Ketamine - PsychonautWiki


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.

Bioavailability 17%[2]
Threshold 50 mg
Light 50 - 100 mg
Common 100 - 300 mg
Strong 300 - 450 mg
Heavy 450 mg+
Onset 10 - 30 minutes
Come up 5 - 20 minutes
Peak 45 - 90 minutes
Offset 3 - 6 hours
After effects 4 - 8 hours

Bioavailability 20%[3] - 29%[4]
Bioavailability 45%[3]
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
Peak 30 - 60 minutes[1]
Offset 3 - 6 hours
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, and others) is a classical dissociative substance of the arylcyclohexylamine class. It is the most well-known and widely-used among the dissociatives, a diverse group that includes phencyclidine (PCP), methoxetamine (MXE), dextromethorphan (DXM), and nitrous oxide. It produces its main effects by binding to and blocking the NMDA receptor; however, its precise mechanism is poorly understood and the subject of ongoing research.

Ketamine was developed in 1963 by Parke-Davis Laboratories as a replacement for the surgical anesthetic phencyclidine (PCP). It is widely used in human and veterinary medicine, typically in surgical and intensive care settings. Recently, it has become the subject of significant clinical research due to the discovery that it can rapidly relieve treatment-resistant depression and suicidal ideation.[5] Recreational use is associated with electronic dance music and the club and rave scenes.[citation needed]

Subjective effects include sedation, motor control loss, pain relief, internal hallucinations, conceptual thinking, euphoria, and dissociation. Dissociation is a complex mental state characterized by perceptual distortions and feelings of detachment from the environment and one's self. Ketamine's effects are similar to dissociatives like PCP and DXM but with a shorter duration and rapid onset. The effects of ketamine are highly dose-dependent: at lower doses, users report alcohol-like disinhibition and relaxation effects while higher doses exceeding a certain threshold are capable of inducing a trance-like state (called a "k-hole") that is commonly described as an out-of-body or near-death experience.

Ketamine is considered to have moderate to high abuse potential. Chronic use is associated with escalating tolerance and psychological dependence. Additionally, the physical health effects of chronic use are not well-known. There is growing evidence that chronic use causes bladder and urinary tract dysfunction.[6] Additionally, chronic use has been linked with cognitive impairment which may indicate neurotoxicity.[7][8] There is also some evidence that it may function as an antibiotic.[9] As a result, it is highly advised to use harm reduction practices if using this substance.

History and culture

Ketamine was first synthesized at Parke Davis Laboratories by the American scientist Calvin Stevens. Stevens was searching for a new anesthetic to replace PCP, which was deemed not suitable for use in humans because of the severe hallucinogenic effects it produced upon recovery of consciousness.[citation needed]

Ketamine began its life 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. Due to its sympathomimetic properties and its wide margin of safety, it was administered as a field anaesthetic to soldiers during the Vietnam War.[10]

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.[11]


Street names include "Special K", "K", "Kit Kat", "kitty", and "horse/dog/cat tranquilizer" (which refers to its use in veterinary medicine), "Cat Valium", and "Jet".[12]


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 mixture of equal amounts of two enantiomers: esketamine and arketamine. Esketamine is a more potent NMDA receptor antagonist and dissociative hallucinogen than arketamine.[13] Because of 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 sufficient effectiveness for depression.[14] 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 a potent alpha-7 nicotinic receptor antagonist may have antidepressive action.[14]


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[15] and to sigma receptors in rats.[16] Also, ketamine interacts with muscarinic receptors, descending monoaminergic pain pathways and voltage-gated calcium channels.[17] 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.[18]

The estimated bioavailability of rectal ketamine is about 25%[19], oral ketamine is about 17% while nasal ketamine is 45%.

Subjective effects

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), a research literature based on collected anecdotal reports and the personal experiences of PsychonautWiki contributors. As a result, they should be regarded with a healthy degree of skepticism. It is worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce a full spectrum of effects. Likewise, adverse effects become much more likely with higher doses and may include addiction, serious injury, or death ☠.

Physical effects

Visual effects

Cognitive effects

Disconnective effects

Multi-sensory effects

Transpersonal effects

Experience reports

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

Additional experience reports can be found here:


Novel antidepressant

Ketamine has been shown to be effective for patients suffering from chronic depression and bipolar disorder. Studies have shown[20][21] 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 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.[22] Arketamine appears to be more effective as a rapid-acting antidepressant than esketamine.[23]

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.[24][25] Arketamine is a AMPA receptor agonist.[26]

Anesthetic doses may not produce an antidepressant effect. While the research is limited, between .5 and 1mg/kg IV given over about 40 mins seems to be the optimal dose. [27] A typical anesthetic dose is 1-2 mg/kg given over 2 minutes, followed by .5-1.8mg/kg/hr. Benzodiazepines and GABA agonist (both of which are often used alongside ketamine in anesthesia) may mitigate the antidepressant effect of ketamine.

