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Dissociative

Ketamine

Also called K, Ket, Kitty, Special K, Cat Tranquilizer, Ketaset, Ketalar, Ketanest, Vitamin K, Purple, Jet

Original Wikipedia articleen.wikipedia.org/wiki/Ketamine revision used (24 October 2026)

Why a "revision used" link? Anyone can edit Wikipedia at any time, so the article you open today may not say what it said when we read it. This link opens the exact version we read on 24 October 2026, frozen as it was. It is the only way to check that every quote on this page matches its source word for word. Newer versions may correct or change things. When we re-check this page against a newer version, the edit log records it. How we cite

Common dose · Insufflated30–75 mg PW
Onset1–3 minutes PW
Total1–2 hours PW
After-effects2–12 hours PW

Dosage

When sources disagree, both rows are shown as published. Nothing is averaged or merged.

Insufflated

SourceThresholdLightCommonStrongHeavy
PsychonautWiki5 mg PW10–30 mg PW30–75 mg PW75–150 mg PW150 mg+ PW
TripSit5–10 mg TS20–50 mg TS50–125 mg TS125–175 mg TS175–250 mg TS

Bioavailability: 45%[40] PW⚠ The source's own markup is broken here, so this is how a reader of the source would see it.

Oral

SourceThresholdLightCommonStrongHeavy
PsychonautWiki50 mg PW50–100 mg PW100–300 mg PW300–450 mg PW450 mg+ PW

Bioavailability: 17%[41] PW⚠ The source's own markup is broken here, so this is how a reader of the source would see it.

NOTE: Ketamine is based on weight. These are figures for the average 150 pound male There is no concrete dose for the "K-Hole" as each user is different. TS

TripSit dose text

TripSit's factsheet also states its doses as text.

Insufflated Threshold: 5-10mg Light: 20-50mg Common: 50-125mg Strong: 125-175mg Heavy: 175-250mg | NOTE: Ketamine is based on weight. These are figures for the average 150 pound male There is no concrete dose for the "K-Hole" as each user is different. TS

What dose are you on? (self-reported, unverified)
Read this first. These numbers come from anonymous visitors typing in a box. Nobody checks them. People misjudge, mistype, troll, or take untested products of unknown strength. They are not a dose guide and never override the sourced table above. They exist only so the sourced ranges can be compared with what people say they take. If you are deciding what to take, use the sourced table, start low, and read the risks section.
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Duration

Route · sourceOnsetCome-upPeakOffsetTotalAfter-effects
Insufflated · PsychonautWiki1–3 minutes PW5–15 minutes PW15–45 minutes[42] PW30–60 minutes PW1–2 hours PW2–12 hours PW
Oral · PsychonautWiki10–30 minutes PW5–20 minutes PW45–90 minutes PW3–6 hours PW–4–8 hours PW

TripSit factsheet

Onset
Insufflated: 7.5-20 minutes · Intramuscular: 2-7.5 minutes · Intravenous: 0-2 minutes · Oral: 10-75 minutes TS
Duration
1-2 hours TS
Aftereffects
1-2 hours TS

Mixing

Acute combinations: what happens when these are taken close together. Entries backed by a medical journal or agency are listed first.

Backed by medical journals

  • Uncertain Grapefruit - Grapefruit juice significantly increases oral absorption of ketamine. This may result in the user having double the concentration of ketamine in their system compared to normal. The ketamine may also have a longer duration of effect. This likely applies to oral, sublingual, and intranasal administration.[43] PW

