From PsychonautWiki
Jump to navigation Jump to search
Skull and crossbones darktextred2.png

Death may occur when Acetylfentanyl is combined with depressants such as opiates, benzodiazepines, barbiturates, gabapentinoids, thienodiazepines or other GABAergic substances.[1]

It is strongly discouraged to combine either heavy or moderate dosages of these substances together.

Summary sheet: Acetylfentanyl
Chemical Nomenclature
Common names Acetylfentanyl
Systematic name N-(1-Phenethylpiperidin-4-yl)-N-phenylacetamide
Class Membership
Psychoactive class Opioid
Chemical class Anilidopiperidine
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.

Threshold 2 mg
Light 5 - 10 mg
Common 10 - 15 mg
Strong 15 - 20 mg
Heavy 20 mg +
Total 1 - 4 hours
Onset 20 - 40 minutes
Threshold 2 mg
Light 5 - 10 mg
Common 10 - 15 mg
Strong 15 - 20 mg
Heavy 20 mg +
Total 3 - 4 hours
Onset 7 - 10 minutes

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.

Serotonin releasers

Acetylfentanyl is a synthetic opioid substance of the anilidopiperidine chemical class that produces analgesic, anxiety suppressing, and euphoric effects when administered. It is a structural analog of fentanyl. Studies have estimated acetylfentanyl to be between five to fifteen times more potent than heroin, eighty times more potent than morphine, and fifteen times less potent than its parent compound, fentanyl.[2][3]

This compound has never been licensed for medical use and has only been sold as a designer drug. Acetylfentanyl was discovered at the same time as fentanyl and was rarely encountered on the illicit market in the late 1980s as it was never commonly used. However, recently in 2013, Canadian police discovered a group distributing over 3 kilograms and 12,400 pills of acetylfentanyl (equal to 117,400 doses).[citation needed]

As a μ-opioid receptor agonist, acetylfentanyl may serve as a direct substitute for heroin or other μ-opioid receptor agonist substances. The side effects of fentanyl analogs are similar to those of fentanyl itself, which include itchiness, nausea and potentially fatal respiratory depression. On the street market, fentanyl and its analogs are often misrepresented as traditional opioids like heroin due to its increased potency and substantially lower production costs. [4]

Fentanyl analogs have killed hundreds of people throughout Europe and the former Soviet republics since the most recent resurgence in use began in Estonia in the early 2000s.[5][6]

It is highly advised to use harm reduction practices such as volumetric dosing if choosing to use this substance.


Acetylfentanyl is a member of the anilidopiperidine class of synthetic opioids. Its structure features a piperidine ring bound at its nitrogen constituent RN to a phenyl ring through an ethyl chain. The opposite carbon of the piperidine ring is bonded to the nitrogen member of a acetamide group, a two carbon chain with a nitrogen constituent adjacent to a carbon bonded to a ketone oxygen. This acetamide group is also substituted with an additional phenyl ring at RN. Acetylfentanyl is a structural homologue to fentanyl, with one less carbon on its amide chain.

Acetyl fentanyl and fentanyl are in the phenylpiperidine class of synthetic opioids. Acetyl fentanyl contains a phenylacetamide group whereas fentanyl has a phenylpropanamide group at the corresponding position. Desmethyl fentanyl is a synonymous name for acetyl fentanyl, likely due to the removal of a methylene group from the structure of fentanyl.[7]


The recreational effects of this compound occur because opioids structurally mimic endogenous endorphins which are naturally found within the body and also work upon the μ-opioid receptor set. The way in which opioids structurally mimic these natural endorphins results in their physical euphoria, pain relief and anxiolytic effects. This is because endorphins are responsible for reducing pain, causing sleepiness, and feelings of pleasure. They can be released in response to pain, strenuous exercise, orgasm, or general excitement.

Acetylfentanyl's strong potency in relation to that of morphine is largely due to its high lipophilicity, which is the ability of a chemical compound to dissolve in fats, oils, and lipids. Because of this, it can more easily penetrate the central nervous system in comparison to other opioids.

