Ketobemidone

Fatal overdose may occur when opiates are combined with other depressants such as benzodiazepines, barbiturates, gabapentinoids, thienodiazepines, alcohol or other GABAergic substances.

It is strongly discouraged to combine these substances, particularly in common to heavy doses.

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Summary sheet: Ketobemidone

Ketobemidone
Chemical Nomenclature
Common names	Cliradon, Cymidon, Ketogan, Ketorax
Substitutive name	Ketobemidone
Systematic name	1-[4-(3-Hydroxyphenyl)-1-methyl-4-piperidyl]propan-1-one
Class Membership
Psychoactive class	Opioid
Chemical class	Piperidine
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. ⇣ Oral Dosage Bioavailability 17% - 62% Threshold 2.5 mg Light 2.5 - 5 mg Common 10 - 15 mg Strong 15 - 25 mg Heavy 25 mg + Duration Total 3 - 5.5 hours Onset 10 - 30 minutes ⇣ Rectal Dosage Bioavailability 44% Threshold 2 - mg Light 2 - 4 mg Common 7.5 - 11.5 mg Strong 11.5 - 20 mg Heavy 20 mg + Duration Total x"x" is not a number. - y"y" is not a number. hours Onset x"x" is not a number. - y"y" is not a number. minutes ⇣ Intravenous Dosage Bioavailability 100% Threshold x"x" is not a number. - mg Light x"x" is not a number. - y"y" is not a number. mg Common x"x" is not a number. - y"y" is not a number. mg Strong x"x" is not a number. - y"y" is not a number. mg Heavy x"x" is not a number. mg + Duration Total 2 - 3 hours Onset 5 - 10 seconds 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.
Interactions
Stimulants
MAOIs
Nitrous
PCP
Alcohol
Benzodiazepines
DXM
GHB
GBL
Ketamine
MXE
Tramadol
Grapefruit
MAOIs
Serotonin releasers
SSRIs
5-HTP

Ketobemidone (also known by the brand names Ketogan, and Ketorax) is a synthetic opioid substance of the piperidine class. It is used to treat severe pain (like cancer pain, postoperative pain, gallstone pain, and kidney pain).

History and culture

Ketobemidone was first synthesized during World War II by German scientists at the I.G. Farbenindustrie laboratory in Höchst, 1942.

Today, Pfizer produces ketobemidone under the brand names Ketogan and Ketorax in tablet and suppository form as well as injection liquids.

Chemistry

Ketobemidone's substitutive name is is 1-methyl-4-(3-hydroxyphenyl)-4-propionylpiperidine. The substance is primarily available as a white, powdered hydrochloride salt.

Pharmacology

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.

Subjective effects

• Euphoria
• Confusion
• Sedation
• Dizziness
• Headache
• Blurred vision
• Bradycardia
• Respiratory depression
• Dry mouth
• Nausea
• Vomiting
• Constipation
• Difficulty urinating
• Decreased blood pressure

Toxicity and harm potential

Dangerous interactions

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
• Stimulants - 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.
• 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

Combinations with the following substances can cause dangerously high serotonin levels. Serotonin syndrome requires immediate medical attention and can be fatal if left untreated.

• 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
• [[Wikipedia:SNRIs|DangerousInteraction::SNRIs]] - Such as tramadol and venlafaxine
• 5-HTP

Legal status

• Australia: S9 (Prohibited substance)
• Canada: Schedule I
• Germany: Anlage II (Authorized trade only, not prescriptible)
• United States: Schedule I
• European Union: Prescription only

See also

• Responsible use
• Opioid
• Dissociative