Other documented combinations

  • Dangerous Alcohol - Both substances cause ataxia and bring a very high risk of vomiting and unconsciousness. If the user falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position. PW
  • Dangerous GHB / GBL - Both substances cause ataxia and bring a risk of vomiting and unconsciousness. If the user falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position. PW
  • Dangerous Opioids - Both substances bring a risk of vomiting and unconsciousness. If the user falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position. PW
  • Dangerous Tramadol - Tramadol lowers the seizure threshold. Both substances increase the risk of vomiting and unconsciousness. PW
  • Uncertain Amphetamines - No unexpected interactions, though likely to increase blood pressure (likely not an issue with sensible doses). Moving around on high doses of this combination may be ill-advised due to risk of physical injury. PW
  • Uncertain Cocaine - No unexpected interactions, though likely to increase blood pressure (likely not an issue with sensible doses). Moving around on high doses of this combination may be ill-advised due to risk of physical injury. PW
  • Uncertain Benzodiazepines - Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. While unconscious, vomit aspiration is a risk if the user is not placed in the recovery position. PW
  • Uncertain MAOIs - MAO-B inhibitors appear to increase the potency of ketamine. MAO-A inhibitors have some negative reports associated with the combination but there isn't much information available PW
  • Uncertain Trazodone - When used as a sleep aid and taken close to that of a dose of ketamine, there is a risk of respiratory depression when high amounts of either are consumed. PW

TripSit combination chart

TripSit rates each pairing. Only pairings with a number carry a citation from TripSit. See the whole chart, with TripSit's note for every pairing.

Dangerous

alcohol TSghb/gbl TSopioids TStramadol TS

Caution

amphetamines TSbenzodiazepines TScocaine TSmaois TS

Low Risk & Synergy

2c-t-x TS2c-x TS5-meo-xxt TSamt TScannabis TSdextromethorphan[44–49] TSdmt TSdox TSlsd TSmdma TSmescaline TSmushrooms TSmxe TSnbomes TSnitrous TSpcp TS

Low Risk & No Synergy

caffeine TSssris TS

Risks and toxicity

Some users have reported positive experience with rectal administration.[50] PW

It is strongly advised to use harm reduction practices if using this substance. PW

There is some evidence that ketamine may have antibiotic properties at higher doses. It is unclear how this affects normal human use.[51] PW

Cognition and well-being

The first large-scale, longitudinal study of ketamine users found that frequent ketamine users (at least 4 days/week, averaging 20 days/month) had increased depression and impaired memory by several measures, including verbal, short-term memory and visual memory. However, infrequent (1–4 days/month, averaging 3.25 days/month) ketamine users and former ketamine users were not found to differ from controls in memory, attention and psychological well-being tests. PW

This suggests the infrequent use of ketamine does not cause cognitive deficits and that any deficits that might occur may be reversible when ketamine use is discontinued. However, abstinent, frequent, and infrequent users all scored higher than controls on a test of delusional symptoms.[52] PW

Urinary tract effects

According to a 2010 systematic review, 110 documented reports of irritative urinary tract symptoms from ketamine dependence exist. Urinary tract symptoms have been collectively referred to as "ketamine-induced ulcerative cystitis" or "ketamine-induced vesicopathy" and they include urge incontinence, decreased bladder compliance, decreased bladder volume, and painful haematuria (blood in urine).[53] PW

The time of onset of lower urinary tract symptoms varies depending, in part, on the severity and chronicity of ketamine use; however, it is unclear whether the severity and chronicity of ketamine use correspond linearly to the presentation of these symptoms. All reported cases where the user consumed greater than 5 grams per day reported symptoms of the lower urinary tract.[29] PW

A study conducted in 2015 demonstrated that co-administration of EGCG (10mM/kg) in rats receiving a daily dose of ketamine (25 mg/kg/d), significantly reduced ketamine-induced bladder damage to almost control levels, showing potential benefits of EGCG consumption to prevent or reverse ketamine-induced cystitis (KIC) and ovariectomy-induced overactive bladder (OAB). However, the application to human use is not clear.[54] PW

NMDA receptor antagonist neurotoxicity (nat)

Also known as Olney's lesions. Short-term exposure of cultures of GABAergic neurons to ketamine at high concentrations led to a significant loss of differentiated cells in one study, and non-cell death-inducing concentrations of ketamine (10 μg/ml) may still initiate long-term alterations of the dendritic arbor in differentiated neurons.[55][56] PW

More recent studies of ketamine-induced neurotoxicity have focused on primates in an attempt to use a more accurate model than rodents. One such study administered daily ketamine doses consistent with typical recreational doses (1 mg/kg IV) to adolescent cynomolgus monkeys for varying periods of time. PW

