View source for Oxycodone

{{Short description|Opioid medication}}
{{For|the naturally occurring peptide hormone|Oxytocin}}
{{Use dmy dates|date=January 2024}}
{{cs1 config|name-list-style=vanc|display-authors=6}}
{{Infobox drug
| verifiedrevid      = 464196835
| image              = Oxycodone.svg
| width              = 183
| alt                = 
| image2             = Oxycodone molecule ball.png
| width2             = 225
| alt2               = 
| caption            = 

<!-- Clinical data -->
| pronounce          = {{IPAc-en|ɒ|k|s|i|ˈ|k|oʊ|d|oʊ|n}}
| tradename          = Roxicodone, OxyContin, Endone, others
| Drugs.com          = {{drugs.com|monograph|oxycodone}}
| MedlinePlus        = a682132
| DailyMedID         = Oxycodone
| pregnancy_AU       = C
| pregnancy_AU_comment = <ref name="Drugs.com pregnancy">{{cite web |title=Oxycodone Use During Pregnancy |website=Drugs.com |date=14 October 2019 |url=https://www.drugs.com/pregnancy/oxycodone.html |access-date=12 April 2020 | archive-date=19 June 2020 |archive-url=https://web.archive.org/web/20200619114900/https://www.drugs.com/pregnancy/oxycodone.html |url-status=live }}</ref>
| pregnancy_category = 
| dependency_liability = High<ref>{{cite book |vauthors=Bonewit-West K, Hunt SA, Applegate E |title=Today's Medical Assistant: Clinical and Administrative Procedures |date=2012 |page=571 |publisher=Elsevier Health Sciences |isbn=978-1-4557-0150-6 |url=https://books.google.com/books?id=YalYPI1KqTQC&pg=PA571 |access-date=20 August 2019 |archive-date=6 October 2022 |archive-url=https://web.archive.org/web/20221006090150/https://books.google.com/books?id=YalYPI1KqTQC&pg=PA571 |url-status=live }}</ref>
| addiction_liability = High<ref>{{cite book |vauthors=Bonewit-West K, Hunt SA, Applegate E |title=Today's Medical Assistant: Clinical and Administrative Procedures |date=2012 |page=571 |publisher=Elsevier Health Sciences |isbn=9781455701506 |url=https://books.google.com/books?id=YalYPI1KqTQC&pg=PA571 |access-date=20 August 2019 |archive-date=10 January 2023 |archive-url=https://web.archive.org/web/20230110030031/https://books.google.com/books?id=YalYPI1KqTQC&pg=PA571 |url-status=live }}</ref>
| routes_of_administration = [[Oral administration|By mouth]], [[sublingual administration|sublingual]], [[intramuscular injection|intramuscular]], [[intravenous injection|intravenous]], [[intranasal administration|intranasal]], [[subcutaneous injection|subcutaneous]], [[transdermal administration|transdermal]], [[rectal administration|rectal]], [[epidural administration|epidural]]<ref name="Kalso2005"/>
| class              = [[Opioid]]
| ATC_prefix         = N02
| ATC_suffix         = AA05
| ATC_supplemental   = ,{{ATC|N02|AJ17}}, {{ATC|N02|AJ18}}, {{ATC|N02|AJ19}}, {{ATC|N02|AA55}}, {{ATC|N02|AA56}}

<!-- Legal status -->
| legal_AU           = Schedule 8
| legal_AU_comment   = 
| legal_BR           = A1
| legal_BR_comment   = 
| legal_CA           = Schedule I
| legal_CA_comment   = 
| legal_DE           = Anlage III
| legal_DE_comment   = 
| legal_NZ           = <!-- Class A, B, C -->
| legal_NZ_comment   = 
| legal_UK           = Class A
| legal_UK_comment   = 
| legal_US           = Schedule II
| legal_US_comment   = 
| legal_UN           = N I
| legal_UN_comment   = 
| legal_status       = <!-- For countries not listed above -->

<!-- Pharmacokinetic data -->
| bioavailability    = By mouth: 60–87%<ref name = MSR>{{cite web |title=Roxicodone, OxyContin (oxycodone) dosing, indications, interactions, adverse effects, and more |work=Medscape Reference |publisher=WebMD |access-date=8 April 2014 |url=http://reference.medscape.com/drug/roxicodone-oxycontin-oxycodone-343321#showall |archive-date=13 April 2014 |archive-url=https://web.archive.org/web/20140413145108/http://reference.medscape.com/drug/roxicodone-oxycontin-oxycodone-343321#showall |url-status=live }}</ref><ref name="ElliottSmith2016"/>
| protein_bound      = 45%<ref name = MSR/>
| metabolism         = [[Liver]]: mainly [[CYP3A]], and, to a much lesser extent, [[CYP2D6]] (~5%);<ref name = MSR/> 95% metabolized (i.e., 5% excreted unchanged)<ref name="SmithPassik2008"/>
| metabolites        = • [[Noroxycodone]] (25%)<ref name=Medscape>{{cite web |title=Roxicodone, OxyContin (oxycodone) dosing, indications, interactions, adverse effects, and more |work=Medscape Reference |publisher=WebMD |access-date=4 January 2019 |url=http://reference.medscape.com/drug/roxicodone-oxycontin-oxycodone-343321#showall |archive-date=13 April 2014 |archive-url=https://web.archive.org/web/20140413145108/http://reference.medscape.com/drug/roxicodone-oxycontin-oxycodone-343321#showall |url-status=live }}</ref><ref name="SmithPassik2008" /><br />• [[Noroxymorphone]] (15%, free and [[Conjugation (biochemistry)|conjugated]])<ref name=Medscape /><ref name="SmithPassik2008" /><br />• [[Oxymorphone]] (11%, conjugated)<ref name=Medscape /><ref name="SmithPassik2008" /><br />• Others (e.g., minor metabolites)<ref name="SmithPassik2008" />
| onset              = {{abbrlink|IR|Instant release}}: 10–30 minutes<ref name="ElliottSmith2016" /><ref name="SmithPassik2008"/><br />{{abbrlink|CR|controlled release}}: 1 hour<ref name="YarbroWujcik2010">{{cite book | vauthors = Yarbro CH, Wujcik D, Gobel BH |title=Cancer Nursing: Principles and Practice |url=https://books.google.com/books?id=Ub6FWXVU7pQC&pg=PA695 |date=15 November 2010 |publisher=Jones & Bartlett Publishers |isbn=978-1-4496-1829-2 |pages=695–}}</ref>
| elimination_half-life = By mouth (IR): 2–3 hrs (same {{abbrlink|t<sub>1/2</sub>|biological half-life}} for all {{abbrlink|ROAs|routes of administration}})<ref name="SmithPassik2008"/><ref name="ElliottSmith2016" /><br />By mouth (CR): 4.5 hrs<ref name="McPhersonPincus2016"/>
| duration_of_action = By mouth (IR): 3–6 hrs<ref name="SmithPassik2008"/><br />By mouth (CR): 10–12 hrs<ref name="sunshine1996"/>
| excretion          = [[Urine]] (83%)<ref name = MSR/>

<!-- Identifiers -->
| index2_label       = as HCl
| CAS_number_Ref     = {{cascite|correct|CAS}}
| CAS_number         = 76-42-6
| CAS_supplemental   = 
| PubChem            = 5284603
| IUPHAR_ligand      = 7093
| DrugBank_Ref       = {{drugbankcite|correct|drugbank}}
| DrugBank           = DB00497
| ChemSpiderID_Ref   = {{chemspidercite|correct|chemspider}}
| ChemSpiderID       = 4447649
| UNII_Ref           = {{fdacite|correct|FDA}}
| UNII               = CD35PMG570
| KEGG_Ref           = {{keggcite|correct|kegg}}
| KEGG               = D05312
| KEGG2_Ref          = {{keggcite|correct|kegg}}
| KEGG2              = D00847
| ChEBI_Ref          = {{ebicite|correct|EBI}}
| ChEBI              = 7852
| ChEMBL_Ref         = {{ebicite|correct|EBI}}
| ChEMBL             = 656
| NIAID_ChemDB       = 
| PDB_ligand         = 
| synonyms           = Eukodal, eucodal; dihydrohydroxycodeinone, 7,8-dihydro-14-hydroxycodeinone, 6-deoxy-7,8-dihydro-14-hydroxy-3-O-methyl-6-oxomorphine<ref name="MerckIndex"/>

<!-- Chemical and physical data -->
| IUPAC_name         = (5''R'',9''R'',13''S'',14''S'')-4,5α-Epoxy-14-hydroxy-3-methoxy-17-methylmorphinan-6-one
| C                  = 18
| H                  = 21
| N                  = 1
| O                  = 4
| SMILES             = O=C4[C@@H]5Oc1c2c(ccc1OC)C[C@H]3N(CC[C@]25[C@@]3(O)CC4)C
| StdInChI_Ref       = {{stdinchicite|correct|chemspider}}
| StdInChI           = 1S/C18H21NO4/c1-19-8-7-17-14-10-3-4-12(22-2)15(14)23-16(17)11(20)5-6-18(17,21)13(19)9-10/h3-4,13,16,21H,5-9H2,1-2H3/t13-,16+,17+,18-/m1/s1
| StdInChI_comment   = 
| StdInChIKey_Ref    = {{stdinchicite|correct|chemspider}}
| StdInChIKey        = BRUQQQPBMZOVGD-XFKAJCMBSA-N
| density            = 
| density_notes      = 
| melting_point      = 219
| melting_high       = 
| melting_notes      = 
| boiling_point      = 
| boiling_notes      = 
| solubility         = 166
| sol_units          = &nbsp;(HCl)
| specific_rotation  = 
}}

