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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.

Summary sheet: Buprenorphine
Chemical Nomenclature
Common names Buprenex, Subutex, Butrans, Cizdol, Addnok, Transtec
Systematic name (2S)-2-[(5R,6R,7R,14S)-9α-cyclopropylmethyl-4,5-epoxy-6,14-ethano-3-hydroxy-6-methoxymorphinan-7-yl]-3,3-dimethylbutan-2-ol
Class Membership
Psychoactive class Opioid
Chemical class Morphinan
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.

Bioavailability 30%[2]
Threshold <=0.3 mg
Light 1 - 2 mg
Common 2 - 4 mg
Strong 4 - 8 mg
Heavy 8mg +
Total 18 - 24 hours
Onset 40 - 80 minutes
Peak 1.5 - 2 hours
After effects 1 - 3 days
Bioavailability 48%[3]
Threshold < 0.2 mg
Light 0.2 - 0.4 mg
Common 0.4 - 0.8 mg
Strong 0.8 - 1.5 mg
Heavy 1.5 mg +
Total 8 - 14 hours
Onset 30 - 60 minutes
Peak 4 - 8 hours
After effects 1 - 3 days

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.


Buprenorphine is a semisynthetic opioid of the morphinan chemical class. It functions as a mixed partial agonist opioid receptor modulator.

At higher dosages, it is used to treat opioid addiction in opioid-dependent individuals. In lower dosages it is used to control moderate-acute pain in non-opioid-tolerant individuals and in even lower dosages it is used to control moderate chronic pain.

Buprenorphine was patented in 1965, and approved for medical use in the United States in 1981.[4] In 2017, 14.6 million prescriptions for the medication were written in the United States.[5] It is also a common medication used to treat opioid use disorders, such as addiction to heroin.[5] Buprenorphine may also be used recreationally by injection or intranasally for the high it produces.[5]


Buprenorphine is a semi-synthetic morphinan derivative of the opioid alkaloid thebaine. Like many opioids, such as codeine or hydrocodone, it is has a morphinan backbone.

Buprenorphine and other molecules of this class contain a polycyclic core of three benzene rings fused in a zig-zag pattern called phenanthrene. A fourth nitrogen containing ring is fused to the phenanthrene at R9 and R13. Buprenophine (along with other morphinans) contains an ether bridge between two of its rings, connecting the benzene and opposite cyclohexane ring through an oxygen group.

Buprenorphine is unique to human medical opioids as it contains an addition fused ring which connects to the lower cyclohexane ring at R6 and R14. This structure is called a endoethenotetrahydrooripavine backbone, often found in veterinarian opioids. It contains a hydroxy group (OH-) substituted on the benzene ring and a methoxy group bound to the lower cyclohexane ring. The backbone of buprenorphine is also substituted with a methyl cyclopropyl moeity on its amino group. Adjacent to its methoxy attachment, the cyclohexane ring is bonded to R2 of a 2-butanol chain.


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This pharmacology section is incomplete.

You can help by adding to it.

Buprenorphine acts as a partial agonist of the μ-opioid receptor with a binding affinity of K~i~ = 1.5 nM in contrast to full agonists like morphine. It also acts as an antagonist of the κ-opioid receptor with a binding affinity of K~i~ = 2.5 nM and the δ-opioid receptor with a binding affinity of K~i~ = 6.1 nM. The ratio of these binding affinities is important, if you compare morphine's binding ratio of 1:50:176 to Buprenorphine's ratio of 15:25:61, it is apparent that the side-effect profile will be much higher to Buprenorphine and μ-opioid stimulation for euphoric effects, sequentially the drug will also bind to delta and kappa opioid receptors to a comparatively high degree.

Buprenorphine exerts its effects by binding to and activating the μ-opioid receptor. This occurs 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.

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

Table from the 2010 ISCD study ranking various drugs (legal and illegal) based on statements by drug-harm experts. Buprenorphine was found to be the 19th overall most dangerous drug.[6]
A 2007 assessment of harm from recreational drug use (mean physical harm and mean dependence liability): Buprenorphine was ranked 9th in dependence, 8th in physical harm, and 11th in social harm.[7]

Buprenorphine has a low toxicity relative to dose: the ceiling dose for buprenorphine is usually between 16mg and 32mg, and anything above this will not produce an increase in respiratory depression (the primary cause of death in opioid overdose is severe respiratory depression, leading to respiratory collapse). Thus increasing the dose of buprenorphine above this level will not continue to increase risk of death in a fashion similar to other μ-opioid receptor agonists. As with all opioids, long-term effects can vary but can include diminished libido, apathy and memory loss.

Regardless of the ceiling dose, an important distinction has to be made in the dose used in opioid naive individuals and opioid experienced individuals. Even low doses in individuals with no tolerance can cause unpleasant side-effects like dizziness, loss of balance, and vomiting. Because of the long half-life of buprenorphine, these side-effects can last a long while in opioid naive individuals which creates the risk of severe dehydration from uncontrollable vomiting.

Buprenorphine is often sold under the brand name Suboxone, which also contains naloxone. Naloxone is not orally active except at higher doses, so when large amounts of Suboxone are taken, the naloxone takes effect and reverses the effects of the buprenorphine. This is done to deter abuse of Suboxone.