Decreased locomotor activity and indicators of increased cell death in the prefrontal cortex were detected in monkeys given daily injections for six months, but not those given daily injections for one month.[57] PW

Dependence and abuse potential

Ketamine has moderate to high abuse potential and produces psychological dependence with chronic use. When dependence has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage. PW

Tolerance to the main effects of ketamine develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. Tolerance can decrease after a break (often called a tolerance break), but the duration required to fully reset tolerance varies. Tolerance returns to half of the original level after 14 days and to baseline after 28 days. This reset period depends on several factors, including an individual’s genetic and physiological makeup, the quantity and frequency of use, and the length of time exposed to the substance. PW

Ketamine presents cross-tolerance with all dissociatives, meaning that after the consumption of ketamine all dissociatives will have a reduced effect. PW

Permatolerance

Dissociatives are reported to be unique from other substances because they are capable of producing a long-term or permanent form of tolerance ("permatolerance") that accumulates slowly and independently from normal tolerance. PW

Many chronic ketamine users report that they need to consume substantially more to achieve dissociation or k-hole compared to their first use, even after taking extended breaks. The cause is not known, although it has been suggested to be a potential indicator of some form of neurotoxicity. PW

Dissociative permatolerance poses an additional problem considering ketamine's negative effects on the urinary tract. As a result, heavy or chronic use of all dissociatives is strongly discouraged. PW

Overdose

Fatal ketamine overdoses are rare. Ketamine's toxicity drastically increases when it is mixed with other substances. Overdoses can cause respiratory depression, vomiting, positional asphyxia, heart problems, rhabdomyolysis causing kidney failure and rarely seizures. However, there is evidence that suggests extremely high doses may result in damage to the brain and other organs.[58] PW⚠ PsychonautWiki itself has flagged this text: citation needed.

Caution for intravenous use

Rapidly injected ketamine (under 2 minutes) can cause cause transient respiratory depression. The effects of ketamine on reflexes and rapid loss of normal consciousness can increase the chances of positional asphyxia (passing out in a position where you can't breath).[59] PW

TripSit factsheet

Avoid
Driving. Moving and walking if possible. Mixing with other depressants like alcohol, benzos and opiates.[2–25] TS

Testing

Awaiting sourceReagent reactions and test kit guidance from a harm reduction testing service.

Effects

A feeling of drunkenness and well being at low doses. As dose increases the user may begin to feel a disconnection from their body. At 'khole' doses the user may become completely disconnected from both body and mind. TS

Overview

Ketamine (also known as 2-Cl-2’-oxo-PCM, Ket, K, Special K, vitamin K, Kitty, 2-CXM, and others) is a classical dissociative substance of the arylcyclohexylamine class. It is perhaps the best-known and archetypal member of the dissociatives, a diverse group which includes PCP, methoxetamine, DXM, and nitrous oxide. The mechanism of action is not fully known, although blocking of the NMDA glutamate receptor is thought to be involved.[1] PW

A short acting dissociative anaesthetic and hallucinogen commonly used in emergency medicine. It is the prototypical dissociative, and is widely used at sub-anesthetic doses recreationally. Small doses are comparable with alcohol, while larger doses are immobilising and lead to psychedelic experiences: the "K-Hole."[2–25] TS

Ketamine is a cyclohexanone-derived dissociative general anesthetic and NMDA receptor antagonist with analgesic and hallucinogenic properties, used medically for anesthesia, depression, and pain management. Ketamine exists as its two enantiomers, S- (esketamine) and R- (arketamine), and has antidepressant action likely involving NMDA antagonism as well as other mechanisms.[26][27] WP

At anesthetic doses, ketamine induces a state of dissociative anesthesia, a trance-like state providing pain relief, sedation, and amnesia. Its distinguishing features as an anesthetic are preserved breathing and airway reflexes, stimulated heart function with increased blood pressure, and moderate bronchodilation. As an anesthetic, it is used especially in trauma, emergency, and pediatric cases. At lower, sub-anesthetic doses, it is used as a treatment for pain and treatment-resistant depression.[28] WP