Reagent results

Exposing compounds to the reagents gives a colour change which is indicative of the compound under test.

Marquis Mecke Mandelin Liebermann Froehde Gallic Robadope
No reaction No reaction Deep brownish orange/red Light yellow No reaction No reaction No reaction
Ehrlich Hofmann Simon’s Zimmermann Scott Folin
No reaction No reaction Orange - Pink - Yellow Slow pink No reaction No reaction

Toxicity and harm potential

This radar plot shows relative physical harm, social harm, and dependence of ketamine.[28]

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. 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.[29]

Urinary tract effects

According to a 2010 systematic review, 110 documented reports of irritative urinary tract symptoms from ketamine dependence exist.[30] 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.[31]

A study conducted in 2015 demonstrated that co-administration of EGCG (10mM/kg) in rats receiving 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).[32]


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.[33][34]

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.[35]

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.

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. 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 if using this substance.


Dissociatives are reported to be unique from other substances because they produce a long-term or permanent form of tolerance ("permatolerance") that accrues slowly and independently from normal tolerance. Many long-term or heavy ketamine users report that they need to take substantially more to achieve dissociation or k-hole compared to their first use, even after taking extended breaks. It is unknown why or how this occurs, although it has been suggested to be a potential indicator of some form of neurotoxicity. Dissociative permatolerance can pose an additional problem considering the negative effects of large doses on the urinary tract. As a result, heavy or chronic use of all dissociatives is strongly discouraged.


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

Dangerous interactions

Although many psychoactive substances are reasonably safe to use on their own, they can suddenly become dangerous or even life-threatening when combined with other substances. The following list includes some known dangerous combinations (although it is not guaranteed to include all of them). Independent research (e.g. Google, DuckDuckGo) should always be conducted to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.

  • Amphetamines - No unexpected interactions, though likely to increase blood pressure but not an issue with sensible doses. Moving around on high doses of this combination may be ill-advised due to risk of physical injury.
  • Cocaine - No unexpected interactions, though likely to increase blood pressure but not an issue with sensible doses. Moving around on high doses of this combination may be ill-advised due to risk of physical injury.
  • 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 not placed in the recovery position.
  • 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
  • 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.
  • GHB - 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.
  • 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.
  • 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.
  • Trazodone - When used as a sleep aid and taken close to that of a dose of ketamine, may bring a risk of respiratory depression when high amounts of each substances are consumed.
  • Tramadol
  • 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.[36] This is likely to apply to oral, sublingual, and intranasal administration.

Legal status

  • Australia: Ketamine is a Schedule 8 drug in Australia, meaning that possession, manufacture or supply without authority is illegal.[37]
  • 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 controlled under Schedule I of the Controlled Drugs and Substances Act[38]. Activities such as sale, possession or production of ketamine are illegal unless authorized for medical, scientific or industrial purposes. In Canada, ketamine has legitimate uses in medicine.[39]
  • 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 a prescription medicine, according to Anlage 1 AMVV.[40]
  • Hong Kong: Ketamine is a Schedule I drug in Hong Kong.[citation needed]
  • Luxembourg: Ketamine is a prohibited substance for recreational use.[41]
  • 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]
  • Spain: Ketamine is a Schedule IV drug in Spain.[42]
  • Sweden: Ketamine is a Schedule IV drug in Sweden.[citation needed]
  • Switzerland: Ketamine is a controlled substance specifically named under Verzeichnis B, when possessed or handled without a license. Medicinal use is permitted.[43]
  • Taiwan: Ketamine is a Schedule III drug in Taiwan.[citation needed]
  • Turkey: Ketamine is a 'green prescription' only substance[44] and illegal when sold or possessed without a prescription.[citation needed]
  • United Kingdom: Ketamine is a Class B drug in the United Kingdom.[45]
  • United States: Ketamine is a Schedule III drug in the United States.[citation needed]
  • Poland: Ketamine is illegal to possess, manufacture and sell except for medical purposes. [46]