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 buprenorphine can be considered moderately 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 buprenorphine 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). Buprenorphine presents cross-tolerance with all other opioids, meaning that after the consumption of buprenorphine all opioids will have a reduced effect.

Precipitated withdrawal syndrome

Buprenorphine has the ability to precipitate withdrawal symptoms in opiate-dependent individuals. This is due to buprenorphine only being a partial agonist, which does not activate the receptor with the appreciable efficacy of a full agonist, as well as having a very high binding affinity for the μ-opioid receptor (Ki = 1.5nM), displacing other agonists that may still be attached when the buprenorphine is ingested.

Note: It is a common misconception that naloxone, in some buprenorphine formulations, is what causes the precipitated withdrawal syndrome to manifest. This is false, as naloxone has a lower binding than Buprenorphine, as well as being inactive through most routes of administration.

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[8]. 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[8]. 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.

Legal status


This legality section is a stub.

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

In the European Union, buprenorphine can be prescribed either alone or in combination with another substance and is approved for the treatment of opioid addiction.[9]

  • Austria: Buprenorphine is legal for medical use under the AMG (Arzneimittelgesetz Österreich) and illegal when sold or possessed without a prescription under the SMG (Suchtmittelgesetz Österreich).[citation needed]
  • Canada: Buprenorphine is a schedule I substance in Canada and is only available with a valid prescription. [10]
  • Germany: Buprenorphine is controlled under Anlage III BtMG (Narcotics Act, Schedule III)[11] as of September 1, 1984.[12] It can only be prescribed on a narcotic prescription form.
  • Netherlands: Buprenorphine a List II drug of the Opium Law, although special rules apply to its prescription and dispensation.[citation needed]
  • Russia: Buprenorphine is a Schedule II controlled substance.[13]
  • Sweden: Buprenorphine is a class IV controlled substance.[14]
  • Switzerland: Buprenorphine is a controlled substance specifically named under Verzeichnis A. Medicinal use is permitted.[15]
  • United States: Buprenorphine, either alone or in combination with naloxone (as, for example, Suboxone), is a Schedule III drug.[citation needed]
    • Prior to the approval of Suboxone in the U.S. for treating opioid addiction, the Drug Addiction Treatment Act of 2000 was passed. This law gives the Secretary of Health and Human Services the authority to grant a waiver to all physicians with appropriate training to prescribe and administer narcotics from Schedules III-V in the treatment of drug addiction. Prior to the passage of this law such authority was restricted solely to physicians working in an outpatient clinic specifically designed for treatment of addiction. The waiver, which requires the physician to undergo an 8-hour training course, initially allowed that physician to treat only 10 patients in this manner; as of 2016, this limit has been increased to 275.[16]

See also

External links


  1. Risks of Combining Depressants - TripSit 
  2. Mendelson, J., Upton, R. A., Everhart, E. T., Jacob, P., Jones, R. T. (January 1997). "Bioavailability of sublingual buprenorphine". Journal of Clinical Pharmacology. 37 (1): 31–37. doi:10.1177/009127009703700106. ISSN 0091-2700. 
  3. Eriksen, J., Jensen, N. H., Kamp-Jensen, M., Bjarnø, H., Friis, P., Brewster, D. (November 1989). "The systemic availability of buprenorphine administered by nasal spray". The Journal of Pharmacy and Pharmacology. 41 (11): 803–805. doi:10.1111/j.2042-7158.1989.tb06374.x. ISSN 0022-3573. 
  4. Fischer, J., Ganellin, C. R. (2006). Analogue-based drug discovery. Wiley-VCH. ISBN 9783527607495. 
  5. 5.0 5.1 5.2 Buprenorphine, Substance Abuse and Mental Health Services Administration, retrieved July 29, 2019 
  6. Nutt DJ, King LA, Phillips LD (November 2010). "Drug harms in the UK: a multicriteria decision analysis". Lancet. 376 (9752): 1558–1565. CiteSeerX accessible. doi:10.1016/S0140-6736(10)61462-6. PMID 21036393.  Unknown parameter |s2cid= ignored (help)
  7. Nutt D, King LA, Saulsbury W, Blakemore C (March 2007). "Development of a rational scale to assess the harm of drugs of potential misuse". Lancet. 369 (9566): 1047–1053. doi:10.1016/S0140-6736(07)60464-4. PMID 17382831.  Unknown parameter |s2cid= ignored (help)
  8. 8.0 8.1 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. 
  9. EMA (2018), Suboxone 
  10. Consolidated federal laws of Canada, Controlled Drugs and Substances Act, 2022 
  11. "Anlage III BtMG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 18, 2019. 
  12. "Erste Verordnung zur Änderung betäubungsmittelrechtlicher Vorschriften" (PDF). Bundesgesetzblatt Jahrgang 1984 Teil I Nr. 36 (in German). Bundesanzeiger Verlag. August 8, 1984. Retrieved December 18, 2019. 
  13. Постановление Правительства РФ от 01.10.2012 N 1002 (ред. от 09.08.2019) 
  14. Läkemedelsverkets föreskrifter (LVFS 1997:12) om förteckningar över narkotika, konsoliderad version t.o.m. LVFS 2010:1
  15. "Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien" (in German). Bundeskanzlei [Federal Chancellery of Switzerland]. Retrieved January 1, 2020. 
  16. Jacobs, H., The Obama administration made a change that could have a huge effect on the opioid epidemic