Ketamine is legally used in medicine but is also tightly controlled, as it is used as a recreational drug for its hallucinogenic and dissociative effects. When used recreationally, it is found both in crystalline, powder and liquid form, and is often referred to by users as "Ket", "Special K" or simply "K". The long-term effects of repeated use are largely unknown and are an area of active investigation. Liver and urinary toxicity have been reported among regular users of high doses of ketamine for recreational purposes. Ketamine can cause dissociation and nausea, and other adverse effects, and is contraindicated in severe heart or liver disease, and uncontrolled psychosis. Ketamine's clinical and antidepressant effects can be influenced by co-administration of other drugs, though these interactions are variable and not yet fully understood.[29–33] WP

Ketamine was first synthesized in 1962; it was derived from phencyclidine in pursuit of a safer anesthetic with fewer hallucinogenic effects. It was approved for use in the United States in 1970. It has been regularly used in veterinary medicine and was extensively used for surgical anesthesia in the Vietnam War. It later gained prominence for its rapid antidepressant effects discovered in 2000, marking a major breakthrough in depression treatment. Racemic ketamine, especially at higher doses, may be more effective and longer-lasting than esketamine in reducing depression severity. It is on the World Health Organization's List of Essential Medicines. It is available as a generic medication.[27][34–39] WP

History

History

Ketamine was first synthesized in 1962 by Calvin L. Stevens, a professor of chemistry at Wayne State University and a Parke-Davis consultant. It was known by the developmental code name CI-581. After promising preclinical research in animals, ketamine was tested in human prisoners in 1964. These investigations demonstrated ketamine's short duration of action and reduced behavioral toxicity made it a favorable choice over phencyclidine (PCP) as an anesthetic. The researchers wanted to call the state of ketamine anesthesia "dreaming", but Parke-Davis did not approve of the name. Hearing about this problem and the "disconnected" appearance of treated people, Edward F. Domino's wife Toni suggested "dissociative anesthesia". Ketamine was first described in the literature in 1963 and its effects in humans were first described by Edward F. Domino and colleagues in 1965.[27][36][60–65] WP

Following FDA approval in 1970, ketamine anesthesia was first given to American soldiers during the Vietnam War.[66] WP

The discovery of antidepressive action of ketamine in 2000 has been described as the single most important advance in the treatment of depression in more than 50 years. It has sparked interest in NMDA receptor antagonists for depression, and has shifted the direction of antidepressant research and development.[67–71] WP

Pharmacology

Mechanism of action

Ketamine is a mixture of equal amounts of two enantiomers: esketamine and arketamine. Esketamine is a far more potent NMDA receptor pore blocker than arketamine. Pore blocking of the NMDA receptor is responsible for the anesthetic, analgesic, and psychotomimetic effects of ketamine. Blocking of the NMDA receptor results in analgesia by preventing central sensitization in dorsal horn neurons; in other words, ketamine's actions interfere with pain transmission in the spinal cord.[34][69][119][120] WP

The mechanism of action of ketamine in alleviating depression is not well understood, but it is an area of active investigation. Due to the hypothesis that NMDA receptor antagonism underlies the antidepressant effects of ketamine, esketamine was developed as an antidepressant. However, multiple other NMDA receptor antagonists, including memantine, lanicemine, rislenemdaz, rapastinel, and 4-chlorokynurenine, have thus far failed to demonstrate significant effectiveness for depression. Furthermore, animal research indicates that arketamine, the enantiomer with a weaker NMDA receptor antagonism, as well as (2R,6R)-hydroxynorketamine, the metabolite with negligible affinity for the NMDA receptor but potent alpha-7 nicotinic receptor antagonist activity, may have antidepressant action. This furthers the argument that NMDA receptor antagonism may not be primarily responsible for the antidepressant effects of ketamine. Acute inhibition of the lateral habenula, a part of the brain responsible for inhibiting the mesolimbic reward pathway and referred to as the "anti-reward center", is another possible mechanism for ketamine's antidepressant effects.[69][113][121–125] WP

