|Summary sheet: Ketobemidone|
|Common names||Cliradon, Cymidon, Ketogan, Ketorax|
|Routes of Administration|
Ketobemidone (also known by the brand names Ketogan, and Ketorax) is an opioid substance of the piperidine class. It belongs to a group of synthetic opioids. The mechanism of action involves binding activity at opioid receptors.
It is commonly prescribed to treat severe pain (i.e. cancer pain, postoperative pain, gallstone pain, and kidney pain). It is marketed in Denmark, Iceland, Norway and Sweden for this purpose.
Subjective effects include sedation, pain relief, muscle relaxation, compulsive redosing, and euphoria. Its effectiveness against pain is in the same range as morphine, and it also has some NMDA-antagonist properties imparted, in part, by its metabolite norketobemidone.
It has high abuse potential comparable to that of morphine. Chronic use is associated with psychological dependence and addiction. It is highly advised to use harm reduction practices if using this substance.
History and culture
Ketobemidone was first synthesized during World War II by German scientists at the I.G. Farbenindustrie laboratory in Höchst, 1942. The first study of it in humans was published in 1946, and it was introduced in clinical medicine shortly after.
Today, Pfizer produces ketobemidone under the brand names Ketogan and Ketorax in tablet and suppository form as well as injection liquids.
Ketobemidone's substitutive name is is 1-methyl-4-(3-hydroxyphenyl)-4-propionylpiperidine. The substance is primarily available as a white, powdered hydrochloride salt.
The synthesis occurs by alkylating (3-methoxyphenyl)acetonitrile with bis(2-chloroethyl)methylamine, followed by a reaction with ethylmagnesium bromide, and finally O-demethylation with hydrobromic acid.
Ketobemidone is metabolized in the liver by N-demethylation, ringhydroxylation, O-methylation, and O-conjugation. The principal phase 1 reaction is N-demethylation, and it is also metabolized by conjugation of the phenolic hydroxyl group. Primary metabolites of ketobemidone are norketobemidone, 4'-hydroxyketobemidone, and hydroxymethoxyketobemidone. The metabolites' pharmacological activity is unknown.
The elimination half-life of ketobemidone is 2 to 2.5 hours for both intravenous and oral administration. Analgesia after 5-10 mg orally or 5-7.5 mg intravenously lasts 3–5 hours. Ketobemidone is also available in preparations with a spasmolytic, which can improve the analgesia.
|This subjective effects section is a stub.|
As such, it is still in progress and may contain incomplete or wrong information.
You can help by expanding or correcting it.
Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.
It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.
- Cognitive euphoria
- Anxiety suppression
- Irritability - While opioids are well known for their ability to improve mood, they can also have the paradoxical effect of increasing the user's sensitivity to irritable stimuli. This can manifest as aloofness and sudden outbursts of anger and aggression (colloquially known as "opiate rage"). It appears to occur more frequently during the comedown of the experience and/or with heavy use.
- Double vision - At high doses, the eyes unfocus and re-focus uncontrollably. This creates a blurred effect and double vision that is present no matter where one focuses their eyes. This can be so intense it becomes impossible to read or drive.
- Acuity suppression
Anecdotal reports which describe the effects of this compound within our experience index include:
Additional experience reports can be found here:
Toxicity and harm potential
This toxicity and harm potential section is a stub.
As a result, it may contain incomplete or even dangerously wrong information! You can help by expanding upon or correcting it.
Dependence and abuse potential
Warning: Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).
Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.
- Alcohol - Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. Place affected patients in the recovery position to prevent vomit aspiration from excess. Memory blackouts are likely
- Amphetamines - Stimulants increase respiration rate which allows for a higher dose of opiates than would otherwise be used. If the stimulant wears off first then the opiate may overcome the user and cause respiratory arrest.
- Benzodiazepines - Central nervous system and/or respiratory-depressant effects may be additively or synergistically present. The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position blackouts/memory loss likely.
- Cocaine - Stimulants increase respiration rate, which allows for a higher dose of opiates than would otherwise be used. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest.
- DXM - Generally considered to be toxic. CNS depression, difficulty breathing, heart issues, and liver toxicity have been observed. Additionally if one takes DXM, their tolerance of opiates goes down slightly, thus causing additional synergistic effects.
- GHB/GBL - The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position
- Ketamine - 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.
