 |
This page has not been fully approved by the PsychonautWiki administrators. It may contain incorrect information, particularly with respect to dosage, duration, subjective effects, toxicity and other risks. It may also not meet PW style and grammar standards. |
Fatal overdose may occur when opiates are combined with other depressants such as benzodiazepines, barbiturates, gabapentinoids, thienodiazepines, alcohol or other GABAergic substances.[1]
It is strongly discouraged to combine these substances, particularly in common to heavy doses.
| Tilidine | |||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
.svg) |
|||||||||||||||||||||||||||||||||
| Chemical Nomenclature | |||||||||||||||||||||||||||||||||
| Common names | Tilidine, Tilidin, Darby, Valoron, Generika | ||||||||||||||||||||||||||||||||
| Substitutive name | Tilidin | ||||||||||||||||||||||||||||||||
| Systematic name | (E)-2-(Dimethylamino)- 1-phenyl-cyclohex-3-en- 1-carbonsäureethylester | ||||||||||||||||||||||||||||||||
| Routes of Administration | |||||||||||||||||||||||||||||||||
|
|||||||||||||||||||||||||||||||||
| Interactions | |||||||||||||||||||||||||||||||||
| Summary sheet: Tilidine |
Tilidine (known under brand names including Valoron, Valtran, Tilicomp) is a synthetic opioid analgesic. Tilidine is mainly used in some European countries such as Germany, Belgium, Luxembourg, Switzerland and also South Africa. As is the case with other opioids, it is also commonly used as a recreational drug.[citation needed]
Pharmacology
Tilidine itself is only a weak µ-opioid agonist. Its pharmacological activity when administered is mediated by its active major metabolite nortilidine, which is further metabolised to the also active bisnortilidine. Tilidine is therefore a prodrug. The demethylation of tilidine to nortilidine and bisnortilidine occures in the liver and is catalysed by the Cytochrome P450 family of enzymes, mainly by CYP3A4 CYP2D6 and CYP2C19. [2]
Subjective effects
 |
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 ☠.
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. |
Lethal dosage
Death with as little as 750 mg has been reported, in combination with barbiturates.
Dangerous interactions
| |
This dangerous interactions section is a stub. As such, it may contain incomplete or invalid information. You can help by expanding upon or correcting it. |
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[3]. 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[3]. 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.
See also
External links
References
- ↑ Risks of Combining Depressants - TripSit
- ↑ J. Weiss, E. Sawa, K.-D. Riedel, W. E. Haefeli, G. Mikus: In vitro metabolism of the opioid tilidine and interaction of tilidine and nortilidine with CYP3A4, CYP2C19, and CYP2D6. In: Naunyn-Schmiedeberg’s Arch. Pharmacol. 378, 2008, S. 275–282, doi:10.1007/s00210-008-0294-7.
- ↑ 3.0 3.1 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.