inventories, each naming itself. They are not scheduling decisions.
Status: Active Update: 31-07-2015 https://echa.europa.eu/registration-dossier/-/registered-dossier/11298
Ketamine: Does not have an individual approval but may be used under an appropriate group standard
The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Ketamine hydrochloride is included on this list. /Ketamine hydrochloride/
Hazardous Substances Data Bank (HSDB)US FDA/Center for Veterinary Medicine; The Green Book - FDA Approved Animal Drug Products. Available from, as of October 29, 2008: https://www.fda.gov/cvm/Green_Book/greenbook.html
Schedule III shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. Each drug or substance has been assigned the DEA Controlled Substances Code Number set forth opposite it. Depressants. ... Unless specifically excepted or unless listed in another schedule, any material, compound, mixture, or preparation which contains any quantity of the following substances having a depressant effect on the central nervous system: Ketamine, its salts, isomers, and salts of isomers. DEA Code Number: 7285.
Hazardous Substances Data Bank (HSDB)21 CFR 1308.13(c) (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
United States federal status only. State law differs, and so does the law of every other country — none of it is represented here. Scheduling changes, and this reflects the DEA records held by PubChem descriptive sections when the monograph was last harvested, not necessarily today. This is a record of what a database publishes, not legal advice.
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.
- 01
Structural basis of opioid receptor activation by PCP and ketamine
Jiang Q, Han J, Fine EJ et al. · Nature structural & molecular biology 2026
- · 6 measurements at 3 targets (EC50, Ki), strongest MOR at 4.94 pX
- 02
Wallach J, Kang H, Colestock T et al. · PloS one 2016
- · 2 measurements at 1 target (Ki), strongest NMDA at 6.49 pX
- 03
Bresink I, Danysz W, Parsons CG et al. · Neuropharmacology 1995
- · 2 measurements at 1 target (Ki), strongest NMDA at 5.92 pX
- 04
Pharmacological characterizations of the 'legal high' fluorolintane and isomers
Wallach J, Colestock T, Agramunt J et al. · European journal of pharmacology 2019
- · 1 measurement at 1 target (Ki), strongest NMDA at 6.49 pX
- 05
Colestock T, Wallach J, Mansi M et al. · Drug testing and analysis 2018
- · 1 measurement at 1 target (Ki), strongest NMDA at 6.49 pX
- 06
Ephenidine: A new psychoactive agent with ketamine-like NMDA receptor antagonist properties
Kang H, Park P, Bortolotto ZA et al. · Neuropharmacology 2017
- · 1 measurement at 1 target (Ki), strongest NMDA at 6.49 pX
- 07
Roth BL, Gibbons S, Arunotayanun W et al. · PloS one 2013
- · 1 measurement at 1 target (Ki), strongest NMDA at 6.18 pX
- 08
The clinical toxicology of ketamine
Schep LJ, Slaughter RJ, Watts M et al. · Clinical toxicology (Philadelphia, Pa.) 2023
- · Plasma elimination half-life
- 09
Baker SC, Shabir S, Georgopoulos NT et al. · The American journal of pathology 2016
- · Mechanism of Action
- 10
Ketamine-Induced Hallucinations
Powers AR 3rd, Gancsos MG, Finn ES et al. · Psychopathology 2015
- · Human Toxicity Excerpts
- 11
Long-term ketamine abuse induces cystitis in rats by impairing the bladder epithelial barrier
Gu D, Huang J, Yin Y et al. · Molecular biology reports 2014
- · Mechanism of Action
- 12
Rasmussen KG · Acta neuropsychiatrica 2014
- · Human Toxicity Excerpts
- 13
Nishitani N, Nagayasu K, Asaoka N et al. · The international journal of neuropsychopharmacology 2014
- · Mechanism of Action
- 14
NMDA receptor antagonist ketamine impairs feature integration in visual perception
Meuwese JD, van Loon AM, Scholte HS et al. · PloS one 2013
- · Human Toxicity Excerpts
- 15
Evans S, Almahdi B, Sultan P et al. · Journal of psychopharmacology (Oxford, England) 2012
- · Human Toxicity Excerpts
- 16
Pharmacokinetics and distribution of ketamine after extradural administration to dogs
Pedraz JL, Calvo MB, Gascon AR et al. · British journal of anaesthesia 1991
- · Biological Half-Life