Acetylfentanyl, similar to fentanyl, possesses opioid-like in vitro binding affinity to µ-opioid receptors as well as produce µ-opioid receptor agonist effects. Acetylfentanyl has also been shown to inhibit the twitch response in electrically stimulated vas deferens preparation. Similarly, in another study using tail flick and phenylquinone writhing tests, acetylfentanyl produced analgesic response in mice. Acetylfentanyl has been shown to completely suppress the signs of withdrawal in morphine-dependent monkeys. Furthermore, acetylfentanyl produce morphine-like subjective effects in drug discrimination study. Besides analgesia, fentanyl-like substances, similar to other opioid analgesics, produce a variety of pharmacological effects including alteration in mood, euphoria, drowsiness, respiratory depression, suppression of cough reflex, constriction of pupils (miosis), and impaired gastrointestinal motility.[7]

Clinical studies evaluating pharmacological effects of acetylfentanyl in humans have not been reported in the scientific literature.[7]

In acute toxicity studies in mice, the LD50 (the dose causing death of 50% of test animals) of acetylfentanyl and fentanyl are 9.3 mg/kg and 62 mg/kg, respectively. Significant bleeding in the small intestines of mice was observed in acetylfentanyl administered mice.[7]

Subjective effects

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 ☠.

Physical effects

Cognitive effects

Visual effects

Experience reports

There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:

Toxicity and harm potential

Fentanyl analogs have killed hundreds of people throughout Europe and the former Soviet republics since the most recent resurgence in use began in Estonia in the early 2000s, and novel derivatives continue to appear.[5][6][8]

The United States Drug Enforcement Administration reported in July of 2015 that at least 52 confirmed fatalities involving acetylfentanyl in the United States had occurred between 2013-2015. Ten fatalities attributed to acetylfentanyl overdose were reported during March of 2013 alone in Rhode Island. [9]

Fentanyl is potentially fatal at heavy dosages and even those with opiate tolerances are at high risk for overdoses. Once the acetylfentanyl is in the user's system, it is extremely difficult to stop its course because of the nature of absorption. Because of the extremely high strength of pure acetylfentanyl powder, it is very difficult to dilute appropriately, and often the resulting mixture may be far too strong and, therefore, very dangerous. It is also potentially lethal when mixed with depressants like alcohol or benzodiazepines.

Like most opioids, unadulterated acetylfentanyl at appropriate dosages does not cause many long-term complications other than extreme physical dependence and constipation. Outside of physical and psychological addiction, the harmful aspects of opioid usage are associated with not taking the necessary precautions in regards to its administration, overdosing on the substance and using impure products within the substance. It is important to consider that particular care must be taken with acetylfentanyl due to its extreme potency and ability to be absorbed through the skin. This means that simply unintentionally spilling a very small amount of acetylfentanyl on one's skin could result in a fatal overdose.

Heavy dosages of acetylfentanyl can result in respiratory depression, leading onto fatal or dangerous levels of anoxia (oxygen deprivation). This occurs because the breathing reflex is suppressed by agonism of μ-opioid receptor proportional to the dosage consumed.

Acetylfentanyl can also cause nausea and vomiting; a significant number of deaths attributed to opioid overdose are caused by aspiration of vomit by an unconscious victim. This is when an unconscious or semi-conscious user who is lying on their back vomits into their mouth and unknowingly suffocates. It can be prevented by ensuring that one is lying on their side with their head tilted downwards so that the airways cannot be blocked in the event of vomiting while unconscious (also known as the recovery position). In case of overdose, it is advised to administer a dose of naloxone intravenously or intramuscularly to reverse the effects of opioid agonism.

It is strongly recommended that one use harm reduction practices when using this substance.