<!-- Definition and medical uses -->
'''Oxycodone''', sold under the brand name '''Roxicodone''' and '''OxyContin''' (which is the extended-release form) among others, is a semi-synthetic [[opioid]] used medically for treatment of moderate to severe [[pain]]. It is highly addictive<ref>{{cite journal | vauthors = Remillard D, Kaye AD, McAnally H | title = Oxycodone's Unparalleled Addictive Potential: Is it Time for a Moratorium? | journal = Current Pain and Headache Reports | volume = 23 | issue = 2 | pages = 15 | date = February 2019 | pmid = 30820686 | doi = 10.1007/s11916-019-0751-7 | s2cid = 73488265 }}</ref> and is a commonly [[drug abuse|abused drug]].<ref name="AHFS2018">{{cite web |title=Oxycodone Monograph for Professionals |url=https://www.drugs.com/monograph/oxycodone.html |website=Drugs.com |publisher=AHFS |access-date=28 December 2018 |archive-date=28 December 2018 |archive-url=https://web.archive.org/web/20181228174726/https://www.drugs.com/monograph/oxycodone.html |url-status=live }}</ref><ref name="Per2018" /> It is usually taken [[oral administration|by mouth]], and is available in [[immediate release|immediate-release]] and [[controlled release|controlled-release]] formulations.<ref name=AHFS2018 /> Onset of [[pain relief]] typically begins within fifteen minutes and lasts for up to six hours with the immediate-release formulation.<ref name=AHFS2018 /> In the United Kingdom, it is available by [[Injection (medicine)|injection]].<ref name=BNF74>{{cite book|title=British national formulary : BNF 74|date=2017|publisher=British Medical Association|isbn=978-0-85711-298-9|page=442|edition=74}}</ref> [[Combination drug|Combination product]]s are also available with [[oxycodone/paracetamol|paracetamol]] (acetaminophen), [[oxycodone/ibuprofen|ibuprofen]], [[oxycodone/naloxone|naloxone]], [[naltrexone]], and [[oxycodone/aspirin|aspirin]].<ref name=AHFS2018 />

<!-- Side effects and mechanism -->
Common side effects include [[euphoria]], [[constipation]], [[nausea]], [[vomiting]], [[Anorexia (symptom)|loss of appetite]], [[Somnolence|drowsiness]], [[dizziness]], [[itch]]ing, [[Xerostomia|dry mouth]], and [[Perspiration|sweating]].<ref name=AHFS2018/> Side effects may also include [[addiction]] and [[Substance dependence|dependence]], [[substance abuse]], [[irritability]], [[Depression (mood)|depression]] or [[mania]], [[delirium]], [[hallucination]]s, [[hypoventilation]], [[gastroparesis]], [[bradycardia]], and [[hypotension]].<ref name=AHFS2018/> Those allergic to [[codeine]] may also be allergic to oxycodone.<ref name=AHFS2018/> Use of oxycodone in early pregnancy appears relatively safe.<ref name=AHFS2018/> [[Opioid withdrawal]] may occur if rapidly stopped.<ref name=AHFS2018/> Oxycodone acts by activating the [[μ-opioid receptor]].<ref name=TalleyFrankum2015>{{cite book| vauthors = Talley NJ, Frankum B, Currow D |title=Essentials of Internal Medicine 3e|url=https://books.google.com/books?id=0Zq9BwAAQBAJ&pg=PA491|date=10 February 2015|publisher=Elsevier Health Sciences|isbn=978-0-7295-8081-6|pages=491–}}</ref> When taken by mouth, it has roughly 1.5 times the [[Equianalgesic#Opioid equivalency table|effect of the equivalent amount]] of [[morphine]].<ref>{{cite web|work=Stanford School of Medicine, Palliative Care|title=Opioid Conversion / Equivalency Table|url=https://palliative.stanford.edu/opioid-conversion/equivalency-table/|date=20 April 2013|access-date=27 October 2017|archive-date=9 September 2020|archive-url=https://web.archive.org/web/20200909012800/https://palliative.stanford.edu/opioid-conversion/equivalency-table/|url-status=dead}}</ref>

<!-- History, society, and culture -->
Oxycodone was originally produced from the [[opium poppy]] opiate alkaloid [[thebaine]] in 1916 in Germany. One year later, it was used medically for the first time in Germany in 1917.<ref>{{cite journal | vauthors = Kalso E | title = Oxycodone | journal = Journal of Pain and Symptom Management | volume = 29 | issue = 5 Suppl | pages = S47–S56 | date = May 2005 | pmid = 15907646 | doi = 10.1016/j.jpainsymman.2005.01.010 | doi-access = free }}</ref> It is on the [[WHO Model List of Essential Medicines|World Health Organization's List of Essential Medicines]].<ref name="WHO23rd">{{cite book | vauthors = ((World Health Organization)) | title = The selection and use of essential medicines 2023: web annex A: World Health Organization model list of essential medicines: 23rd list (2023) | year = 2023 | hdl = 10665/371090 | author-link = World Health Organization | publisher = World Health Organization | location = Geneva | id = WHO/MHP/HPS/EML/2023.02 | hdl-access=free }}</ref> It is available as a [[generic medication]].<ref name=AHFS2018/> In 2022, it was the 60th most commonly prescribed medication in the United States, with more than 11{{nbsp}}million prescriptions.<ref>{{cite web | title=The Top 300 of 2022 | url=https://clincalc.com/DrugStats/Top300Drugs.aspx | website=ClinCalc | access-date=30 August 2024 | archive-date=30 August 2024 | archive-url=https://web.archive.org/web/20240830202410/https://clincalc.com/DrugStats/Top300Drugs.aspx | url-status=live }}</ref><ref>{{cite web | title = Oxycodone Drug Usage Statistics, United States, 2013 - 2022 | website = ClinCalc | url = https://clincalc.com/DrugStats/Drugs/Oxycodone | access-date = 30 August 2024 }}</ref> A number of abuse-deterrent formulations are available, such as in [[oxycodone/naloxone|combination with naloxone]] or [[naltrexone]].<ref name=Per2018>{{cite journal | vauthors = Pergolizzi JV, Taylor R, LeQuang JA, Raffa RB | title = Managing severe pain and abuse potential: the potential impact of a new abuse-deterrent formulation oxycodone/naltrexone extended-release product | journal = Journal of Pain Research | volume = 11 | pages = 301–311 | date = 2018 | pmid = 29445297 | pmc = 5810535 | doi = 10.2147/JPR.S127602 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Dart RC, Iwanicki JL, Dasgupta N, Cicero TJ, Schnoll SH | title = Do abuse deterrent opioid formulations work? | journal = Journal of Opioid Management | volume = 13 | issue = 6 | pages = 365–378 | date = 2017 | pmid = 29308584 | doi = 10.5055/jom.2017.0415 }}</ref>
{{TOC limit}}

==Medical uses==
Oxycodone is used for managing moderate to severe acute or chronic [[pain]] when other treatments are not sufficient.<ref name=AHFS2018/> It may improve [[quality of life]] in certain types of pain.<ref name="Riley2008">{{cite journal | vauthors = Riley J, Eisenberg E, Müller-Schwefe G, Drewes AM, Arendt-Nielsen L | title = Oxycodone: a review of its use in the management of pain | journal = Current Medical Research and Opinion | volume = 24 | issue = 1 | pages = 175–192 | date = January 2008 | pmid = 18039433 | doi = 10.1185/030079908X253708 | s2cid = 9099037 }}</ref> Numerous studies have been completed, and the appropriate use of this compound does improve the quality of life of patients with long term chronic pain syndromes.<ref>{{cite journal | vauthors = Ueberall MA, Eberhardt A, Mueller-Schwefe GH | title = Quality of life under oxycodone/naloxone, oxycodone, or morphine treatment for chronic low back pain in routine clinical practice | journal = International Journal of General Medicine | volume = 9 | pages = 39–51 | date = 24 February 2016 | pmid = 26966387 | pmc = 4771398 | doi = 10.2147/IJGM.S94685 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Dowell D, Haegerich TM, Chou R | title = CDC Guideline for Prescribing Opioids for Chronic Pain - United States, 2016 | language = en-us | journal = MMWR. Recommendations and Reports | volume = 65 | issue = 1 | pages = 1–49 | date = March 2016 | pmid = 26987082 | doi = 10.15585/mmwr.rr6501e1er | doi-access = free | pmc = 6390846 }}</ref><ref>{{cite journal | vauthors = Roth AR, Lazris A, Haskell H, James J | title = Appropriate Use of Opioids for Chronic Pain | language = en-US | journal = American Family Physician | volume = 102 | issue = 6 | pages = 335–337 | date = September 2020 | pmid = 32931211 | url = https://www.aafp.org/pubs/afp/issues/2020/0915/p335.html }}</ref>

Oxycodone is available as a [[time release technology|controlled-release]] tablet.<ref name="Biancofiore_20060901">{{cite journal | vauthors = Biancofiore G | title = Oxycodone controlled release in cancer pain management | journal = Therapeutics and Clinical Risk Management | volume = 2 | issue = 3 | pages = 229–234 | date = September 2006 | pmid = 18360598 | pmc = 1936259 | doi = 10.2147/tcrm.2006.2.3.229 | doi-access = free }}</ref> A 2006 review found that controlled-release oxycodone is comparable to immediate-release oxycodone, [[morphine]], and [[hydromorphone]] in management of moderate to severe [[cancer pain]], with fewer side effects than morphine. The author concluded that the controlled-release form is a valid alternative to morphine and a first-line treatment for cancer pain.<ref name="Biancofiore_20060901" /> In 2014, the European Association for Palliative Care recommended oxycodone by mouth as a second-line alternative to morphine by mouth for cancer pain.<ref name="pmid11237376">{{cite journal | vauthors = Hanks GW, Conno F, Cherny N, Hanna M, Kalso E, McQuay HJ, Mercadante S, Meynadier J, Poulain P, Ripamonti C, Radbruch L, Casas JR, Sawe J, Twycross RG, Ventafridda V | title = Morphine and alternative opioids in cancer pain: the EAPC recommendations | journal = British Journal of Cancer | volume = 84 | issue = 5 | pages = 587–593 | date = March 2001 | pmid = 11237376 | pmc = 2363790 | doi = 10.1054/bjoc.2001.1680 }}</ref>

