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Ketamine 2-(2-chlorophenyl)-2-(methylamino)cyclohexan-1-one, also known as special K, lady k, super k, vitamin K, cat tranquilizer, ket, ketaset, ketalar, kittens, kitkat, is a dissociative drug of arylcyclohexylamine class. In medicine, it is used as anesthetic agent, causes dissociative anesthesia, sedation and amnesia. A distinctive feature of ketamine is the preservation of the respiratory reflexes and the stimulation of cardiac activity. Ketamine is a racemic mixture consisting of S- and R-enantiomers and has been used in clinical practice since 1970. It is a water-soluble arylcyclohexylamine with a molecular weight of 238 g/mol and a pKa of 7.5. Ketamine, used as hydrochloride in slightly acidic water solution, sometimes includes benzethonium chloride or chlorobutanol as preservatives. The second carbon of the cyclohexane radical is asymmetric. The active enantiomer is S-ketamine. It is 3-4 times more active than its right-handed isomer.

It is most often available as a solution for parenteral administration in concentrations of 500 mg / 10 ml, 500 mg / 5 ml, 100 mg / 10 ml, 10 mg / 1 ml, 1000 mg / 10 ml, 2 mg / 1 ml, or in the form of small crystals of white or slightly yellowish colour. On the black market it is sold in the form of powder, capsules with ketamine powder or blotters, soaked with ketamine solution of a particular concentration. It has an appearance of white or almost white crystalline powder with a faint characteristic odor, soluble in water. The melting point is 262-263 degrees Celsius. It is soluble in water at a concentration of 20 g / 100 ml, easily soluble in methanol, alcohol, moderately soluble in chloroform. It can change colour to yellow and form a precipitate after prolonged exposure to light. When heated, it releases toxic vapors of chloride and nitrogen oxides. Ketamine mustn't be mixed with benzodiazepines and barbiturates in one syringe. It should be stored in a place protected from light, with an air temperature of no more than 25 degrees. Ketamine solution is usually considered expired after 3 years.


Pharmacokinetics and Pharmacodynamics.
Ketamine undergoes extensive metabolism and is initially demethylated to norketamine, a reaction that is catalyzed by cytochrome p450 CYPB6 and CYP3A4 liver enzymes. Demethylation occurs in a stereoselective manner, since 3A4 demethylates the S-enantiomer faster than the right-handed form, whereas 2B6 demethylates both enantiomers with equal efficiency and speed. Next, norketamine is metabolized into hydroxynorketamine dehydronorketamine (NHK and DHNK, respectively). CYP3A4 and CYP3A5 are responsible for the formation of 2S; 4S; 2R; 4R. The alpha phase lasts about 45 minutes with a half-life of 10 to 15 minutes and corresponds to the anesthetic effect of the drug. With intramuscular administration, bioavailability reaches 93%, and peak plasma concentrations are reached within 5-30 minutes after administration.

Oral bioavailability of ketamine is only 16-29%, and peak concentrations are reached within 20-120 minutes, which is associated with intensive liver metabolism during the first passage of the substance. Intranasal and intrarectal bioavailability ranges from 25% to 45%. Ketamine is rapidly distributed in tissues with high perfusion capacity including the brain and binds to plasma proteins from 10% to 50%, which explains a large volume of distribution of 3-5 l/kg. A single intravenous bolus injection of ketamine at a dose of 2 mg / kg leads to equal concentrations of enantiomers in plasma after 1 minute with a maximum concentration of 1800 ng / ml.


The elimination half-life is 186 minutes with intravenous administration (with a total clearance of 19.1 ml / min) and 155 minutes with intramuscular administration, with a total clearance of 23.2 ml/ min. About 85-95% of ketamine metabolites are excreted in urine, low concentrations of ketamine are excreted in bile and feces. After intravenous administration, 91% of the administered dose after distribution is excreted in urine and 3% in feces. In the central nervous system and cerebrospinal fluid, the maximum concentration is reached faster than in blood plasma. There, ketamine is distributed mainly in brainstem, while norketamine and dehydronorketamine are distributed mainly in the cerebellum and kidneys. Median lethal dose with intravenous administration in mice is 224 mg / kg, with intraperitoneal administration is 400 mg / kg.


