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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: Oxycodone
Chemical Nomenclature
Common names OxyContin, Oxy, Roxicodone, Oxecta, OxyIR, Endone, Oxynor, Codilek, Oxydor, Redocam, Oxygesic, Percodan, Percocet
Substitutive name Oxycodone
Systematic name (5R,9R,13S,14S)-4,5α-epoxy-14-hydroxy-3-methoxy-17-methylmorphinan-6-one
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.

Threshold 1 mg
Light 2.5 - 10 mg
Common 10 - 25 mg
Strong 25 - 40 mg
Heavy 40 mg +
Total 4 - 6 hours
Onset 20 - 40 minutes

Threshold 1 mg
Light 2.5 - 7.5 mg
Common 7.5 - 15 mg
Strong 15 - 25 mg
Heavy 25 mg +
Total 3 - 5 hours
Onset 2 - 5 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.


Oxycodone (also known under brand names including Roxicodone, OxyContin, Percocet, Oxecta, OxyIR, Endone, Oxynorm, and OxyNEO) is a semi-synthetic opioid synthesized from poppy-derived thebaine. It is a narcotic analgesic within the morphinan chemical class and is generally indicated for relief of moderate to severe pain. It was developed in 1916 in Germany[2][3] as one of several new semi-synthetic opioids in an attempt to improve on the existing opioids.[4]

Oxycodone is available as single-ingredient medication in immediate release and controlled release. Combination products, such as Percocet, formulated with non-narcotic ingredients such as NSAIDs and paracetamol (acetaminophen) are also available.


Oxycodone, or dihydro hydroxy codeinone, is an opioid of the morphinan class. Oxycodone and other molecules of this class contain a polycyclic core of three benzene rings fused in a zig-zag pattern called a phenanthrene. A fourth nitrogen containing ring is fused to the phenanthrene at R9 and R13, with the nitrogen member looking at R17 of the combined structure. This structure is called morphinan.

Oxycodone, along with other morphinans, contains an ether bridge between two of its rings, connecting R4 and R5 through an oxygen group. It contains a carbonyl group bound at R6 and a methyl group located on the nitrogen atom at R17. The carbon-oxygen double bond of the carbonyl saturates the benzene ring it is bonded with. Thus oxycodone lacks the double bond on that ring found in codeine. Oxycodone also shares the 3-methoxy substitution found in codeine; however, it contains an additional hydroxy group at R14. Oxycodone is analogous to the other morphinans including dihydrocodeine, heroin, ethylmorphine, and codeine.


Oxycodone produces effects that are typical of μ-opioid agonists, suggesting a pharmacological similarity to more traditional opioids, such as codeine and morphine. These compounds exert their 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.

In 2006, research by a Japanese group suggested the effect of oxycodone is mediated by different receptors in different situations. Specifically in diabetic mice, the κ-opioid receptor appears to be involved in the direct pain relief caused by oxycodone,[5] while in nondiabetic mice, the μ1-opioid receptor seems to be primarily responsible for these effects.[6]


Oxycodone has 3 metabolites: noroxycodone (CYP3A4/5), oxymorphone (CYP2D6), and 6α-/6β-oxycodol (6-Ketoreduction). Of these, oxymorphone is the active one. Anywhere from 5-19% of oxycodone is metabolized to oxymorphone, the rest being mostly noroxycodone (45-70%) and 6-oxycodols (~2-14%). Grapefruit juice inhibits CYP3A4 activity, allowing more oxycodone to be metabolized into oxymorphone which potentiates oxycodone.[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

Anecdotal reports which describe the effects of this compound within our experience index include:

Additional experience reports can be found here:

Toxicity and harm potential

Oxycodone has a low toxicity relative to dose. As with all opioids, long-term effects can vary but can include diminished libido, apathy, and memory loss. It is also potentially lethal when mixed with depressants like alcohol or benzodiazepines.

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 oxycodone 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 oxycodone 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). Oxycodone presents cross-tolerance with all other opioids, meaning that after the consumption of oxycodone 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.[8] 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.[9]

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[10]. 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[10]. 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 issues

Oxycodone is subject to international conventions on narcotic drugs. In addition, oxycodone is subject to national laws that differ by country. The 1931 Convention for Limiting the Manufacture and Regulating the Distribution of Narcotic Drugs of the League of Nations included oxycodone.[11] The 1961 Single Convention on Narcotic Drugs of the United Nations, which replaced the 1931 convention, categorized oxycodone in Schedule I.[12]