In children between 11 and 16, the extended-release formulation is FDA-approved for the relief of cancer pain, trauma pain, or pain due to major surgery (for those already treated with opioids, who can tolerate at least 20&nbsp;mg per day of oxycodone) – this provides an alternative to Duragesic ([[fentanyl]]), the only other extended-release [[opioid]] [[analgesic]] approved for children.<ref>{{cite web|url=https://www.msn.com/en-us/news/us/fda-approves-oxycontin-for-kids-11-to-16/ar-BBlK3zS?ocid=spartandhp|title=FDA approves OxyContin for kids 11 to 16|website=www.msn.com|access-date=11 February 2018|archive-url=https://web.archive.org/web/20170630065901/http://www.msn.com/en-us/news/us/fda-approves-oxycontin-for-kids-11-to-16/ar-BBlK3zS?ocid=spartandhp|archive-date=30 June 2017|url-status=dead}}</ref>

Oxycodone, in its extended-release form and/or in combination with [[naloxone]], is sometimes used [[off-label use|off-label]] in the treatment of severe and refractory [[restless legs syndrome]].<ref>{{Cite web |title=Restless Legs Syndrome {{!}} Baylor Medicine |url=https://www.bcm.edu/healthcare/specialties/neurology/parkinsons-disease-and-movement-disorders/restless-legs-syndrome |access-date=6 November 2023 |website=www.bcm.edu }}</ref>

===Available forms===
{{See also|Oxycodone/paracetamol|Oxycodone/aspirin|Oxycodone/ibuprofen|Oxycodone/naloxone}}
{{Multiple image
|width=125
|image1=OxyContin branded oxycodone 10mg (OC side).jpg
|image2=OxyContin branded oxycodone 10mg (number side).jpg
|footer=Both sides of a single 10mg OxyContin pill.
}}

Oxycodone is available in a variety of formulations for [[oral administration|by mouth]] or [[sublingual administration|under the tongue]]:<ref name="ElliottSmith2016" >{{cite book |vauthors=Elliott JA, Smith HS |title=Handbook of Acute Pain Management |url=https://books.google.com/books?id=Em7OBQAAQBAJ&pg=PA82 |date=19 April 2016 |publisher=CRC Press |isbn=978-1-4665-9635-1 |pages=82–}}</ref><ref name="PhD2006">{{cite book |vauthors=Gould III HJ |title=Understanding Pain: What It Is, Why It Happens, and How It's Managed |url=https://books.google.com/books?id=eKPudFvllpsC&pg=PA71|date=11 December 2006|publisher=Demos Medical Publishing|isbn=978-1-934559-82-6|pages=71–}}</ref><ref name="Graves2015">{{cite book|vauthors=Graves K |title=Drug I.D. & Symptom Guide |edition=6th |series=QWIK-CODE |url=https://books.google.com/books?id=yGyfCgAAQBAJ&pg=PT99 |date=29 September 2015|publisher=LawTech Publishing Group|isbn=978-1-56325-225-9 |pages=99–}}</ref><ref name="Skidmore-Roth2015">{{cite book |vauthors=Skidmore-Roth L |title=Mosby's Drug Guide for Nursing Students, with 2016 Update |url=https://books.google.com/books?id=g_BwCgAAQBAJ&pg=PA789 |date=16 July 2015 |publisher=Elsevier Health Sciences |isbn=978-0-323-17297-4 |pages=789– |access-date=5 October 2016 |archive-date=7 October 2022 |archive-url=https://web.archive.org/web/20221007000409/https://books.google.com/books?id=g_BwCgAAQBAJ&pg=PA789 |url-status=live}}</ref>

* Immediate-release oxycodone (OxyFast, OxyIR, OxyNorm, Roxicodone)
* Controlled-release oxycodone (OxyContin, Xtampza ER) – 10–12 hour duration<ref name="sunshine1996">{{cite journal |vauthors=Sunshine A, Olson NZ, Colon A, Rivera J, Kaiko RF, Fitzmartin RD, Reder RF, Goldenheim PD |date=July 1996 |title=Analgesic efficacy of controlled-release oxycodone in postoperative pain |journal=Journal of Clinical Pharmacology |volume=36 |issue=7 |pages=595–603 |doi=10.1002/j.1552-4604.1996.tb04223.x |pmid=8844441 |s2cid=35076787 |quote=Treatment with CR oxycodone was safe and effective in this study, and its characteristics will be beneficial in the treatment of pain.}}</ref>
* Oxycodone tamper-resistant (OxyContin OTR)<ref>{{cite web|url=http://www.accessdata.fda.gov/drugsatfda_docs/nda/2013/022272Orig1s014ClinPharmR.pdf|title=accessdata.fda.gov|access-date=11 February 2018|archive-date=12 February 2017|archive-url=https://web.archive.org/web/20170212033248/http://www.accessdata.fda.gov/drugsatfda_docs/nda/2013/022272Orig1s014ClinPharmR.pdf|url-status=live}}</ref>
* Immediate-release oxycodone with [[paracetamol]] (acetaminophen) (Percocet, Endocet, Roxicet, Tylox)
* Immediate-release oxycodone with [[aspirin]] (Endodan, Oxycodan, Percodan, Roxiprin)
* Immediate-release oxycodone with [[ibuprofen]] (Combunox)<ref name="SinatraLeon-Cassasola2009">{{cite book|vauthors=Sinatra RS, de Leon-Cassasola OA|title=Acute Pain Management|url=https://books.google.com/books?id=ORpBaZnBSaQC&pg=PA198|date=27 April 2009|publisher=Cambridge University Press|isbn=978-0-521-87491-5|pages=198–|access-date=5 October 2016|archive-date=7 October 2022|archive-url=https://web.archive.org/web/20221007000410/https://books.google.com/books?id=ORpBaZnBSaQC&pg=PA198|url-status=live}}</ref>
* Controlled-release oxycodone with [[naloxone]] (Targin, Targiniq, Targinact)<ref name="StaatsSilverman2016">{{cite book|vauthors=Staats PS, Silverman SM|title=Controlled Substance Management in Chronic Pain: A Balanced Approach|url=https://books.google.com/books?id=-WxBDAAAQBAJ&pg=PA172|date=28 May 2016|publisher=Springer|isbn=978-3-319-30964-4|pages=172–|access-date=5 October 2016|archive-date=7 October 2022|archive-url=https://web.archive.org/web/20221007000410/https://books.google.com/books?id=-WxBDAAAQBAJ&pg=PA172|url-status=live}}</ref> – 10–12 hour duration<ref name="sunshine1996" />
* Controlled-release oxycodone with [[naltrexone]] (Troxyca) – 10–12 hour duration<ref name="sunshine1996"/><ref name="Pfizer2018">{{cite web |title=FDA Approves Troxyca® ER (Oxycodone Hydrochloride and Naltrexone Hydrochloride) Extended-release Capsules CII with Abuse-deterrent Properties for the Management of Pain |date=19 August 2016 |url=https://www.pfizer.com/news/press-release/press-release-detail/fda_approves_troxyca_er_oxycodone_hydrochloride_and_naltrexone_hydrochloride_extended_release_capsules_cii_with_abuse_deterrent_properties_for_the_management_of_pain |access-date=21 June 2018 |archive-date=25 September 2020 |archive-url=https://web.archive.org/web/20200925173435/https://www.pfizer.com/news/press-release/press-release-detail/fda_approves_troxyca_er_oxycodone_hydrochloride_and_naltrexone_hydrochloride_extended_release_capsules_cii_with_abuse_deterrent_properties_for_the_management_of_pain |url-status=live}}</ref>
[[File:Oxycodone Syrup 10mg per ml.jpg|thumb|A liquid solution containing 10mg of oxycodone per 1ml]]
In the US, oxycodone is only approved for use by mouth, available as tablets and oral solutions. [[Parenteral]] formulations of oxycodone (brand name OxyNorm) are also available in other parts of the world, however, and are widely used in the European Union.<ref name="Davis2009">{{cite book |vauthors=Davis MP |title=Opioids in Cancer Pain |url=https://books.google.com/books?id=aEzg6i2nPMQC&pg=PA158 |date=28 May 2009 |publisher=OUP Oxford |isbn=978-0-19-923664-0 |pages=155–158 |access-date=5 October 2016 |archive-date=7 October 2022 |archive-url=https://web.archive.org/web/20221007000410/https://books.google.com/books?id=aEzg6i2nPMQC&pg=PA158 |url-status=live}}</ref><ref name="Forbes2007">{{cite book |vauthors=Forbes K |title=Opioids in Cancer Pain |url=https://books.google.com/books?id=X7PjroLnaYQC&pg=PA64 |date=29 November 2007 |publisher=OUP Oxford |isbn=978-0-19-921880-6 |pages=64–65}}</ref><ref name="BradburyHodge2013">{{cite book |vauthors=Bradbury H, Hodge BS |title=Practical Prescribing for Medical Students |url=https://books.google.com/books?id=U5L3AgAAQBAJ&pg=PT93 |date=8 November 2013 |publisher=SAGE Publications |isbn=978-1-4462-9753-7 |pages=93– |access-date=5 October 2016 |archive-date=7 October 2022 |archive-url=https://web.archive.org/web/20221007000411/https://books.google.com/books?id=U5L3AgAAQBAJ&pg=PT93 |url-status=live}}</ref> In [[Spain]], the [[Netherlands]] and the [[United Kingdom]], oxycodone is approved for [[intravenous therapy|intravenous]] (IV) and [[intramuscular injection|intramuscular]] (IM) use. When first introduced in [[Germany]] during [[World War I]], both IV and IM administrations of oxycodone were commonly used for postoperative pain management of [[Central Powers]] soldiers.<ref name="Kalso2005">{{cite journal |vauthors=Kalso E |title=Oxycodone |journal=Journal of Pain and Symptom Management |volume=29 |issue=5 Suppl |pages=S47–S56 |date=May 2005 |pmid=15907646 |doi=10.1016/j.jpainsymman.2005.01.010 |doi-access=free}}</ref>