Tolerance and addiction potential

As with other opioids, the chronic use of acetylfentanyl can be considered extremely addictive with a high potential for abuse and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and withdrawal symptoms may occur if a person suddenly stops their usage.

Tolerance to many of the effects of acetylfentanyl develops with prolonged and repeated use. The rate at which this occurs develops at different rates for different effects, with tolerance to the constipation-inducing effects developing particularly slowly for instance. 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). Acetylfentanyl presents cross-tolerance with all other opioids, meaning that after the consumption of acetylfentanyl all opioids will have a reduced effect.

The risk of fatal opioid overdoses rise sharply after a period of cessation and relapse, largely because of reduced tolerance.[10] To account for this lack of tolerance, it is safer to only dose a fraction of one's usual dosage if relapsing. It has also been found that the environment one is in can play a role in opioid tolerance. In one scientific study, rats with the same history of heroin administration were significantly more likely to die after receiving their dose in an environment not associated with the drug in contrast to a familiar environment.[11]

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
  • 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[12]. 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[12]. 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.

Legal status

In 2016, acetylfentanyl was placed under international control, in Schedule I and Schedule IV of the 1961 UN Single Convention on Narcotic Drugs.[14]

  • Austria: Acetylfentanyl is a controlled substance under the SMG.[15]
  • Canada: Acetylfentanyl is a Schedule 1 controlled substance as it is an analog of fentanyl.[16]
  • China: Acetylfentanyl is a controlled substance as of October 1, 2015.[17][15]
  • Cyprus: Acetylfentanyl is a controlled substance since 2013.[15]
  • Estonia: Acetylfentanyl is a controlled substance as of June 8, 2015.[15]
  • Finland: Acetylfentanyl is a Liite 4 (Annex 4) controlled substance as of September 28, 2015.[15]
  • Germany: Acetylfentanyl is controlled under Anlage II BtMG (Narcotics Act, Schedule II)[18] as of June 20, 2017.[19] It is illegal to manufacture, possess, import, export, buy, sell, procure or dispense it without a license.[20]
  • Ireland: Acetylfentanyl is listed in Schedule I of the Misuse of Drugs Regulation 1988.[15]
  • Latvia: Acetylfentanyl is a List I controlled substance.[15]
  • Lithuania: Acetylfentanyl is a controlled substance.[15]
  • Norway: Acetylfentanyl is controlled by the Medicines Act.[15]
  • Poland: Acetylfentanyl is controlled under new psychoactive substances control legislation.[15]
  • Russia: Acetylfentanyl is a Schedule I controlled substance.[21]
  • Sweden: Acetylfentanyl is a controlled substance as of August 18, 2015.[15]
  • Switzerland: Acetylfentanyl is a controlled substance specifically named under Verzeichnis D.[22]
  • Turkey: Acetylfentanyl is illegal in Turkey as of February 2016.[23]
  • United Kingdom: Acetylfentanyl was made a Class A controlled substance as an analogue of fentanyl in 1986.[24]
  • United States: Acetylfentanyl is a Schedule I controlled substance as of May 2015.[25] The illegality of the drug has been supported by the charges against individuals for distribution of acetylfentanyl and possession with the intent to distribute acetylfentanyl.[26] One individual was sentenced to 3 years in prison by a federal court.

