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Summary sheet: Ketamine
Chemical Nomenclature
Common names Ketamine, K, Ket, Kitty, "Special K", "Cat Tranquilizer", Ketaset, Ketalar, Ketanest
Substitutive name Ketamine
Systematic name (RS)-2-(2-Chlorophenyl)-2-(methylamino)cyclohexanone
Class Membership
Psychoactive class Dissociative
Chemical class Arylcyclohexylamine
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.

Threshold 50 mg
Light 50 - 100 mg
Common 100 - 300 mg
Strong 300 - 450 mg
Heavy 450 mg+
Onset 10 - 30 minutes
Peak 45 - 90 minutes
After effects 4 - 8 hours

Threshold 5 mg
Light 10 - 30 mg
Common 30 - 75 mg
Strong 75 - 150 mg
Heavy 150 mg +
Total 1 - 1.5 hours
Onset 2 - 5 minutes
Come up 5 - 10 minutes
After effects 2 - 12 hours

DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.

Ketamine (also known as ket, K, special K, kitty, horse/dog/vet tranquilizer, and others) is a dissociative substance of the arylcyclohexylamine class. Ketamine is chemically related to phencyclidine (PCP) and methoxetamine (MXE). Like other dissociatives, it acts by blocking NMDA receptors in the brain.

Ketamine was developed in 1963 by Parke-Davis Laboratories as part of an effort to find a replacement for the surgical anesthetic phencyclidine (PCP). It became available by prescription in 1969 under the name Ketalar.[1] Today, ketamine is widely used in human and veterinary medicine, primarily for general anesthesia for surgical procedures.[citation needed] It is also used illicitly as a recreational substance and is associated with the clubbing and raving scenes.[citation needed]

Typical effects of ketamine include sedation, hallucinations, and dissociation, which is characterized by perceptual distortions and feelings of detachment from the environment and ones self. The effects of ketamine are similar to those of PCP but ketamine is much less potent and its effects are of much shorter duration. The effects of ketamine are highly dose dependent. At lower doses, users report disinhibition and relaxation effects similar to those of alcohol. Higher doses exceeding a certain threshold are capable of inducing experiences described as out-of-body or near-death experiences.

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

History and culture

Ketamine began as a veterinary anaesthetic when it was patented in Belgium in 1963. After being patented by Parke-Davis for human and animal use in 1966, ketamine became available by prescription in 1969 in the form of ketamine hydrochloride, under the name of Ketalar. It was officially approved for human consumption by the United States Food and Drug Administration in 1970 and, because of its sympathomimetic properties and its wide margin of safety, was administered as a field anaesthetic to soldiers during the Vietnam war.[1]

Ketamine is on the World Health Organization’s “Essential Drugs List”, a list of the safest and most effective drugs needed in a modern health system.[2]


Ketamine, or (RS)-2-(2-Chlorophenyl)-2-(methylamino)cyclohexanone, is a member of the arylcyclohexylamine chemical class. Arylcyclohexylamines are named for their chemical structures which include a cyclohexane ring bound to an aromatic ring along with an amine group. Ketamine is comprised of a phenyl ring with a chlorine substituent at R2 bonded to a cyclohexane ring substituted with an -Oxo group (cyclohexanone). An amino methyl chain (-N-CH3) is bound to the same location (R1) of the cyclohexanone ring.

Ketamine is a chiral molecule and is typically produced as a racemate.[citation needed] Enantiopure versions such as esketamine (S-ketamine) and arketamine (R-ketamine) are sometimes used.[citation needed]


Further information: NMDA receptor antagonist

Ketamine acts as a non-competitive antagonist of the NMDA receptor, an ionotropic glutamate receptor. NMDA receptors allow for electrical signals to pass between neurons in the brain and spinal column; for the signals to pass, the receptor must be open. Dissociatives close the NMDA receptors by blocking them. This disconnection of neurons leads to loss of feeling, difficulty moving, and eventually the notorious state known as the “K-hole”.

At high, fully anesthetic level doses, ketamine has also been found to bind to μ-opioid receptors type 2 in cultured human neuroblastoma cells without agonist activity[3] and to sigma receptors in rats.[4] Also, ketamine interacts with muscarinic receptors, descending monoaminergic pain pathways and voltage-gated calcium channels.[5] At subanesthetic and fully anesthetic doses, ketamine has been found to block serotonin depletion in the brain by inhibiting 5-HT receptors rather than through monoamine oxidase inhibition.[6]

Subjective effects

The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. These effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances of inducing a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include serious injury or death.