Possible biochemical mechanisms of ketamine's antidepressant action include direct action on the NMDA receptor and downstream effects on regulators such as brain-derived neurotrophic factor (BDNF) and mTOR. It is not clear whether ketamine alone is sufficient for antidepressant action or its metabolites are also important; the active metabolite of ketamine, hydroxynorketamine, which does not significantly interact with the NMDA receptor but nonetheless indirectly activates AMPA receptors, may also or alternatively be involved in the rapid-onset antidepressant effects of ketamine. As an NMDA receptor antagonist, ketamine triggers a paradoxical acute burst of glutamate by selectively blocking inhibitory GABAergic neurons. This surge activates AMPA receptors, which modulate downstream signaling pathways in the limbic system to produce rapid antidepressant effects. Such downstream actions of the activation of AMPA receptors include upregulation of BDNF and activation of its signaling receptor tropomyosin receptor kinase B (TrkB), activation of the mammalian target of rapamycin (mTOR) pathway, deactivation of glycogen synthase kinase 3 (GSK-3), and inhibition of the phosphorylation of the eukaryotic elongation factor 2 (eEF2) kinase.[119][123][126–130] WP

Molecular targets

Ketamine principally acts as a pore blocker of the NMDA receptor, an ionotropic glutamate receptor. The S-(+) and R-(–) stereoisomers of ketamine bind to the dizocilpine site of the NMDA receptor with different affinities, the former showing approximately 3- to 4-fold greater affinity for the receptor than the latter. As a result, the S isomer is a more potent anesthetic and analgesic than its R counterpart.[131][132] WP

Ketamine may interact with and inhibit the NMDAR via another allosteric site on the receptor.[133] WP

With a couple of exceptions, ketamine's actions at other receptors are far weaker than its antagonism of the NMDA receptor (see the activity table to the right).[90][134] WP

Although ketamine is a very weak ligand of the monoamine transporters (Kᵢ > 60 μM), it has been suggested that it may interact with allosteric sites on the monoamine transporters to produce monoamine reuptake inhibition. However, no functional inhibition (IC₅₀) of the human monoamine transporters has been observed with ketamine or its metabolites at concentrations of up to 10,000 nM. Moreover, animal studies and at least three human case reports have found no interaction between ketamine and the monoamine oxidase inhibitor (MAOI) tranylcypromine, which is of importance as the combination of a monoamine reuptake inhibitor with an MAOI can produce severe toxicity such as serotonin syndrome or hypertensive crisis. Collectively, these findings shed doubt on the involvement of monoamine reuptake inhibition in the effects of ketamine in humans. Ketamine has been found to increase dopaminergic neurotransmission in the brain, but instead of being due to dopamine reuptake inhibition, this may be via indirect/downstream mechanisms, namely through antagonism of the NMDA receptor.[103][109][131][135][136] WP

Whether ketamine is an agonist of D₂ receptors is controversial. Early research by the Philip Seeman group found ketamine to be a D₂ partial agonist with a potency similar to that of its NMDA receptor antagonism. However, later studies by different researchers found the affinity of ketamine of >10 μM for the regular human and rat D₂ receptors, Moreover, whereas D₂ receptor agonists such as bromocriptine can rapidly and powerfully suppress prolactin secretion, subanesthetic doses of ketamine have not been found to do this in humans and in fact, have been found to dose-dependently increase prolactin levels. Imaging studies have shown mixed results on inhibition of striatal [¹¹C] raclopride binding by ketamine in humans, with some studies finding a significant decrease and others finding no such effect. However, changes in [¹¹C] raclopride binding may be due to changes in dopamine concentrations induced by ketamine rather than binding of ketamine to the D₂ receptor.[103][108][109][110][137–142] WP