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. "Hall D, Robinson AINTRANASAL KETAMINE FOR PROCEDURAL SEDATIONEmergency Medicine Journal 2014;31:789-790."
  2. Clements, J.A.; Nimmo, W.S.; Grant, I.S. (1982). "Bioavailability, Pharmacokinetics, and Analgesic Activity of Ketamine in Humans". Journal of Pharmaceutical Sciences. 71 (5): 539–542. doi:10.1002/jps.2600710516. ISSN 0022-3549. 
  3. 3.0 3.1 "Yanagihara, Y., Ohtani, M., Kariya, S., Uchino, K., Hiraishi, T., Ashizawa, N., et al. (2003). Plasma concentration profiles of ketamine and norketamine after administration of various ketamine preparations to healthy Japanese volunteers. Biopharm. Drug Dispos. 24, 37–43. doi: 10.1002/bdd.336
  4. Rolan, Paul; Lim, Stephen; Sunderland, Vivian; Liu, Yandi; Molnar, Valeria (2013). "The absolute bioavailability of racemic ketamine from a novel sublingual formulation". British Journal of Clinical Pharmacology. 77 (6): 1011–1016. doi:10.1111/bcp.12264. ISSN 0306-5251. 
  5. Murrough, J. W., Perez, A. M., Pillemer, S., Stern, J., Parides, M. K., aan het Rot, M., ... & Iosifescu, D. V. (2013). Rapid and longer-term antidepressant effects of repeated ketamine infusions in treatment-resistant major depression. Biological psychiatry, 74(4), 250-256.
  6. Tsai, T. H., Cha, T. L., Lin, C. M., Tsao, C. W., Tang, S. H., Chuang, F. P., ... & Chang, S. Y. (2009). Ketamine‐associated bladder dysfunction. International journal of urology, 16(10), 826-829.
  7. Morgan, Celia J. A.; Muetzelfeldt, Leslie; Curran, H. Valerie (2010). "Consequences of chronic ketamine self-administration upon neurocognitive function and psychological wellbeing: a 1-year longitudinal study". Addiction. 105 (1): 121–133. doi:10.1111/j.1360-0443.2009.02761.x. ISSN 0965-2140. 
  8. Liang, H.J.; Lau, C.G.; Tang, A.; Chan, F.; Ungvari, G.S.; Tang, W.K. (2013). "Cognitive impairments in poly-drug ketamine users". Addictive Behaviors. 38 (11): 2661–2666. doi:10.1016/j.addbeh.2013.06.017. ISSN 0306-4603. 
  10. Mion, Georges (2017). "History of anaesthesia". European Journal of Anaesthesiology. 34 (9): 571–575. doi:10.1097/EJA.0000000000000638. ISSN 0265-0215. 
  11. WHO Model List of Essential Medicines |
  13. Hashimoto K (October 2019). "Rapid-acting antidepressant ketamine, its metabolites and other candidates: A historical overview and future perspective". Psychiatry and Clinical Neurosciences. 73 (10): 613–627. doi:10.1111/pcn.12902. PMC 6851782. PMID 31215725.
  14. 14.0 14.1 Hashimoto K (October 2019). "Rapid-acting antidepressant ketamine, its metabolites and other candidates: A historical overview and future perspective". Psychiatry and Clinical Neurosciences. 73 (10): 613–627. doi:10.1111/pcn.12902. PMC 6851782. PMID 31215725.
  15. Interaction of ketamine with μ2 opioid receptors in SH-SY5Y human neuroblastoma cells |
  16. putative sigma1 receptor antagonist NE-100 attenuates the discriminative stimulus effects of ketamine in rats |
  17. Pharmaceutical Society of Australia. "2.1.1 IV general anaesthetics". Australian Medicines Handbook. 2011. Australian Medicines Handbook Pty Ltd. p. 13.
  18. Ketamine inhibits serotonin uptake in vivo. ( / NCBI) |
  20. Ketamine Improves Bipolar Depression Within Minutes -
  21. Could A Club Drug Offer 'Almost Immediate' Relief From Depression? -
  22. Nishimura, M., & Sato, K. (1999). Ketamine stereoselectively inhibits rat dopamine transporter. Neuroscience Letters, 274(2), 131-134. PMID: 10553955.
  23. 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. 
  24. Tyler, M. W., Yourish, H. B., Ionescu, D. F., & Haggarty, S. J. (2017). Classics in Chemical Neuroscience: Ketamine. ACS Chemical Neuroscience.
  25. 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.
  26. 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.
  27. [1]
  28. Development of a rational scale to assess the harm of drugs of potential misuse (ScienceDirect) |
  29. "Addiction Users Study: Consequences of chronic ketamine self-administration upon neurocognitive function and psychological well-being: a 1-year longitudinal study -
  30. Ketamine-induced vesicopathy: a literature review |
  31. Ketamine use: a review |
  32. The protective effect of green tea catechins on ketamine-induced cystitis in a rat model
  33. Low concentrations of ketamine initiate dendritic atrophy of differentiated GABAergic neurons in culture (ScienceDirect) |
  34. Neuroprotective NMDA antagonists: the controversy over their potential for adverse effects on cortical neuronal morphology ( / NCBI) |
  35. Chronic ketamine exposure induces permanent impairment of brain functions in adolescent cynomolgus monkeys |
  36. [2]
  38. Controlled Drugs and Substances Act
  39. Heatlh Canada
  41. Règlement grand-ducal du 13 décembre 1985 modifiant l'annexe du règlement grand-ducal du 4 mars 1974 concernant certaines substances toxiques. |
  43. "Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien" (in German). Bundeskanzlei [Federal Chancellery of Switzerland]. Retrieved January 1, 2020. 
  45. Drugs penalties, GOV.UK, 3 September 2016. Retrieved on 25 November 2017.