  • Australia: Oxycodone is in Schedule I (derived from the Single Convention on Narcotic Drugs) of the Commonwealth's Narcotic Drugs Act 1967.[13] In addition, it is in Schedule 8 of the Australian Standard for the Uniform Scheduling of Drugs and Poisons ("Poisons Standard"), meaning it is a "controlled drug... which should be available for use but require[s] restriction of manufacture, supply, distribution, possession and use to reduce abuse, misuse and physical or psychological dependence".[14]
  • Austria: Oxycodone 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: Oxycodone is a controlled substance under Schedule I of the Controlled Drugs and Substances Act (CDSA).[15]
  • Germany: The drug is in Appendix III of the Narcotics Act (Betäubungsmittelgesetz or BtMG).[16] The law allows only physicians, dentists, and veterinarians (Ärzte, Zahnärzte und Tierärzte) to prescribe oxycodone and the federal government to regulate the prescriptions (e.g., by requiring reporting).[16]
  • Hong Kong: Oxycodone is regulated under Part I of Schedule 1 of Hong Kong's Chapter 134 Dangerous Drugs Ordinance.[17]
  • Russia: Oxycodone is a Schedule II controlled substance.[18]
  • Singapore: Oxycodone is listed as a Class A drug in the Misuse of Drugs Act of Singapore, which means offences in relation to the drug attract the most severe level of punishment. A conviction for unauthorized manufacture of the drug attracts a minimum sentence of 10 years of imprisonment and corporal punishment of five strokes of the cane, and a maximum sentence of life imprisonment or 30 years of imprisonment and 15 strokes of the cane.[19] The minimum and maximum penalties for unauthorized trafficking in the drug are respectively five years of imprisonment and five strokes of the cane, and 20 years of imprisonment and 15 strokes of the cane.[20]
  • Switzerland: Oxycodone is a controlled substance specifically named under Verzeichnis A. Medicinal use is permitted.[21]
  • Turkey: Oxycodone is a 'red prescription' only substance[22] and illegal when sold or possessed without a prescription.[citation needed]
  • UK: Oxycodone is a Class A drug under the Misuse of Drugs Act.[23]
  • USA: Oxycodone is a Schedule II controlled substance.[24]

See also

External links


  1. Risks of Combining Depressants - TripSit 
  2. Publication of DE296916C 
  3. Sneader, W. (2005). Drug discovery: a history. Wiley. ISBN 9780471899792. 
  4. Kalso, E. (May 2005). "Oxycodone". Journal of Pain and Symptom Management. 29 (5 Suppl): S47–56. doi:10.1016/j.jpainsymman.2005.01.010. ISSN 0885-3924. 
  5. Nozaki, C., Saitoh, A., Kamei, J. (27 March 2006). "Characterization of the antinociceptive effects of oxycodone in diabetic mice". European Journal of Pharmacology. 535 (1): 145–151. doi:10.1016/j.ejphar.2006.02.002. ISSN 0014-2999. 
  6. Nozaki, C., Kamei, J. (10 April 2007). "Involvement of μ1-opioid receptor on oxycodone-induced antinociception in diabetic mice". European Journal of Pharmacology. 560 (2): 160–162. doi:10.1016/j.ejphar.2007.01.021. ISSN 0014-2999. 
  7. Nieminen, Tuija H., et al. “Grapefruit juice enhances the exposure to oral oxycodone.” Basic & Clinical Pharmacology & Toxicology, vol. 107, no. 4, 2010, pp. 782–788, https://doi.org/10.1111/j.1742-7843.2010.00582.x.
  8. Why Heroin Relapse Often Ends In Death - Lauren F Friedman (Business Insider) | http://www.businessinsider.com.au/philip-seymour-hoffman-overdose-2014-2
  9. Siegel, 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. 
  10. 10.0 10.1 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. 
  11. VI.8a Convention for limiting the Manufacture and regulating the Distribution of Narcotic Drugs. Geneva, 13 July 1931 | https://treaties.un.org/doc/Treaties/1931/07/19310713%2006-44%20AM/Ch_VI_8_ap.pdf
  12. "United Nations conference for the adoption of a single convention on narcotic drugs. Final act | https://treaties.un.org/doc/Treaties/1964/12/19641213%2002-14%20AM/Ch_VI_15p.pdf
  13. Narcotic Drugs Act 1967 
  14. http://www.comlaw.gov.au/ComLaw/Legislation/LegislativeInstrument1.nsf/0/3BBB39C4645284BCCA2574A6001C711F/$file/PoisonsStandard2008.pdf
  15. Branch, L. S. (2022), Consolidated federal laws of Canada, Controlled Drugs and Substances Act 
  16. 16.0 16.1 BtMG - Gesetz über den Verkehr mit Betäubungsmitteln 
  17. CAP 134 DANGEROUS DRUGS ORDINANCE Schedule 1 (Replaced 62 of 1994 s. 9) 
  18. Постановление Правительства РФ от 01.10.2012 N 1002 (ред. от 09.08.2019) 
  19. http://statutes.agc.gov.sg/aol/search/display/view.w3p;page=0;query=DocId%3Ac13adadb-7d1b-45f8-a3bb-92175f83f4f5%20Depth%3A0%20Status%3Ainforce;rec=0
  20. Misuse of Drugs Act (Singapore), section 5(1).
  21. "Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien" (in German). Bundeskanzlei [Federal Chancellery of Switzerland]. Retrieved January 1, 2020. 
  22. KIRMIZI REÇETEYE TABİ İLAÇLAR | https://www.titck.gov.tr/storage/Archive/2019/contentFile/K%C4%B1rm%C4%B1z%C4%B1%20Re%C3%A7eteye%20Tabi%20%C4%B0la%C3%A7lar%2005072019_ebcc7e92-6661-4983-870a-fe8983a9c2b7.pdf
  23. Drugs licensing 
  24. http://www.deadiversion.usdoj.gov/schedules/