Pharmacokinetics

Ketamine can be absorbed by many different routes due to its water and lipid solubility. Intravenous ketamine bioavailability is 100% by definition, intramuscular injection bioavailability is slightly lower at 93%, and epidural bioavailability is 77%. Subcutaneous bioavailability has never been measured but is presumed to be high. Among the less invasive routes, the intranasal route has the highest bioavailability (45–50%) and oral – the lowest (16–20%). Sublingual and rectal bioavailabilities are intermediate at approximately 25–50%.[69][90][143][144][145] WP

After absorption ketamine is rapidly distributed into the brain and other tissues. The plasma protein binding of ketamine is variable at 23–47%.[34][146] WP

In the body, ketamine undergoes extensive metabolism. It is biotransformed by CYP3A4 and CYP2B6 isoenzymes into norketamine, which, in turn, is converted by CYP2A6 and CYP2B6 into hydroxynorketamine and dehydronorketamine. Low oral bioavailability of ketamine is due to the first-pass effect and, possibly, ketamine intestinal metabolism by CYP3A4. As a result, norketamine plasma levels are several-fold higher than ketamine following oral administration, and norketamine may play a role in anesthetic and analgesic action of oral ketamine. This also explains why oral ketamine levels are independent of CYP2B6 activity, unlike subcutaneous ketamine levels.[90][119][147][148] WP

After an intravenous injection of tritium-labelled ketamine, 91% of the radioactivity is recovered from urine and 3% from feces. The medication is excreted mostly in the form of metabolites, with only 2% remaining unchanged. Conjugated hydroxylated derivatives of ketamine (80%) followed by dehydronorketamine (16%) are the most prevalent metabolites detected in urine.[36][149] WP

Detection

Ketamine may be quantified in blood or plasma to confirm a diagnosis of poisoning in hospitalized people, provide evidence in an impaired driving arrest, or assist in a medicolegal death investigation. Blood or plasma ketamine concentrations are usually in a range of 0.5–5.0 mg/L in persons receiving the drug therapeutically (during general anesthesia), 1–2 mg/L in those arrested for impaired driving, and 3–20 mg/L in victims of acute fatal overdosage. Urine is often the preferred specimen for routine drug use monitoring purposes. The presence of norketamine, a pharmacologically active metabolite, is useful for confirmation of ketamine ingestion.[150][151][152] WP

Receptor binding · Wikipedia

Ketamine and biological targets (with Kᵢ below 100 μM)

SiteValue (μM)TypeActionSpecies
NMDA (PCP)0.25–0.66KᵢAntagonistHuman[102][103] WP
MOR (μ-Opioid receptor)42KᵢAntagonistHuman[104] WP
MOR₂ (μ-Opioid receptor)12.1KᵢAntagonistHuman[105] WP
KOR (κ-Opioid receptor)28; 25Kᵢ; KᵢAntagonist; AgonistHuman[104][106] WP
σ₂26KᵢND (No data)Rat[107] WP
D₂0.5; >10Kᵢ; KᵢAgonist; ND (No data)Human[103][108][109][110] WP
M₁45KᵢND (No data)Human[111] WP
α₂β₂ (Nicotinic acetylcholine receptor)92IC₅₀AntagonistHuman[112] WP
α₂β₄ (Nicotinic acetylcholine receptor)29IC₅₀AntagonistHuman[112] WP
α₃β₂50IC₅₀AntagonistHuman[112] WP
α₃β₄9.5IC₅₀AntagonistHuman[112] WP
α₄β₂72IC₅₀AntagonistHuman[112] WP
α₄β₄18IC₅₀AntagonistHuman[112] WP
α₇3.1 (HNK)IC₅₀NAMRat[113] WP
ERα (Estrogen receptor alpha)0.34KᵢND (No data)Human[114] WP
NET (Norepinephrine transporter)82–291IC₅₀InhibitorHuman[115][116] WP
DAT (Dopamine transporter)63KᵢInhibitorRat[115] WP
HCN1 (Hyperpolarization-activated cyclic nucleotide-gated channel 1)8–16EC₅₀InhibitorMouse[117] WP
TRPV11-100KᵢAgonistRat[118] WP