Ketamine binds with allosteric phencyclidine site, which is situated inside of NMDAR channel, and thus uncompetitively blocks the receptor. Ketamine has relatively high binding capacity of this receptor (about 86%), and the affinity is in the range from 0.18 to 3.1 in the presence of magnesium ions. This very blockade underlies dissociative anesthetic and amnestic effects of the substance as well as its antidepressive, analgesic and psychosomatic effects. It has been proven that cognitive deficits are also associated with inhibition of this type of receptor. S-ketamine has higher binding capacity to NMDA-receptor than right-handed isomer (2,5-3 times higher). In the membrane fractions of brain cell homogenates, IC50 = 1.6-1.9. In studies using electrophysiological recordings of whole human embryonic kidney (HEK) 293T cells, transfixed with various NMDAR subunits, it was shown, that in the absence of intracellular magnesium, ketamine inhibits receptors consisting of GluN1/GluN2A, GluN2B, GluND и GluN2C. That is why the inhibition of each particular subtype of receptors depends on the concentration of intracellular magnesium. Also, ketamine inhibits HCN1 and HCN2 channels with ЕС50 = 8,2, which is associated with anaesthetic and antidepressive effects of ketamine. In high concentrations' ketamine potentiates GABA-activeated receptors, and it is also proved that ketamine has inhibitory effect on the absorption of this type of receptors with IC50=45. The functional significance of ketamine affecting these types of receptors is unclear; however, there is a theoretical explanation of the positive effect provided by this mechanism of action, which consists in leveling hallucinogenic potency when using ketamine. So, if for some genetic reasons there is a mutation of channels and ketamine affects this type of receptors more strongly, then there can be no hallucinations during anesthesia. Ketamine also binds both to muscarinic and nicotinic acetylcholine receptors (mAChR and nAChR, respectively).


There is evidence that ketamine affects DA carriers, and the affinity to D2 receptors is about 0.06-1, and the substance itself acts as an agonist of these receptors with EC50 = 0.9 M, which explains psychomimetic effects of ketamine. Binding of ketamine to 5-HT2 receptors (affinity to them is about 15) may be related to the analgesic effects of the substance and in studies, the levels of extracellular serotonin in the prefrontal cortex and in the dorsal raphe nucleus in mice are significantly increased. Finally, ketamine acts as an inhibitor of norepinephrine reuptake, however, this fact has no clinically significant effects. To this date, only one study has been published concerning the effect of ketamine metabolites on monoaminergic receptors and carriers, in which norketamine had affinity to DA. Another place of ketamine action is sigma-receptor. There are two subtypes, though it was once assumed that there is a third subtype. Ketamine binds to both of them and has affinity of IC50=15. Given the fact that the activation of this receptor is promising in the context of targeted therapy for depression treatment, it can be assumed that the study of these mechanisms will provide positive results in the search for new methods of using ketamine and its effects.


Also, ketamine effect on this type of receptors can have positive influence on neuroplasticity. There are studies that describe the effect of ketamine (in concentrations from 30 to 300 µl) on tonic suppression induction of sodium channel flow in isolated ventricular myocytes of guinea pigs. This may be one of the application points in using it as a local anesthetic, however, the concentrations required for this are much higher than normal therapeutic ones. Ketamine is an inhibitor of voltage-gated L-type calcium channels (VDCC), so, by activating АМРА-receptors, followed by increased release of brain neurotrophic factor and activation of rapamycin complex, it realizes its antidepressant effects.

Clinical effects of ketamine.
As for the desirable positive effects of recreational use of ketamine, it has a moderate or pronounced sedative effect. Extremely pronounced effects related to "spontaneous bodily sensations", with an increase in the dose, are leveled. Euphoria from ketamine use is described as slight or moderate. At high doses, general motor activity and motor skills are disrupted, proportionally the increase in dose, "Optical sliding" effects appear, dizziness, the level of anxiety decreases up to its complete absence (however, with the dose increased, anxiety level can increase as well. In some users' anxiety level can build up even when using low doses. This is an indication for discontinuation of use).


At low and medium doses, the effects of "Conceptual thinking", "Immersion enhancement", "Increased music appreciation" and "Introspection" occur. The appearance of various sound and optical illusions are also considered positive by users. "Existential self-realization" and "Spirituality enhancement" are subjective personal effects of ketamine. With ketamine used, blood pressure increases by an average of 25%, and the heart rate increases by 20%, as well as cardiac output and oxygen consumption by the myocardium. The positive inotropic effect is associated with an increase in the internal calcium flow modulated by cAMP. Ketamine can significantly increase the pressure in the pulmonary artery, pulmonary vascular resistance and intra-pulmonary shunt. Hemodynamic effects of ketamine are not dose-dependent, and repeated administration of this substance causes less or even opposite effects. It is likely that the mechanism of the changes above is due to the fact that ketamine suppresses the function of baroreceptors through the effect on the NMDA receptors of the nucleus tractus solitarii, as well as due to the sympathetic-neuronal release of norepinephrine.