==Side effects==
{{Anchor|Adverse effects}}

[[File:Side effects of Oxycodone.png|thumb|upright=1.5|Main [[adverse effect|side effects]] of oxycodone<ref>{{cite web |author=American Society of Health-System Pharmacists |title=Oxycodone |publisher=U.S. National Library of Medicine, MedlinePlus |date=23 March 2009 |url=https://www.nlm.nih.gov/medlineplus/druginfo/meds/a682132.html |access-date=27 March 2009 |archive-date=24 March 2009 |archive-url=https://web.archive.org/web/20090324041355/http://www.nlm.nih.gov/medlineplus/druginfo/meds/a682132.html |url-status=live }}</ref>]]
[[File:GT-Oxycodon-Sicherheitsblister.jpg|thumb|Two tablets (10 mg) of oxycodone and safety blisters]]

Most common side effects of oxycodone include reduced sensitivity to pain, delayed gastric emptying, [[euphoria]], [[anxiolytic|anxiolysis]] (a reduction in anxiety), feelings of [[relaxation (psychology)|relaxation]], and [[Hypoventilation|respiratory depression]].<ref name="FitzgibbonLoeser2012" /> Common side effects of oxycodone include [[constipation]] (23%), [[nausea]] (23%), [[vomiting]] (12%), [[somnolence]] (23%), [[dizziness]] (13%), [[pruritus|itching]] (13%), [[dry mouth]] (6%), and [[sweating]] (5%).<ref name="FitzgibbonLoeser2012" /><ref name="drugscomSE">{{cite web |title=Oxycodone Side Effects |url=https://www.drugs.com/sfx/oxycodone-side-effects.html |publisher=Drugs.com |access-date=22 May 2013 |archive-date=21 June 2013 |archive-url=https://web.archive.org/web/20130621052514/http://www.drugs.com/sfx/oxycodone-side-effects.html |url-status=live }}</ref> Less common side effects (experienced by less than 5% of patients) include [[anorexia (symptom)|loss of appetite]], [[anxiety|nervousness]], [[abdominal pain]], [[diarrhea]], [[urinary retention]], [[dyspnea]], and [[hiccups]].<ref name="OxyContinInsertUS" />

Most side effects generally become less intense over time, although issues related to constipation are likely to continue for the duration of use.<ref>{{cite journal | vauthors = Ordóñez Gallego A, González Barón M, Espinosa Arranz E | title = Oxycodone: a pharmacological and clinical review | journal = Clinical & Translational Oncology | volume = 9 | issue = 5 | pages = 298–307 | date = May 2007 | pmid = 17525040 | doi = 10.1007/s12094-007-0057-9 | s2cid = 44986791 }}</ref> Chronic use of this compound and associated constipation issues can become very serious, and have been implicated in life-threatening [[bowel perforation]]s,<ref>{{cite journal | vauthors = Poitras R, Warren D, Oyogoa S | title = Opioid drugs and stercoral perforation of the colon: Case report and review of literature | journal = International Journal of Surgery Case Reports | volume = 42 | pages = 94–97 | date = 7 December 2017 | pmid = 29232630 | pmc = 5730425 | doi = 10.1016/j.ijscr.2017.11.060 }}</ref> a number of specific medications including [[naloxegol]]<ref>{{Cite web |title=Movantik for the Treatment of Opioid-Induced Constipation |url=https://www.clinicaltrialsarena.com/projects/movantik-for-the-treatment-of-opioid-induced-constipation/ |access-date=11 November 2023 |website=Clinical Trials Arena }}</ref> have been developed to address opioid induced constipation.

[[Oxycodone/naloxone|Oxycodone in combination]] with [[naloxone]] in managed-release tablets has been formulated to both deter abuse and reduce [[Opioid#Constipation|opioid-induced constipation]].<ref>{{cite journal | vauthors = Simpson K, Leyendecker P, Hopp M, Müller-Lissner S, Löwenstein O, De Andrés J, Troy Ferrarons J, Bosse B, Krain B, Nichols T, Kremers W, Reimer K | title = Fixed-ratio combination oxycodone/naloxone compared with oxycodone alone for the relief of opioid-induced constipation in moderate-to-severe noncancer pain | journal = Current Medical Research and Opinion | volume = 24 | issue = 12 | pages = 3503–3512 | date = December 2008 | pmid = 19032132 | doi = 10.1185/03007990802584454 | s2cid = 73061000 }}</ref>

===Dependence and withdrawal===
{{See also|Opioid dependence}}

The risk of experiencing severe [[Drug withdrawal|withdrawal]] symptoms is high if a patient has become physically dependent and discontinues oxycodone abruptly. Medically, when the drug has been taken regularly over an extended period, it is withdrawn gradually rather than abruptly. People who regularly use oxycodone recreationally or at higher than prescribed doses are at even higher risk of severe withdrawal symptoms. The symptoms of oxycodone withdrawal, as with other opioids, may include "[[anxiety]], [[panic attack]], [[nausea]], [[insomnia]], [[muscle pain]], [[muscle weakness]], [[fever]]s, and other [[flu-like syndrome|flu-like symptoms]]".<ref name="CESAR2005">{{cite web |url=http://www.cesar.umd.edu/cesar/drugs/oxycodone.asp |title=Oxycodone |access-date=25 March 2009 |date=2 May 2005 |publisher=Center for Substance Abuse Research |archive-date=6 April 2009 |archive-url=https://web.archive.org/web/20090406010900/http://www.cesar.umd.edu/cesar/drugs/oxycodone.asp |url-status=dead }}</ref><ref>{{cite web|title=Tapering off opioids: When and how|publisher=Mayo Clinic|url=https://www.mayoclinic.org/diseases-conditions/prescription-drug-abuse/in-depth/tapering-off-opioids-when-and-how/art-20386036|access-date=10 October 2020}}</ref>

Withdrawal symptoms have also been reported in newborns whose mothers had been either injecting or orally taking oxycodone during pregnancy.<ref>{{cite journal | vauthors = Rao R, Desai NS | title = OxyContin and neonatal abstinence syndrome | journal = Journal of Perinatology | volume = 22 | issue = 4 | pages = 324–325 | date = June 2002 | pmid = 12032797 | doi = 10.1038/sj.jp.7210744 | s2cid = 22539877 | doi-access =  }}</ref>

===Hormone levels===
{{See also|Opioid#Low sex hormone levels}}

As with other opioids, chronic use of oxycodone (particularly with higher doses) can often cause concurrent [[hypogonadism]] (low [[sex hormone]] levels).<ref name="pmid30343356">{{cite journal |vauthors=Coluzzi F, Billeci D, Maggi M, Corona G |title=Testosterone deficiency in non-cancer opioid-treated patients |journal=[[Journal of Endocrinological Investigation]] |volume=41 |issue=12 |pages=1377–1388 |date=December 2018 |pmid=30343356 |pmc=6244554 |doi=10.1007/s40618-018-0964-3}}</ref><ref name="pmid23414717">{{cite journal | vauthors = Brennan MJ | title = The effect of opioid therapy on endocrine function | journal = The American Journal of Medicine | volume = 126 | issue = 3 Suppl 1 | pages = S12–S18 | date = March 2013 | pmid = 23414717 | doi = 10.1016/j.amjmed.2012.12.001 }}</ref>

==Overdose==
In high doses, [[overdose]]s, or in some persons not tolerant to opioids, oxycodone can cause [[shallow breathing]], [[bradycardia|slowed heart rate]], cold/clammy skin, [[apnea|pauses in breathing]], [[hypotension|low blood pressure]], [[miosis|constricted pupils]], [[circulatory collapse]], [[respiratory arrest]], and [[death]].<ref name="OxyContinInsertUS" />

In 2011, it was the leading cause of drug-related deaths in the U.S.<ref name=CDC2018Death>{{cite web |title=Drugs Most Frequently Involved in Drug Overdose Deaths: United States, 2011–2016 |url=https://www.cdc.gov/nchs/data/nvsr/nvsr67/nvsr67_09-508.pdf |website=CDC |access-date=21 December 2018 |date=12 December 2018 |archive-date=13 December 2018 |archive-url=https://web.archive.org/web/20181213221854/https://www.cdc.gov/nchs/data/nvsr/nvsr67/nvsr67_09-508.pdf |url-status=live }}</ref> However, from 2012 onwards, [[heroin]] and [[fentanyl]] have become more common causes of drug-related deaths.<ref name=CDC2018Death/>

Oxycodone overdose has also been described to cause spinal cord infarction in high doses and [[Brain ischemia|ischemic damage to the brain]], due to prolonged [[Hypoxia (medical)|hypoxia]] from suppressed breathing.<ref>{{cite journal | vauthors = Ntranos A, Shoirah H, Dhamoon MS, Hahn D, Naidich TP, Shin S | title = Clinical Reasoning: A young woman with respiratory failure, hearing loss, and paraplegia | journal = Neurology | volume = 88 | issue = 10 | pages = e78–e84 | date = March 2017 | pmid = 28265044 | doi = 10.1212/WNL.0000000000003684 | doi-access = free }}</ref>