See also

External links


  1. Risks of Combining Depressants - TripSit 
  2. Janssen, P. A. J., Eycken, C. A. M. van der (August 1968). Burger, A., Dekker, M., eds. "Drugs affecting the central nervous system". Journal of Pharmaceutical Sciences. 57 (8): 51–54. doi:10.1002/jps.2600570852. ISSN 0022-3549. 
  3. Higashikawa, Y., Suzuki, S. (1 June 2008). "Studies on 1-(2-phenethyl)-4-(N-propionylanilino)piperidine (fentanyl) and its related compounds. VI. Structure-analgesic activity relationship for fentanyl, methyl-substituted fentanyls and other analogues". Forensic Toxicology. 26 (1): 1–5. doi:10.1007/s11419-007-0039-1. ISSN 1860-8973. 
  4. Fentanyl, CDC’s Response to the Opioid Overdose Epidemic, CDC, 2022 
  5. 5.0 5.1 Mounteney, J., Giraudon, I., Denissov, G., Griffiths, P. (July 2015). "Fentanyls: Are we missing the signs? Highly potent and on the rise in Europe". International Journal of Drug Policy. 26 (7): 626–631. doi:10.1016/j.drugpo.2015.04.003. ISSN 0955-3959. 
  6. 6.0 6.1 Ruangyuttikarn, W., Law, M. Y., Rollins, D. E., Moody, D. E. (1 May 1990). "Detection of Fentanyl and its Analogs by Enzyme-Linked Immunosorbent Assay*". Journal of Analytical Toxicology. 14 (3): 160–164. doi:10.1093/jat/14.3.160. ISSN 1945-2403. 
  7. 7.0 7.1 7.2 7.3
  8. Centers for Disease Control and Prevention (CDC) (30 August 2013). "Acetyl fentanyl overdose fatalities--Rhode Island, March-May 2013". MMWR. Morbidity and mortality weekly report. 62 (34): 703–704. ISSN 1545-861X. 
  9. Acetylfentanyl Critical Review Report (World Health Organization)|
  10. Why Heroin Relapse Often Ends In Death - Lauren F Friedman (Business Insider) |
  11. SSiegel, S., Hinson, R. E., Krank, M. D., McCully, J. (23 April 1982). "Heroin "Overdose" Death: Contribution of Drug-Associated Environmental Cues". Science. 216 (4544): 436–437. doi:10.1126/science.7200260. ISSN 0036-8075. 
  12. 12.0 12.1 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. 
  13. Gillman, P. K. (2005). "Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity". British Journal of Anaesthesia. 95 (4): 434–441. doi:10.1093/bja/aei210Freely accessible. eISSN 1471-6771. ISSN 0007-0912. OCLC 01537271. PMID 16051647. 
  14. "Control measures". European Monitoring Centre for Drugs and Drug Addiction (EMCDDA). Retrieved October 20, 2020. 
  15. 15.00 15.01 15.02 15.03 15.04 15.05 15.06 15.07 15.08 15.09 15.10 "Acetylfentanyl: EMCDDA–Europol Joint Report on a new psychoactive substance: N-phenyl-N-[1-(2-phenylethyl)piperidin-4-yl]acetamide (acetylfentanyl)" (PDF). European Monitoring Centre for Drugs and Drug Addiction. ISSN 1977-7868. Retrieved December 29, 2019. 
  16. Controlled Drugs and Substances Act : Legislative history · Schedule I · Section 16: Fentanyls 
  17. 关于印发《非药用类麻醉药品和精神药品列管办法》的通知 |
  18. "Anlage II BtMG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 18, 2019. 
  19. "Achtzehnte Verordnung zur Änderung von Anlagen des Betäubungsmittelgesetztes" (PDF). Bundesgesetzblatt Jahrgang 2017 Teil I Nr. 38 (in German). Bundesanzeiger Verlag. June 20, 2017. Retrieved December 18, 2019. 
  20. "§ 29 BtMG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 18, 2019. 
  21. Постановление Правительства РФ от 01.10.2012 N 1002 (ред. от 09.08.2019) 
  22. "Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien" (in German). Bundeskanzlei [Federal Chancellery of Switzerland]. Retrieved January 1, 2020. 
  23. "Karar Sayısı : 2016/8548" (PDF) (in Turkish). Resmi Gazete. Retrieved January 15, 2020. 
  24. The Misuse of Drugs Act 1971 (Modification) Order 1986 
  25. 80 FR 29227 - Schedules of Controlled Substances: Temporary Placement of Acetyl Fentanyl into Schedule I |
  26. Two Charged With Witness Tampering In Joint Woonsocket Police, DEA Investigation, 2015