Physical effects

Visual effects

Experience reports

Anecdotal reports which describe the effects of this compound within our experience index include:

Additional experience reports can be found here:

Medical uses

Novel antidepressant

It has been demonstrated that ketamine, even if taken in small doses, is effective for patients suffering from chronic depression and bipolar disorder. Studies have shown[7][8] that the effect of the drug is immediate or within 2 hours and consistent in relieving a patient’s depressive and/or suicidal symptoms, lasting up to 3 days after a single dose. In comparison, common antidepressants such as Prozac, are entirely ineffective for 40% of the population and can take weeks to show effects. This gives ketamine the potential to become an indispensable tool in the treatment of depression and bipolar disorder, which is currently being held back by institutionalized drug prohibition.

Ketamine is a racemate that comprises the R-(−)-ketamine enantiomer (arketamine) and the S-(+)-ketamine enantiomer (esketamine). Esketamine inhibits the reuptake of the dopamine transporter about 8-fold more potently than does arketamine, and so is about 8 times more potent as a dopamine reuptake inhibitor.[9] Arketamine appears to be more effective as a rapid-acting antidepressant than esketamine.[10]

A study conducted in mice found that ketamine's antidepressant activity is not caused by ketamine inhibiting NMDAR, but rather by sustained activation of a different glutamate receptor, the AMPA receptor, by a metabolite, (2R,6R)-hydroxynorketamine; as of 2017 it was unknown if this was happening in humans.[11][12] Arketamine is a AMPA receptor agonist.[13]

Psychedelic therapy

Ketamine psychedelic therapy (KPT) is used for preparation for death (thanatological, Death-Rebirth Psychotherapy)[14]

Toxicity and harm potential


This toxicity and harm potential section is a stub.

As such, it may contain incomplete or even dangerously wrong information. You can help by expanding or correcting it.
We also recommend that you conduct independent research and use harm reduction practices when using this substance.

This radar plot shows relative physical harm, social harm, and dependence of ketamine.[15]

Fatal ketamine overdoses are particularly rare, but not unheard of. However, the exact toxic dosage is unknown.

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. 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.[16]

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.[17][18]

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. 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.[19]

Urinary tract effects

According to a 2010 systematic review, 110 documented reports of irritative urinary tract symptoms from ketamine dependence exist.[20] 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).

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 corresponds 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.[21]

Dependence and abuse potential

As with other NMDA receptor antagonists, ketamine produces dependence with chronic use and has high abuse potential. When dependence has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage.

Tolerance to the main effects of ketamine develops with prolonged and repeated use|Time to full tolerance::readily develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). Ketamine presents cross-tolerance with all dissociatives, meaning that after the consumption of ketamine all dissociatives will have a reduced effect.

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

Dangerous interactions

Although many psychoactive substances are safe to use on their own, they can quickly become dangerous or even life-threatening when combined with other substances. The following lists some known dangerous combinations, but may not include all of them. A combination that appears to be safe in low doses can still increase the risk of injury or death. Independent research should always be conducted to ensure that a combination of two or more substances is safe to consume.

  • Stimulants - Both stimulants and dissociatives carry the risk of adverse psychological reactions like anxiety, mania, delusions and psychosis and these risks are exacerbated when the two substances are combined.
  • Depressants - Because both depress the respiratory system, this combination can result in an increased risk of suddenly falling unconscious, vomiting and choking to death from the resulting suffocation. If nausea or vomiting occurs, users should attempt to fall asleep in the recovery position or have a friend move them into it.

Legal status

  • Australia: Ketamine is a Schedule IV drug in Australia.[citation needed]
  • Austria: Ketamine is legal for medical and veterinary use and illegal when sold or possessed without a prescription under the NPSG (Neue-Psychoaktive-Substanzen-Gesetz Österreich).[citation needed]
  • Belgium: Ketamine is legal for medical and veterinary use and illegal when sold or possessed without a prescription.[citation needed]
  • Brazil: Ketamine is legal for veterinary use and illegal when sold or possessed for human use.[citation needed]
  • Canada: Ketamine is a Schedule I drug.[22]
  • China: Ketamine is a Schedule II drug.[citation needed]
  • Czech Republic: Ketamine is legal for medical and veterinary use and illegal when sold or possessed without a prescription.[citation needed]
  • Denmark: Ketamine is legal for medical and veterinary use and illegal when sold or possessed without a prescription.[citation needed]
  • France: Ketamine is a Schedule IV drug in France.[citation needed]
  • Germany: Ketamine is legal for medical and veterinary use and illegal when sold or possessed without a prescription.[citation needed]
  • Hong Kong: Ketamine is a Schedule I drug in Hong Kong.[citation needed]
  • Malaysia: Ketamine is illegal to sell and possess in Malaysia.[citation needed]
  • Mexico: Ketamine is a Category 3 drug in Mexico.[citation needed]
  • New Zealand: Ketamine is a Class C drug in New Zealand.[citation needed]
  • Norway: Ketamine is a Class A drug in Norway.[citation needed]
  • Singapore: Ketamine is a Class A drug in Singapore.[citation needed]
  • Slovakia: Ketamine is a Schedule II drug in Slovakia.[citation needed]
  • South Korea: Ketamine is illegal to possess and sell in South Korea.[citation needed]
  • Sweden: Ketamine is a Schedule IV drug in Sweden.[citation needed]
  • Taiwan: Ketamine is a Schedule III drug in Taiwan.[citation needed]
  • United Kingdom: Ketamine is a Class B drug in the United Kingdom.[23]
  • United States: Ketamine is a Schedule III drug in the United States.[citation needed]