== Interactions ==

Oxycodone is [[metabolism|metabolized]] by the [[enzyme]]s [[CYP3A4]] and [[CYP2D6]]. Therefore, its [[clearance (pharmacology)|clearance]] can be altered by [[enzyme inhibitor|inhibitor]]s and [[enzyme inducer|inducer]]s of these enzymes, increasing and decreasing [[half-life]], respectively.<ref name="Forbes2007" /> (For lists of CYP3A4 and CYP2D6 inhibitors and inducers, see [[CYP3A4#Ligands|here]] and [[CYP2D6#Ligands|here]], respectively.) Natural [[genetic variation]] in these enzymes can also influence the clearance of oxycodone, which may be related to the wide inter-individual variability in its half-life and [[potency (pharmacology)|potency]].<ref name="Forbes2007" />

[[Ritonavir]] or [[lopinavir/ritonavir]] greatly increase [[Blood plasma|plasma]] concentrations of oxycodone in healthy human volunteers due to inhibition of CYP3A4 and CYP2D6.<ref name="NieminenHagelberg2010">{{cite journal | vauthors = Nieminen TH, Hagelberg NM, Saari TI, Neuvonen M, Neuvonen PJ, Laine K, Olkkola KT | title = Oxycodone concentrations are greatly increased by the concomitant use of ritonavir or lopinavir/ritonavir | journal = European Journal of Clinical Pharmacology | volume = 66 | issue = 10 | pages = 977–985 | date = October 2010 | pmid = 20697700 | doi = 10.1007/s00228-010-0879-1 | s2cid = 25770818 | url = https://hal.archives-ouvertes.fr/hal-00614173/file/PEER_stage2_10.1007%252Fs00228-010-0879-1.pdf }}</ref> [[Rifampicin]] greatly reduces plasma concentrations of oxycodone due to strong induction of CYP3A4.<ref name="NieminenHagelberg2009">{{cite journal | vauthors = Nieminen TH, Hagelberg NM, Saari TI, Pertovaara A, Neuvonen M, Laine K, Neuvonen PJ, Olkkola KT | title = Rifampin greatly reduces the plasma concentrations of intravenous and oral oxycodone | journal = Anesthesiology | volume = 110 | issue = 6 | pages = 1371–1378 | date = June 2009 | pmid = 19417618 | doi = 10.1097/ALN.0b013e31819faa54 | doi-access = free }}</ref> There is also a case report of [[fosphenytoin]], a CYP3A4 inducer, dramatically reducing the analgesic effects of oxycodone in a chronic pain patient.<ref name="Pon, Hwang, 2015">{{cite journal | vauthors = Pon D, Hwang J, Lo T, Zyl CV | title = Decreased responsiveness to oxycodone: A case of a pharmacokinetic drug interaction? | journal = Journal of Opioid Management | volume = 11 | issue = 4 | pages = 357–361 | year = 2015 | pmid = 26312962 | doi = 10.5055/jom.2015.0284 }}</ref> Dosage or medication adjustments may be necessary in each case.<ref name="NieminenHagelberg2010" /><ref name="NieminenHagelberg2009" /><ref name="Pon, Hwang, 2015" />

==Pharmacology==
{{contradicts other|Equianalgesic|there|morphine vs. oxycodone|section's equianalgesic table|date=October 2023}}

===Pharmacodynamics===

{| class="wikitable floatright" style="text-align: center;"
|+ Oxycodone (and metabolite) at opioid receptors
|-
! rowspan="2" | Compound || colspan="3" | [[Binding affinity|Affinities]] ({{abbrlink|K<sub>i</sub>|Inhibitor constant}}) || Ratio || rowspan="2" |{{Abbr|Ref.|Reference}}
|-
! {{abbrlink|MOR|μ-Opioid receptor}} !! {{abbrlink|DOR|δ-Opioid receptor}} !! {{abbrlink|KOR|κ-Opioid receptor}} !! MOR:DOR:KOR
|-
| Oxycodone || 18 nM || 958 nM || 677 nM || 1:53:38 || <ref name="Kalso2005"/>
|-
| Oxymorphone || 0.78 nM || 50 nM || 137 nM || 1:64:176 || <ref name="CorbettPaterson1993">{{cite book | vauthors = Corbett AD, Paterson SJ, Kosterlitz HW |chapter=Selectivity of Ligands for Opioid Receptors |title=Opioids |volume=104 |issue=1 |year=1993 |pages=645–679 |issn=0171-2004 |doi=10.1007/978-3-642-77460-7_26 |series=Handbook of Experimental Pharmacology |isbn=978-3-642-77462-1}}</ref>
|}

{| class="wikitable floatright"
|+ <br />Equianalgesic doses<ref name="King2010">{{cite book| vauthors = King TL, Brucker MC |title=Pharmacology for Women's Health|url=https://books.google.com/books?id=o_rHHCsIpckC&pg=PA332|date=25 October 2010|publisher=Jones & Bartlett Publishers|isbn=978-1-4496-1073-9|pages=332–}}</ref><ref name="ChestnutWong2014">{{cite book|vauthors=Chestnut DH, Wong CA, Tsen LC, Ngan Kee WD, Beilin YM, Mhyre J|title=Chestnut's Obstetric Anesthesia: Principles and Practice E-Book|url=https://books.google.com/books?id=FMU0AwAAQBAJ&pg=PA611|date=28 February 2014|publisher=Elsevier Health Sciences|isbn=978-0-323-11374-8|pages=611–|access-date=22 June 2018|archive-date=6 October 2022|archive-url=https://web.archive.org/web/20221006145548/https://books.google.com/books?id=FMU0AwAAQBAJ&pg=PA611|url-status=live}}</ref><ref name="Tiziani2013">{{cite book|vauthors=Tiziani AP|title=Havard's Nursing Guide to Drugs|url=https://books.google.com/books?id=XpzQAgAAQBAJ&pg=PA933|date=1 June 2013|publisher=Elsevier Health Sciences|isbn=978-0-7295-8162-2|pages=933–|access-date=22 June 2018|archive-date=6 October 2022|archive-url=https://web.archive.org/web/20221006145548/https://books.google.com/books?id=XpzQAgAAQBAJ&pg=PA933|url-status=live}}</ref>
|-
! Compound !! [[Route of administration|Route]] !! [[Dose (biochemistry)|Dose]]
|-
| [[Codeine]] || {{abbr|PO|Oral administration}} || 200&nbsp;mg
|-
| [[Hydrocodone]] || {{abbr|PO|Oral administration}} || 20–30&nbsp;mg
|-
| [[Hydromorphone]] || {{abbr|PO|Oral administration}} || 7.5&nbsp;mg
|-
| [[Hydromorphone]] || {{abbr|IV|Intravenous administration}} || 1.5&nbsp;mg
|-
| [[Morphine]] || {{abbr|PO|Oral administration}} || 30&nbsp;mg
|-
| [[Morphine]] || {{abbr|IV|Intravenous administration}} || 10&nbsp;mg
|-
| Oxycodone || {{abbr|PO|Oral administration}} || 20&nbsp;mg
|-
| Oxycodone || {{abbr|IV|Intravenous administration}} || 10&nbsp;mg
|-
| [[Oxymorphone]] || {{abbr|PO|Oral administration}} || 10&nbsp;mg
|-
| [[Oxymorphone]] || {{abbr|IV|Intravenous administration}} || 1&nbsp;mg
|}

Oxycodone, a semi-synthetic opioid, is a highly [[binding selectivity|selective]] [[full agonist]] of the [[μ-opioid receptor]] (MOR).<ref name="Davis2009" /><ref name="Forbes2007" /> This is the main [[biological target]] of the [[endogenous]] opioid [[neuropeptide]] [[β-endorphin]].<ref name="TalleyFrankum2015" /> Oxycodone has low [[affinity (pharmacology)|affinity]] for the [[δ-opioid receptor]] (DOR) and the [[κ-opioid receptor]] (KOR), where it is an [[agonist]] similarly.<ref name="Davis2009" /><ref name="Forbes2007" /> After oxycodone binds to the MOR, a [[G protein]]-complex is released, which inhibits the release of [[neurotransmitter]]s by the cell by decreasing the amount of [[cyclic adenosine monophosphate|cAMP]] produced, closing [[calcium channel]]s, and opening [[potassium channel]]s.<ref>{{cite journal | vauthors = Chahl L |year = 1996 |title = Opioids- mechanism of action |journal = Aust Prescr |volume = 19 |issue = 3|pages = 63–65 |doi=10.18773/austprescr.1996.063|doi-access = free }}</ref> Opioids like oxycodone are thought to produce their analgesic effects via activation of the MOR in the [[midbrain]] [[periaqueductal gray]] (PAG) and [[rostral ventromedial medulla]] (RVM).<ref name="Stein1999">{{cite book|vauthors=Stein C|title=Opioids in Pain Control: Basic and Clinical Aspects|url=https://books.google.com/books?id=4Rfr8cQayvgC&pg=PA46|year=1999|publisher=Cambridge University Press|isbn=978-0-521-62269-1|pages=46–|access-date=21 June 2018|archive-date=7 October 2022|archive-url=https://web.archive.org/web/20221007000411/https://books.google.com/books?id=4Rfr8cQayvgC&pg=PA46|url-status=live}}</ref> Conversely, they are thought to produce [[Reward system|reward]] and addiction via activation of the MOR in the [[mesolimbic reward pathway]], including in the [[ventral tegmental area]], [[nucleus accumbens]], and [[ventral pallidum]].<ref name="SquireBerg2012">{{cite book |vauthors=Squire L, Berg D, Bloom FE, du Lac S, Ghosh A, Spitzer NC |title=Fundamental Neuroscience |url=https://books.google.com/books?id=QGzJFu_NyzcC&pg=PA884 |date=17 December 2012 |publisher=Academic Press |isbn=978-0-12-385871-9 |pages=884– |access-date=21 June 2018 |archive-date=7 October 2022 |archive-url=https://web.archive.org/web/20221007000411/https://books.google.com/books?id=QGzJFu_NyzcC&pg=PA884 |url-status=live }}</ref><ref name="KringelbachBerridge2010">{{cite book | vauthors = Kringelbach ML, Berridge KC |title=Pleasures of the Brain |url=https://books.google.com/books?id=yl2yAwAAQBAJ&pg=PA33 |year=2010|publisher=Oxford University Press |isbn=978-0-19-533102-8|pages=33–}}</ref> [[Drug tolerance|Tolerance]] to the analgesic and rewarding effects of opioids is complex and occurs due to receptor-level tolerance (e.g., MOR [[downregulation and upregulation|downregulation]]), cellular-level tolerance (e.g., cAMP upregulation), and system-level tolerance (e.g., [[neuroplasticity|neural adaptation]] due to induction of [[ΔFosB]] expression).<ref name="SinatraJahr2010">{{cite book| vauthors = Sinatra RS, Jahr JS, Watkins-Pitchford JM |title=The Essence of Analgesia and Analgesics |url=https://books.google.com/books?id=ZwPIjKg0XukC&pg=PA167 |date=14 October 2010|publisher=Cambridge University Press|isbn=978-1-139-49198-3|pages=167–}}</ref>