Negative undesirable effects of ketamine recreational use include: pronounced sedation up to deep deafening and coma, complete loss of control over motor skills and consciousness, hypersalivation, nausea and vomiting, decreased libido, physical autonomy, impaired urination up to the complete impossibility of emptying the bladder (in some cases, cystitis, hydronephrosis, dysuria, the appearance of blood in the urine and other similar pathology associated with the urinary system, which is one of the main forms of ketamine toxicity, especially with prolonged use); there is also depersonalization and derealization, frequent déjà vu (some users attribute this symptom to positive effects), the impossibility of logical and abstract thinking, confusion, inability to focus on a specific task, short-term memory impairment (with high doses - complete retrograde amnesia), suppression of personal prejudices, psychosis, synesthesia, spatial and temporal disorientation, distortion of the sense of time, pronounced auditory and visual hallucinations (true and false).


Hallucinations are the most frequent and, at medium and high doses, are described as bright, fast-moving colorful and complex geometric patterns, or constants of shape, fractals and colors, organized or disorganized, structureless or structural, located far beyond the perception of the user's thoughts, can be accompanied by visual noise, bright flashes, images of real people, objects. When using ketamine, addiction can be developed; however, its potential is quite low and remains at the psychosomatic level without physical manifestations. Also, side effects of ketamine use include: anaphylactic reactions (rarely) and hypersensitivity reactions, anorexia (with prolonged use), delirium, "flashbulb" symptom, dysphoria, insomnia, diplopia, nystagmus, increased skeletal muscle tone and tonic-clonic seizures, increased intraocular pressure, bradycardia, arrhythmia, laryngospasm, increased frequency of respiratory movements (with induction doses).

Methods of use and doses.
  • When administered orally, ketamine doses vary from 1.5 mg/kg to 4 mg/kg. Such way of administration helps to avoid irritation of the nasal mucosa, pain. It is advisable to use capsules (if ketamine is in the form of powder). The duration of action with oral administration is on average 1-2 hours, and the onset of action gradually begins after 10-40 minutes.
  • When administered intranasally, effects manifest after 5-15 minutes and have a total duration of up to two hours (on average 1-1.5 hours). With this way of administration, it is easy to monitor and control one's condition and frequency of use. Starting (low) dose of ketamine is 0,2-0,8 mg/kg, medium dose is 0,8-1,5 mg/kg. Doses more than 1.85 mg/kg are considered as high and increase the risk of side effects, hallucinations, retrograde amnesia and loss of consciousness with respiratory depression.
  • When administered parenterally (intravenously and intramuscularly), doses start from 0.05 mg/kg and provide particular subjective feelings during ketamine trip. However, in case of increasing the dose, there is a risk of getting general anesthesia at the tip of the needle, which is characterized by retrograde amnesia and inability to recall the feeling of ketamine trip, which is why thorough titration or low starting dose are advised.

Special instructions, dangerous interactions with other substances.
Ketamine is not recommended for recreational use by people with thyroid gland diseases, kidneys, mental disorders, infectious diseases, brain tumors or contusions, chronic severe (or moderate) diseases of the cardiovascular system, lungs, liver and kidneys. When ketamine is used together with ethanol, phenothiazines, antihistamines, any sleeping pills, it may worsen the depression of the central nervous system, which increases the risk of developing central respiratory failure.


Low risk when used together with ketamine (or amplification of ketamine effects): mushrooms, LSD, DMT, DOx, NBOMes, 2C-x, 2C-Tx, aMT, 5-MeO-xxT, cannabis, MXE, PCP, N20, MDMA, Mescaline, DXM, SSRIS, caffeine.
High risk when used together with ketamine: Amphetamines, Cocaine, Benzodiazepines, MAOIs.
Extremely high risk when used together with ketamine: Alcohol, GHB/GBL, Opioids, Tramadol.

In people taking a course of hormone therapy, recreational use of ketamine in any doses is not recommended due to the high risk of increased blood pressure. In some cases, after intake of a high ketamine dose, there may be a depressive state, short-term and long-term memory impairment (including verbal and visual). This cognitive deficit recovers for some time without pharmacological therapy. Absolute contraindications for ketamine use are: severe cardiovascular diseases (for example, uncontrolled hypertension or unstable angina), uncontrolled psychosis or schizophrenia, pregnancy at any term, severe liver diseases (cirrhosis, active hepatitis of any etiology, hepatocellular carcinoma, and so on).​
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