See also

External links



  • Durieux, M., & Kohrs, R.T. (1998). Ketamine: teaching an old drug new tricks. Anesthesia and A nalgesia, 87 5, 1186-93. PMID: 9806706
  • Mion, G. (2017). History of anaesthesia: The ketamine story–past, present and future. European Journal of Anaesthesiology (EJA), 34(9), 571-575.
  • Krystal, J. H., Karper, L. P., Seibyl, J. P., Freeman, G. K., Delaney, R., Bremner, J. D., . . . Charney, D. S. (1994). Subanesthetic effects of the noncompetitive NMDA antagonist, ketamine, in humans: Psychotomimetic, perceptual, cognitive, and neuroendocrine responses. Archives of General Psychiatry, 51(3), 199-214.
  • Morris, H., & Wallach, J. (2014). From PCP to MXE: A comprehensive review of the non-medical use of dissociative drugs. Drug Testing and Analysis, 6(7–8), 614–632.


  1. 1.0 1.1 Mion, G. (2017). History of anaesthesia: The ketamine story–past, present and future. European Journal of Anaesthesiology (EJA), 34(9), 571-575.
  2. WHO Model List of Essential Medicines |
  3. Interaction of ketamine with μ2 opioid receptors in SH-SY5Y human neuroblastoma cells |
  4. putative sigma1 receptor antagonist NE-100 attenuates the discriminative stimulus effects of ketamine in rats |
  5. Pharmaceutical Society of Australia. "2.1.1 IV general anaesthetics". Australian Medicines Handbook. 2011. Australian Medicines Handbook Pty Ltd. p. 13.
  6. Ketamine inhibits serotonin uptake in vivo. ( / NCBI) |
  7. Ketamine Improves Bipolar Depression Within Minutes -
  8. Could A Club Drug Offer 'Almost Immediate' Relief From Depression? -
  9. Nishimura, M., & Sato, K. (1999). Ketamine stereoselectively inhibits rat dopamine transporter. Neuroscience Letters, 274(2), 131-134. PMID: 10553955.
  10. Zhang JC, Li SX, Hashimoto K (2014). "R (-)-ketamine shows greater potency and longer-lasting antidepressant effects than S (+)-ketamine". Pharmacol. Biochem. Behav. 116: 137–41. doi:10.1016/j.pbb.2013.11.033. PMID 24316345. 
  11. Tyler, M. W., Yourish, H. B., Ionescu, D. F., & Haggarty, S. J. (2017). Classics in Chemical Neuroscience: Ketamine. ACS Chemical Neuroscience.
  12. Zanos, P., Moaddel, R., Morris, P. J., Georgiou, P., Fischell, J., Elmer, G. I., ... & Dossou, K. S. (2016). NMDAR inhibition-independent antidepressant actions of ketamine metabolites. Nature, 533(7604), 481-486.
  13. Yang, C., Zhou, W., Li, X., Yang, J., Szewczyk, B., Pałucha-Poniewiera, A., ... & Nowak, G. (2012). A bright future of researching AMPA receptor agonists for depression treatment. Expert opinion on investigational drugs.
  15. Development of a rational scale to assess the harm of drugs of potential misuse (ScienceDirect) |
  16. "Addiction Users Study: Consequences of chronic ketamine self-administration upon neurocognitive function and psychological well-being: a 1-year longitudinal study -
  17. Low concentrations of ketamine initiate dendritic atrophy of differentiated GABAergic neurons in culture (ScienceDirect) |
  18. Neuroprotective NMDA antagonists: the controversy over their potential for adverse effects on cortical neuronal morphology ( / NCBI) |
  19. Chronic ketamine exposure induces permanent impairment of brain functions in adolescent cynomolgus monkeys |
  20. Ketamine-induced vesicopathy: a literature review |
  21. Ketamine use: a review |
  22. Controlled Drugs and Substances Act of Canada
  23. Drugs penalties, GOV.UK, 3 September 2016. Retrieved on 25 November 2017.