Taken orally, 20&nbsp;mg of immediate-release oxycodone is considered to be [[equianalgesic|equivalent in analgesic effect]] to 30&nbsp;mg of morphine,<ref name="Merck">{{Cite web|url=http://www.merckmanuals.com/professional/neurologic-disorders/pain/treatment-of-pain|title=Treatment of Pain|website=Merck Manuals Professional Edition|access-date=24 April 2016|archive-date=3 May 2016|archive-url=https://web.archive.org/web/20160503150513/http://www.merckmanuals.com/professional/neurologic-disorders/pain/treatment-of-pain|url-status=live}}</ref><ref name="FerrellPasero2010">{{Cite book |chapter-url=https://books.google.com/books?id=Q5iNSuBma0AC |title=Pain Assessment and Pharmacologic Management |vauthors=Ferrell BR, Pasero C, McCaffery M |date=2010 |publisher=Elsevier Health Sciences |isbn=978-0-323-08263-1 |chapter=Table 16-1 Equianalgesic Dose Chart |access-date=24 April 2016 |archive-date=7 October 2022 |archive-url=https://web.archive.org/web/20221007000412/https://books.google.com/books?id=Q5iNSuBma0AC |url-status=live }}</ref> while extended release oxycodone is considered to be twice as potent as oral morphine.<ref name="LevyVictor2007">{{cite book|vauthors=Levy EF, Victor J|title=Opioids in medicine a comprehensive review on the mode of action and the use of analgesics in different clinical pain states|year=2007|publisher=Springer Science+Business Media B.V.|location=New York|isbn=978-1-4020-5947-6|page=371|url=https://books.google.com/books?id=ybtX0GZGhk8C&pg=PA371|access-date=1 February 2016|archive-date=7 October 2022|archive-url=https://web.archive.org/web/20221007000913/https://books.google.com/books?id=ybtX0GZGhk8C&pg=PA371|url-status=live}}</ref>

Similarly to most other opioids, oxycodone increases [[prolactin]] secretion, but its influence on [[testosterone]] levels is unknown.<ref name="Davis2009" /> Unlike morphine, oxycodone lacks [[immunosuppressive]] activity (measured by [[natural killer cell]] activity and [[interleukin 2]] production ''[[in vitro]]''); the clinical relevance of this has not been clarified.<ref name="Davis2009" />

====Active metabolites====
A few of the [[metabolite]]s of oxycodone have also been found to be active as MOR agonists, some of which notably have much higher [[affinity (pharmacology)|affinity]] for (as well as higher [[intrinsic activity|efficacy]] at) the MOR in comparison.<ref name="LalovicKharasch2006">{{cite journal | vauthors = Lalovic B, Kharasch E, Hoffer C, Risler L, Liu-Chen LY, Shen DD | title = Pharmacokinetics and pharmacodynamics of oral oxycodone in healthy human subjects: role of circulating active metabolites | journal = Clinical Pharmacology and Therapeutics | volume = 79 | issue = 5 | pages = 461–479 | date = May 2006 | pmid = 16678548 | doi = 10.1016/j.clpt.2006.01.009 | s2cid = 21372271 }}</ref><ref name="KlimasWitticke2013">{{cite journal | vauthors = Klimas R, Witticke D, El Fallah S, Mikus G | title = Contribution of oxycodone and its metabolites to the overall analgesic effect after oxycodone administration | journal = Expert Opinion on Drug Metabolism & Toxicology | volume = 9 | issue = 5 | pages = 517–528 | date = May 2013 | pmid = 23488585 | doi = 10.1517/17425255.2013.779669 | s2cid = 22857902 }}</ref><ref name="LembergSiiskonen2008">{{cite journal | vauthors = Lemberg KK, Siiskonen AO, Kontinen VK, Yli-Kauhaluoma JT, Kalso EA | title = Pharmacological characterization of noroxymorphone as a new opioid for spinal analgesia | journal = Anesthesia and Analgesia | volume = 106 | issue = 2 | pages = 463–70, table of contents | date = February 2008 | pmid = 18227301 | doi = 10.1213/ane.0b013e3181605a15 | s2cid = 16524280 | doi-access = free }}</ref> [[Oxymorphone]] possesses 3- to 5-fold higher affinity for the MOR than does oxycodone,<ref name="SmithPassik2008">{{cite book |vauthors=Smith H, Passik S |title=Pain and Chemical Dependency |url=https://books.google.com/books?id=T88C-9VTDXMC&pg=PA195 |date=25 April 2008 |publisher=Oxford University Press USA |isbn=978-0-19-530055-0 |pages=195– |access-date=5 October 2016 |archive-date=7 October 2022 |archive-url=https://web.archive.org/web/20221007000913/https://books.google.com/books?id=T88C-9VTDXMC&pg=PA195 |url-status=live }}</ref> while [[noroxycodone]] and [[noroxymorphone]] possess one-third of and 3-fold higher affinity for the MOR, respectively,<ref name="SmithPassik2008"/><ref name="LembergSiiskonen2008" /> and MOR activation is 5- to 10-fold less with noroxycodone but 2-fold higher with noroxymorphone relative to oxycodone.<ref name="Preedy2016" /> Noroxycodone, noroxymorphone, and oxymorphone also have longer [[biological half-life|biological half-lives]] than oxycodone.<ref name="LalovicKharasch2006" /><ref name="FiresteinBudd2016">{{cite book |vauthors=Firestein GS, Budd RC, Gabriel SE, McInnes IB, O'Dell JR |title=Kelley and Firestein's Textbook of Rheumatology |url=https://books.google.com/books?id=kBZ6DAAAQBAJ&pg=PA1080 |date=21 June 2016 |publisher=Elsevier Health Sciences |isbn=978-0-323-31696-5 |lccn=2016009254 |pages=1080– |access-date=5 October 2016 |archive-date=7 October 2022 |archive-url=https://web.archive.org/web/20221007000913/https://books.google.com/books?id=kBZ6DAAAQBAJ&pg=PA1080 |url-status=live }}</ref>

{| class="wikitable"
|+ Pharmacology of oxycodone and metabolites<ref name="FitzgibbonLoeser2012" /><ref name="Preedy2016" />
|-
! Compound !! {{abbrlink|K<sub>i</sub>|Inhibitor constant}} !! {{abbrlink|EC<sub>50</sub>|Half-maximal effective concentration}} !! [[Cmax (pharmacology)|{{abbr|C<sub>max</sub>|Peak serum concentrations}}]] !! [[Area under the curve (pharmacokinetics)|{{abbr|AUC|Area under the curve}}]]
|-
| Oxycodone || 16.0 nM || 343 nM || 23.2 ± 8.6&nbsp;ng/mL || 236 ± 102&nbsp;ng/h/mL
|-
| [[Oxymorphone]] || 0.36 nM || 42.8 nM || 0.82 ± 0.85&nbsp;ng/mL || 12.3 ± 12&nbsp;ng/h/mL
|-
| [[Noroxycodone]] || 57.1 nM || 1930 nM || 15.2 ± 4.5&nbsp;ng/mL || 233 ± 102&nbsp;ng/h/mL
|-
| [[Noroxymorphone]] || 5.69 nM || 167 nM || {{abbr|ND|No data}} || {{abbr|ND|No data}}
|- class="sortbottom"
| colspan="5" style="width: 1px;" |{{Small|K<sub>i</sub> is for [<sup>3</sup>H]diprenorphine displacement. (Note that diprenorphine is a non-selective opioid receptor ligand, so this is not MOR-specific.) EC<sub>50</sub> is for hMOR1 GTPyS binding. C<sub>max</sub> and AUC levels are for 20&nbsp;mg CR oxycodone.}}
|}

However, despite the greater ''in vitro'' activity of some of its metabolites, it has been determined that oxycodone itself is responsible for 83.0% and 94.8% of its analgesic effect following oral and intravenous administration, respectively.<ref name="KlimasWitticke2013" /> Oxymorphone plays only a minor role, being responsible for 15.8% and 4.5% of the analgesic effect of oxycodone after oral and intravenous administration, respectively.<ref name="KlimasWitticke2013" /> Although the [[CYP2D6]] [[genotype]] and the [[route of administration]] result in differential rates of oxymorphone formation, the unchanged parent compound remains the major contributor to the overall analgesic effect of oxycodone.<ref name="KlimasWitticke2013" /> In contrast to oxycodone and oxymorphone, noroxycodone and noroxymorphone, while also potent MOR agonists, poorly cross the [[blood–brain barrier]] into the [[central nervous system]], and for this reason are only minimally analgesic in comparison.<ref name="LalovicKharasch2006" /><ref name="Preedy2016" /><ref name="KlimasWitticke2013" /><ref name="LembergSiiskonen2008" />