- MAOIs - Coadministration of monoamine oxidase inhibitors (MAOIs) with certain opioids has been associated with rare reports of severe adverse reactions. There appear to be two types of interaction, an excitatory and a depressive one. Symptoms of the excitatory reaction may include agitation, headache, diaphoresis, hyperpyrexia, flushing, shivering, myoclonus, rigidity, tremor, diarrhea, hypertension, tachycardia, seizures, and coma. Death has occurred in some cases.
- MXE - MXE can potentiate the effects of opioids but also increases the risk of respiratory depression and organ toxicity.
- Nitrous - 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. Memory blackouts are common.
- PCP - PCP may reduce opioid tolerance, increasing the risk of overdose.
- Tramadol - Increased risk of seizures. Tramadol itself is known to induce seizures and it may have additive effects on seizure threshold with other opioids. Central nervous system- and/or respiratory-depressant effects may be additively or synergistically present.
- Grapefruit - While grapefruit is not psychoactive, it may affect the metabolism of certain opioids. Tramadol, oxycodone, and fentanyl are all primarily metabolized by the enzyme CYP3A4, which is potently inhibited by grapefruit juice. This may cause the drug to take longer to clear from the body. it may increase toxicity with repeated doses. Methadone may also be affected. Codeine and hydrocodone are metabolized by CYP2D6. People who are on medicines that inhibit CYP2D6, or that lack the enzyme due to a genetic mutation will not respond to codeine as it can not be metabolized into its active product: morphine.
Serotonin syndrome risk
- MAOIs - Such as banisteriopsis caapi, syrian rue, phenelzine, selegiline, and moclobemide.
- Serotonin releasers - Such as MDMA, 4-FA, methamphetamine, methylone and αMT.
- SSRIs - Such as citalopram and sertraline
- SNRIs - Such as tramadol and venlafaxine
This legality section is a stub.
As such, it may contain incomplete or wrong information. You can help by expanding it.
- Australia: S9 (Prohibited substance).
- Canada: Schedule I.
- Germany: Anlage II (Authorized trade only, not prescriptible).
- United States: Ketobemidone is a Schedule I substance.
- European Union: Available by prescription only
- Risks of Combining Depressants - TripSit
- Wikipedia contributors. (2021, March 28). Ketobemidone. In Wikipedia, The Free Encyclopedia. Retrieved 20:57, May 28, 2021, from https://en.wikipedia.org/w/index.php?title=Ketobemidone&oldid=1014750378
- Brayfield A, ed. (9 January 2017). "Ketobemidone Hydrochloride: Martindale: The Complete Drug Reference". MedicinesComplete. London, UK: Pharmaceutical Press.
- Ebert B, Thorkildsen C, Andersen S, Christrup LL, Hjeds H (September 1998). "Opioid analgesics as noncompetitive N-methyl-D-aspartate (NMDA) antagonists". Biochemical Pharmacology. 56 (5): 553–9. doi:10.1016/S0006-2952(98)00088-4. PMID 9783723.
- GB patent 609763, "Manufacture of piperidyl ketones", published 1948-10-06, assigned to Ciba Ltd.
- US patent 2486796, Meischer, K.; Kaegi, H., "Esters of 1-alkyl-4-hydroxyphenyl-piperidil-4-ketones", issued 1949-11-01
- William Andrew Publishing (2013). "Cetobemidone" (excerpt). Pharmaceutical Manufacturing Encyclopedia. Elsevier. ISBN 9780815518563.
- Bondesson U, Hartvig P, Danielsson B (1981). "Quantitative determination of the urinary excretion of ketobemidone and four of its metabolites after intravenous and oral administration in man". Drug Metabolism and Disposition. 9 (4): 376–80. PMID 6114838.
- Ershad, M., Cruz, M. D., Mostafa, A., Mckeever, R., Vearrier, D., Greenberg, M. I. (March 2020). "Opioid Toxidrome Following Grapefruit Juice Consumption in the Setting of Methadone Maintenance". Journal of Addiction Medicine. 14 (2): 172–174. doi:10.1097/ADM.0000000000000535. ISSN 1932-0620.
- Gillman, P. K. (2005). "Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity". British Journal of Anaesthesia. 95 (4): 434–441. doi: . eISSN 1471-6771. ISSN 0007-0912. OCLC 01537271. PMID 16051647.