Chemistry

Formula
C13H16ClNO PC
CAS number
6740-88-1 PC
Molar mass (g/mol)
237.72 PC
IUPAC name (computed by PubChem)
2-(2-chlorophenyl)-2-(methylamino)cyclohexan-1-one PC
SMILES
CNC1(CCCCC1=O)C2=CC=CC=C2Cl PC
InChIKey
YQEZLKZALYSWHR-UHFFFAOYSA-N PC
PubChem CID
3821

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References

  1. Other Ketamine: Dreams and Realities, p129, p172
  2. Journal / agency Comparative and interactive human psychopharmacologic effects of ketamine and amphetamine: implications for glutamatergic and dopaminergic model ps
  3. Journal / agency The effect of ketamine on opioid-induced acute tolerance: can it explain reduction of opioid consumption with ketamine-opioid analgesic combinations
  4. Journal / agency Subanesthetic ketamine infusion therapy: a retrospective analysis of a novel therapeutic approach to complex regional pain syndrome
  5. Journal / agency Effects of ketamine on precipitated opiate withdrawal
  6. Journal / agency Low-dose ketamine with multimodal postcesarean delivery analgesia: a randomized controlled trial
  7. Journal / agency Chronic ketamine exposure induces permanent impairment of brain functions in adolescent cynomolgus monkeys
  8. Journal / agency GLYX-13, a NMDA receptor glycine-site functional partial agonist, induces antidepressant-like effects without ketamine-like side effects
  9. Journal / agency From "Special K" to "Special M": the evolution of the recreational use of ketamine and methoxetamine
  10. Journal / agency Daily oral ketamine for the treatment of depression and anxiety in patients receiving hospice care: a 28-day open-label proof-of-concept trial
  11. Journal / agency Brain damages in ketamine addicts as revealed by magnetic resonance imaging
  12. Journal / agency Antidepressant efficacy of ketamine in treatment-resistant major depression: a two-site randomized controlled trial
  13. Journal / agency Are sexes affected differently by ketamine? An exploratory study in ketamine users
  14. Journal / agency Therapeutic infusions of ketamine: do the psychoactive effects matter
  15. Journal / agency The absolute bioavailability of racemic ketamine from a novel sublingual formulation
  16. Journal / agency The mood stabilizer lithium potentiates the antidepressant-like effects and ameliorates oxidative stress induced by acute ketamine in a mouse model
  17. Journal / agency The promise of ketamine for treatment-resistant depression: current evidence and future directions
  18. Journal / agency Antidepressants do not increase the lethality of ketamine in mice
  19. Journal / agency Effect of ketamine, an NMDA receptor inhibitor, in acute and chronic orofacial pain
  20. Journal / agency Ketamine and norketamine plasma concentrations after i.v., nasal and rectal administration in children
  21. Journal / agency Tissue distribution of ketamine in a mixed drug fatality
  22. Journal / agency From the racemate to the eutomer: (S)-ketamine. Renaissance of a substance?
  23. Journal / agency Chronic abuse has led to a case of kidney and liver damage
  24. Other ketamine in the hospital setting can raise blood pressure and is something to be considered when using it: "Emergency care in the streets"
  25. Other Ketamine shows promise in treating suicidal ideation in patients with depression
  26. Journal / agency Ketamine
  27. Journal / agency Sachdeva B, Sachdeva P, Ghosh S, Ahmad F, Sinha JK. Ketamine as a therapeutic agent in major depressive disorder and posttraumatic stress disorder: Potential medicinal and deleterious effects. Ibrain. March 2023. doi:10.1002/ibra.12094 · PMID 37786516 · PMC10528797
  28. Journal / agency Green SM, Roback MG, Kennedy RM, Krauss B. Clinical practice guideline for emergency department ketamine dissociative sedation: 2011 update. Annals of Emergency Medicine. May 2011. doi:10.1016/j.annemergmed.2010.11.030 · PMID 21256625
  29. Journal / agency Morgan CJ, Curran HV. Ketamine use: a review. Addiction. January 2012. doi:10.1111/j.1360-0443.2011.03576.x · PMID 21777321
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