====κ-opioid receptor====
In 1997, a group of Australian researchers proposed (based on a study in rats) that oxycodone acts on KORs, unlike morphine, which acts upon MORs.<ref>{{cite journal | vauthors = Ross FB, Smith MT | title = The intrinsic antinociceptive effects of oxycodone appear to be kappa-opioid receptor mediated | journal = Pain | volume = 73 | issue = 2 | pages = 151–157 | date = November 1997 | pmid = 9415500 | doi = 10.1016/S0304-3959(97)00093-6 | s2cid = 53165907 }}</ref> Further research by this group indicated the drug appears to be a high-affinity κ<sub>2b</sub>-opioid receptor agonist.<ref>{{cite journal | vauthors = Smith MT | title = Differences between and combinations of opioids re-visited | journal = Current Opinion in Anesthesiology | volume = 21 | issue = 5 | pages = 596–601 | date = October 2008 | pmid = 18784485 | doi = 10.1097/ACO.0b013e32830a4c4a | s2cid = 14293344 }}</ref> However, this conclusion has been disputed, primarily on the basis that oxycodone produces effects that are typical of MOR agonists.<ref name="pmid17961923">{{cite journal | vauthors = Kalso E | title = How different is oxycodone from morphine? | journal = Pain | volume = 132 | issue = 3 | pages = 227–228 | date = December 2007 | pmid = 17961923 | doi = 10.1016/j.pain.2007.09.027 | s2cid = 45689872 }}</ref> In 2006, research by a Japanese group suggested the effect of oxycodone is mediated by different receptors in different situations.<ref name="pmid16533506">{{cite journal | vauthors = Nozaki C, Saitoh A, Kamei J | title = Characterization of the antinociceptive effects of oxycodone in diabetic mice | journal = European Journal of Pharmacology | volume = 535 | issue = 1–3 | pages = 145–151 | date = March 2006 | pmid = 16533506 | doi = 10.1016/j.ejphar.2006.02.002 }}</ref> Specifically in diabetic mice, the KOR appears to be involved in the antinociceptive effects of oxycodone, while in nondiabetic mice, the μ<sub>1</sub>-opioid receptor seems to be primarily responsible for these effects.<ref name="pmid16533506" /><ref name="pmid17292346">{{cite journal | vauthors = Nozaki C, Kamei J | title = Involvement of mu1-opioid receptor on oxycodone-induced antinociception in diabetic mice | journal = European Journal of Pharmacology | volume = 560 | issue = 2–3 | pages = 160–162 | date = April 2007 | pmid = 17292346 | doi = 10.1016/j.ejphar.2007.01.021 }}</ref>

===Pharmacokinetics===

====Instant-release absorption profiles and Tmax====
Oxycodone can be administered orally, intravenously, via [[intravenous]], [[intramuscular]], or [[subcutaneous injection]]. Along with [[suppository|rectal]], [[sublingual]], [[Buccal administration|buccal]] or [[intranasal drug delivery]]. The [[bioavailability]] of [[oral administration]] of oxycodone averages within a range of 60 to 87%, with rectal administration yielding the same results; [[Intranasal]] administration of oxycodone has a bioavailability of ~77%, the same [[half life]] as oral oxycodone, along with faster [[Tmax (pharmacology)|Tmax]]<ref>{{cite journal | vauthors = Lofwall MR, Moody DE, Fang WB, Nuzzo PA, Walsh SL | title = Pharmacokinetics of intranasal crushed OxyContin and intravenous oxycodone in nondependent prescription opioid abusers | journal = Journal of Clinical Pharmacology | volume = 52 | issue = 4 | pages = 600–606 | date = April 2012 | pmid = 21610203 | pmc = 4006196 | doi = 10.1177/0091270011401620 }}</ref> previously reported as 47% for nasal spray administration due to the solution in the study exceeding the 0.3- to 0.4-mL nasal mucosa limit.<ref>Analgesic Expert Group. Therapeutic Guidelines: Analgesic. Version 4. Melbourne: Therapeutic Guidelines Ltd, 2007.</ref> Buccal bioavailability ~55%, [[Tmax (pharmacology)|Tmax]] ~60 min.<ref>{{cite journal | vauthors = Kinnunen M, Piirainen P, Kokki H, Lammi P, Kokki M | title = Updated Clinical Pharmacokinetics and Pharmacodynamics of Oxycodone | journal = Clinical Pharmacokinetics | volume = 58 | issue = 6 | pages = 705–725 | date = June 2019 | pmid = 30652261 | doi = 10.1007/s40262-018-00731-3 | quote = Data indicate that after buccal and sublingual administration of oxycodone 0.1 mg/kg, the rate and extent of absorption is appropriate for clinical use. After transmucosal administration, C<sub>max</sub> was between 16 and 22 ng/mL, T<sub>max</sub> was 60 min, and bioavailability was 55% | doi-access = free }}</ref> Sublingual bioavailability 20% (non alkalized) ~55% (alkalized) [[Tmax (pharmacology)|Tmax]] ~60 minutes.<ref>{{cite journal | vauthors = Kinnunen M, Piirainen P, Kokki H, Lammi P, Kokki M | title = Updated Clinical Pharmacokinetics and Pharmacodynamics of Oxycodone | journal = Clinical Pharmacokinetics | volume = 58 | issue = 6 | pages = 705–725 | date = June 2019 | pmid = 30652261 | doi = 10.1007/s40262-018-00731-3 }}</ref><ref>{{cite journal | vauthors = Li Y, Sun D, Palmisano M, Zhou S | title = Slow drug delivery decreased total body clearance and altered bioavailability of immediate- and controlled-release oxycodone formulations | journal = Pharmacology Research & Perspectives | volume = 4 | issue = 1 | pages = e00210 | date = February 2016 | pmid = 26977300 | pmc = 4777261 | doi = 10.1002/prp2.210 }}</ref>

After a dose of conventional (immediate-release) oral oxycodone, the [[onset of action]] is 10 to 30 minutes,<ref name="SmithPassik2008"/><ref name="ElliottSmith2016" /> and peak plasma levels of the drug are attained within roughly 30 to 60 minutes;<ref name="SmithPassik2008"/><ref name="ElliottSmith2016" /><ref name="LalovicKharasch2006" /> in contrast, after a dose of OxyContin (an oral controlled-release formulation), [[peak plasma levels]] of oxycodone occur in about three hours.<ref name="OxyContinInsertUS">{{cite book|title=1. Package insert Oxycontin|publisher=Purdue Pharma L.P|date=5 November 2007|location=Stamfbord, CT|url=http://www.purduepharma.com/PI/Prescription/Oxycontin.pdf|access-date=23 March 2009|url-status=dead|archive-url=https://web.archive.org/web/20090326125214/http://www.purduepharma.com/PI/Prescription/Oxycontin.pdf|archive-date=26 March 2009}}</ref> The duration of instant-release oxycodone is 3 to 6 hours, although this can be variable depending on the individual.<ref name="SmithPassik2008"/>

====Distribution====
Oxycodone has a [[volume of distribution]] of 2.6L/kg,<ref name="Drugbank">{{cite web |title=Oxycodone |url=https://www.drugbank.ca/drugs/DB00497 |website=www.drugbank.ca |access-date=24 January 2019 |archive-date=25 January 2019 |archive-url=https://web.archive.org/web/20190125074846/https://www.drugbank.ca/drugs/DB00497 |url-status=live }}</ref> in the blood it is distributed to [[skeletal muscle]], liver, intestinal tract, lungs, [[spleen]], and brain.<ref name="OxyContinInsertUS" /> At equilibrium the unbound concentration in the brain is threefold higher than the unbound concentration in blood.<ref>{{cite journal | vauthors = Boström E, Simonsson US, Hammarlund-Udenaes M | title = In vivo blood-brain barrier transport of oxycodone in the rat: indications for active influx and implications for pharmacokinetics/pharmacodynamics | journal = Drug Metabolism and Disposition | volume = 34 | issue = 9 | pages = 1624–1631 | date = September 2006 | pmid = 16763013 | doi = 10.1124/dmd.106.009746 | s2cid = 772550 }}</ref> Conventional oral preparations start to reduce pain within 10 to 15 minutes on an empty stomach; in contrast, OxyContin starts to reduce pain within one hour.<ref name=AHFS2018/>

====Metabolism====
The [[metabolism]] of oxycodone in humans occurs in the [[liver]] mainly via the [[cytochrome P450]] system and is extensive (about 95%) and complex, with many minor [[metabolic pathway|pathway]]s and resulting [[metabolite]]s.<ref name="SmithPassik2008" /><ref name="pmid14516487">{{cite journal | vauthors = Moore KA, Ramcharitar V, Levine B, Fowler D | title = Tentative identification of novel oxycodone metabolites in human urine | journal = Journal of Analytical Toxicology | volume = 27 | issue = 6 | pages = 346–352 | date = September 2003 | pmid = 14516487 | doi = 10.1093/jat/27.6.346 | doi-access = free }}</ref> Around 10% (range 8–14%) of a dose of oxycodone is excreted essentially unchanged (unconjugated or [[conjugation (biochemistry)|conjugated]]) in the [[urine]].<ref name="SmithPassik2008"/> The major metabolites of oxycodone are [[noroxycodone]] (70%), [[noroxymorphone]] ("relatively high concentrations"),<ref name="FitzgibbonLoeser2012">{{cite book| vauthors = Fitzgibbon DR, Loeser JD |title=Cancer Pain|url=https://books.google.com/books?id=17vaJQVtDN0C&pg=PA198|date=28 March 2012|publisher=Lippincott Williams & Wilkins|isbn=978-1-4511-5279-1|pages=198–}}</ref> and [[oxymorphone]] (5%).<ref name="LalovicKharasch2006" /><ref name="Preedy2016">{{cite book| vauthors = Preedy VR |title=Neuropathology of Drug Addictions and Substance Misuse Volume 3: General Processes and Mechanisms, Prescription Medications, Caffeine and Areca, Polydrug Misuse, Emerging Addictions and Non-Drug Addictions|url=https://books.google.com/books?id=Yu9eBwAAQBAJ&pg=PA462|date=25 April 2016|publisher=Elsevier Science|isbn=978-0-12-800677-1|pages=462–464}}</ref> The immediate metabolism of oxycodone in humans is as follows:<ref name="SmithPassik2008"/><ref name="McPhersonPincus2016" >{{cite book | vauthors = McPherson RA, Pincus MR |title=Henry's Clinical Diagnosis and Management by Laboratory Methods |url=https://books.google.com/books?id=xAzhCwAAQBAJ&pg=PA336 |date=31 March 2016 |publisher=Elsevier Health Sciences |isbn=978-0-323-41315-2 |pages=336–}}</ref><ref name="AnzenbacherZanger2012">{{cite book|vauthors=Anzenbacher P, Zanger UM|title=Metabolism of Drugs and Other Xenobiotics|url=https://books.google.com/books?id=ulcB7zYIresC&pg=PA420|date=29 May 2012|publisher=John Wiley & Sons|isbn=978-3-527-32903-8|pages=420–|access-date=5 October 2016|archive-date=7 October 2022|archive-url=https://web.archive.org/web/20221007000913/https://books.google.com/books?id=ulcB7zYIresC&pg=PA420|url-status=live}}</ref>

