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This substance is extraordinarily potent (i.e. active in the microgram range), to the point that the pure powder can result in a fatal overdose if spilled on one's skin. For this reason, it should never be eyeballed. Sufentanil can also be fatal when combined with depressants such as opiates, benzodiazepines, barbiturates, gabapentinoids, thienodiazepines or other GABAergic substances.[1]

It is strongly encouraged to wear gloves while handling, use volumetric dosing combined with a milligram scale, and to not consume either moderate or heavy dosages of other depressants in combination with this drug.

Summary sheet: Sufentanil
Chemical Nomenclature
Common names Sufentanil, sufentanyl, Sufenta, Chronogesic,
Systematic name N-[4-(Methoxymethyl)-1-(2-thiofuran-2-ylethyl)-4-piperidyl]-N-phenylpropanamide
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 0.1 μg
Light 1 - 5 μg
Common 5 - 10 μg
Strong 10 - 25 μg
Heavy 25 μg +
Onset 1 - 2 minutes
Peak 5 - 10 minutes
After effects 1 - 12 hours

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

Sufentanil, also known as sufentanyl and by the brand name Sufenta, is an extremely potent synthetic anilidopiperidine opioid analgesic. Sufentanil has a rapid onset and short mechanism and is used medically as an analgesic in surgical procedures or for the management of post-operative pain. Sufentanil is roughly 500 to 1,000 times more potent than pharmaceutical grade morphine and is approximately 10 times more potent than pharmaceutical grade fentanyl. The subjective effects of sufentanil are similar to those of heroin, with the exception that many users report a significantly less euphoric "high" associated with the drug and stronger respiratory depression, sedation and pain relief. Sufentanil is the most potent opioid analgesic currently used in human medicine.


Sufentanil is synthetic anilidopiperidine that is similar in structure to both fentanyl and acetylfentanyl. One of the key differences is that one of the phenyl groups in sufentanil has been replaced with a thiophene or thiofuran group. Thiophene groups can typically replace phenyl groups without a significant drop in potency. The empirical formula of sufentanil is C22H30N2O2S and has a molar mass of 386.552 grams per mole.

Sufentanil Citrate Injection, is an opioid agonist, available as a solution containing 50 mcg/mL eq. of Sufentanil base, adjusted to pH 3.5 to 6.0. The chemical name is N-[4-(methyoxymethyl)-1-[2-(2-thienyl)ethyl]-4-piperidinyl]-N-phenylpropanamide: 2-hydroxy-1,2,3-propanetricarboxylate (1:1). The molecular weight is 578.68. Sufentanil Citrate Injection, is a sterile, non-pyrogenic, preservative free aqueous solution for intravenous or epidural injection.[2]


The recreational effects of sufentanil 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 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. Like endorphins, sufentanil is an extremely potent μ-opioid agonist. Sufentanil has an extremely short biological half life of only 162 minutes.

Because of its extremely high potency, it is often used in surgery and post-operative pain management for patients that are heavily opioid dependent/opioid tolerant because of long term opiate use for chronic pain or illicit opiate use. Currently sufentanil is the most potent opioid painkiller available for use in humans. Although more potent narcotic pain medications do exist, all medications stronger than sufentanil are approved for veterinary use only. It is also used in surgery and postoperative pain control in patients that are taking high dose buprenorphine for chronic pain because it is the only opioid that has a potency and binding affinity strong enough to displace buprenorphine from the opioid receptors in the central nervous system and provide analgesia.[3]

Subjective effects

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), a research literature based on anecdotal reports and the personal experiences of PsychonautWiki contributors. As a result, they should be regarded with a healthy degree of skepticism. It is 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 much more likely with higher doses and may include addiction, serious injury, or death.

Physical effects

Cognitive effects

Toxicity and harm potential

Recreational use of sufentanil by individuals without opioid tolerance is extremely dangerous due to its potency. It is potentially fatal at heavy dosages and even those with opiate tolerances are at high risk for overdoses. Once the sufentanil 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 sufentanil 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 sufentanil at appropriate dosages does not cause many long-term complications other than dependence and constipation. Outside of the extremely powerful addiction and physical dependence, the harmful or toxic aspects of opioid usage are exclusively associated with not taking the necessary precautions in regards to its administration, overdosing and using impure products.

It is important to consider that particular care must be taken with sufentanil due to its extreme potency and ability to be absorbed through the skin. This means that simply unintentionally spilling a very small amount of sufentanil on one's skin could result in a fatal overdose.

Heavy dosages of sufentanil 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 receptors proportional to the dosage consumed.

Sufentanil 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 has been noted that naloxone is not very effective for the management of opioid overdoses in cases where extremely potent opioids like sufentanil have been used. In the case of sufentanil, naltrexone should be used in case of an overdose.

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

Tolerance and addiction potential

As with other opioids, the chronic use of sufentanil 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 sufentanil 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. It is unknown how long it takes for sufentanil tolerance to decrease to baseline (no distinguishable tolerance). Sufentanil presents cross-tolerance with all other opioids, meaning that after the consumption of sufentanil 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.[4] 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.[5]

Dangerous interactions

Although many psychoactive substances are reasonably safe to use on their own, they can suddenly become dangerous or even life-threatening when combined with other substances. The following list includes some known dangerous combinations (although it is not guaranteed to include all of them). Independent research (e.g. Google, DuckDuckGo) should always be conducted 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[6]. 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[6]. 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


This legality section is a stub.

As such, it may contain incomplete or wrong information. You can help by expanding it.

  • Germany: Sufentanil is a controlled substance under Anlage III of the BtMG. It can only be prescribed on a narcotic prescription form.[8]
  • Russia: Sufentanil is a Schedule II controlled substance.[9]
  • Switzerland: Sufentanil is a controlled substance specifically named under Verzeichnis A. Medicinal use is permitted.[10]
  • United States: Sufentanil is classified as a Schedule II Controlled Substance under the Controlled Substances Act.[11]

See also

External links


  1. Risks of Combining Depressants (Tripsit) |
  3. "Fentanyl Citrate - Drug Summary".
  4. Why Heroin Relapse Often Ends In Death - Lauren F Friedman (Business Insider) |
  5. Siegel, S., Hinson, R., Krank, M., & McCully, J. (1982). Heroin “overdose” death: contribution of drug-associated environmental cues. Science, 216(4544), 436–437.
  6. 6.0 6.1 [1]
  7. 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. 
  9. Постановление Правительства РФ от 01.10.2012 N 1002 (ред. от 09.08.2019) |
  10. "Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien" (in German). Bundeskanzlei [Federal Chancellery of Switzerland]. Retrieved January 1, 2020. 
  11. Controlled Drugs |