* N-[[Demethylation]] to [[noroxycodone]] predominantly via [[CYP3A4]]
* O-Demethylation to [[oxymorphone]] predominantly via [[CYP2D6]]
* 6-[[wikt:ketoreduction|Ketoreduction]] to [[6α-oxycodol|6α-]] and [[6β-oxycodol]]
* N-[[Oxidation]] to [[oxycodone-N-oxide]]

In humans, N-demethylation of oxycodone to noroxycodone by CYP3A4 is the major metabolic pathway, accounting for 45% ± 21% of a dose of oxycodone, while O-demethylation of oxycodone into oxymorphone by CYP2D6 and 6-ketoreduction of oxycodone into 6-oxycodols represent relatively minor metabolic pathways, accounting for 11% ± 6% and 8% ± 6% of a dose of oxycodone, respectively.<ref name="SmithPassik2008"/><ref name="Davis2009" />

Several of the immediate metabolites of oxycodone are subsequently conjugated with [[glucuronic acid]] and excreted in the [[urine]].<ref name="SmithPassik2008"/> 6α-Oxycodol and 6β-oxycodol are further metabolized by N-demethylation to [[nor-6α-oxycodol]] and [[nor-6β-oxycodol]], respectively, and by N-oxidation to [[6α-oxycodol-N-oxide]] and [[6β-oxycodol-N-oxide]] (which can subsequently be [[glucuronidation|glucuronidated]] as well).<ref name="SmithPassik2008"/><ref name="McPhersonPincus2016" /> Oxymorphone is also further metabolized, as follows:<ref name="SmithPassik2008"/><ref name="McPhersonPincus2016" /><ref name="AnzenbacherZanger2012" />

* 3-Glucuronidation to [[oxymorphone-3-glucuronide]] predominantly via [[UGT2B7]]
* 6-Ketoreduction to [[oxymorphol|6α-oxymorphol]] and [[oxymorphol|6β-oxymorphol]]
* N-Demethylation to [[noroxymorphone]]

The first pathway of the above three accounts for 40% of the metabolism of oxymorphone, making oxymorphone-3-glucuronide the main metabolite of oxymorphone, while the latter two pathways account for less than 10% of the metabolism of oxymorphone.<ref name="AnzenbacherZanger2012" /> After N-demethylation of oxymorphone, [[noroxymorphone]] is further glucuronidated to [[noroxymorphone-3-glucuronide]].<ref name="AnzenbacherZanger2012" />

Because oxycodone is metabolized by the cytochrome P450 system in the liver, its pharmacokinetics can be influenced by [[genetic polymorphism]]s and [[drug interaction]]s concerning this system, as well as by [[liver function]].<ref name="OxyContinInsertUS" /> Some people are [[fast metabolizer]]s of oxycodone, while others are [[slow metabolizer]]s, resulting in polymorphism-dependent alterations in relative analgesia and toxicity.<ref name="pmid15625333">{{cite journal | vauthors = Gasche Y, Daali Y, Fathi M, Chiappe A, Cottini S, Dayer P, Desmeules J | title = Codeine intoxication associated with ultrarapid CYP2D6 metabolism | journal = The New England Journal of Medicine | volume = 351 | issue = 27 | pages = 2827–2831 | date = December 2004 | pmid = 15625333 | doi = 10.1056/NEJMoa041888 | doi-access = free }}</ref><ref name="pmid8477556">{{cite journal | vauthors = Otton SV, Wu D, Joffe RT, Cheung SW, Sellers EM | title = Inhibition by fluoxetine of cytochrome P450 2D6 activity | journal = Clinical Pharmacology and Therapeutics | volume = 53 | issue = 4 | pages = 401–409 | date = April 1993 | pmid = 8477556 | doi = 10.1038/clpt.1993.43 | s2cid = 39724277 }}</ref> While higher CYP2D6 activity increases the effects of oxycodone (owing to increased conversion into oxymorphone), higher CYP3A4 activity has the opposite effect and decreases the effects of oxycodone (owing to increased metabolism into noroxycodone and noroxymorphone).<ref name="SamerDaali2010">{{cite journal | vauthors = Samer CF, Daali Y, Wagner M, Hopfgartner G, Eap CB, Rebsamen MC, Rossier MF, Hochstrasser D, Dayer P, Desmeules JA | title = Genetic polymorphisms and drug interactions modulating CYP2D6 and CYP3A activities have a major effect on oxycodone analgesic efficacy and safety | journal = British Journal of Pharmacology | volume = 160 | issue = 4 | pages = 919–930 | date = June 2010 | pmid = 20590588 | pmc = 2935998 | doi = 10.1111/j.1476-5381.2010.00709.x }}</ref> The dose of oxycodone must be reduced in patients with [[hepatic impairment|reduced liver function]].<ref name=AHFS>{{cite web |title=Oxycodone |url=https://www.drugs.com/monograph/oxycodone.html |work=The American Society of Health-System Pharmacists |access-date=3 April 2011 |archive-date=28 December 2018 |archive-url=https://web.archive.org/web/20181228174726/https://www.drugs.com/monograph/oxycodone.html |url-status=live }}</ref>

====Elimination====
The clearance of oxycodone is 0.8&nbsp;L/min.<ref name="Drugbank"/> Oxycodone and its metabolites are mainly [[excretion|excreted]] in urine.<ref name="DavisCladis2016">{{cite book| vauthors = Davis PJ, Cladis FP |title=Smith's Anesthesia for Infants and Children E-Book |url=https://books.google.com/books?id=SGljDQAAQBAJ&pg=PA234 |date=15 October 2016 |publisher=Elsevier Health Sciences |isbn=978-0-323-38869-6 |pages=234–}}</ref> Therefore, oxycodone accumulates in patients with [[renal|kidney]] impairment.<ref name="AHFS" /> Oxycodone is [[elimination (pharmacology)|eliminated]] in the urine 10% as unchanged oxycodone, 45% ± 21% as ''N''-demethylated metabolites (noroxycodone, noroxymorphone, noroxycodols), 11 ± 6% as ''O''-demethylated metabolites (oxymorphone, oxymorphols), and 8% ± 6% as 6-keto-reduced metabolites (oxycodols).<ref name="DavisCladis2016" /><ref name="LalovicKharasch2006"/>

====Duration of action====
Oral oxycodone has a half-life of 4.5 hours.<ref name="Drugbank"/> It is available as a [[generic medication]].<ref name="AHFS2018" /> The manufacturer of OxyContin, a controlled-release preparation of oxycodone, [[Purdue Pharma]], claimed in their 1992 patent application that the duration of action of OxyContin is 12 hours in "90% of patients". It has never performed any clinical studies in which OxyContin was given at more frequent intervals. In a separate filing, Purdue claims that controlled-release oxycodone "provides pain relief in said patient for at least 12 hours after administration".<ref name="latimes2016">{{cite news |vauthors=Ryan H, Girion L, Glover S |title=You want a description of hell?' OxyContin's 12-hour problem |url=https://www.latimes.com/projects/oxycontin-part1/ |access-date=8 July 2018 |work=Los Angeles Times |date=7 July 2016 |archive-date=1 July 2018 |archive-url=https://web.archive.org/web/20180701135355/http://www.latimes.com/projects/oxycontin-part1/ |url-status=live }}</ref> However, in 2016 an investigation by the ''[[Los Angeles Times]]'' found that "the drug wears off hours early in many people", inducing symptoms of [[opiate withdrawal]] and intense cravings for OxyContin. One doctor, Lawrence Robbins, told journalists that over 70% of his patients would report that OxyContin would only provide 4–7 hours of relief. Doctors in the 1990s often would switch their patients to a dosing schedule of once every eight hours when they complained that the duration of action for OxyContin was too short to be taken only twice a day.<ref name="latimes2016"/><ref name="oxycontinfiles">{{cite news |title='Q12' Workshops, 2001 |url=http://documents.latimes.com/q12-workshops-2001/ |newspaper=Los Angeles Times |access-date=8 July 2018 |archive-date=21 April 2018 |archive-url=https://web.archive.org/web/20180421121121/http://documents.latimes.com/q12-workshops-2001/ |url-status=live }}</ref>

Purdue strongly discouraged the practice: Purdue's medical director Robert Reder wrote to one doctor in 1995 that "OxyContin has been developed for [12-hour] dosing...I request that you not use a [8-hourly] dosing regimen." Purdue repeatedly released memos to its sales representatives ordering them to remind doctors not to deviate from a 12-hour dosing schedule. One such memo read, "There is no Q8 dosing with OxyContin... [8-hour dosing] needs to be nipped in the bud. NOW!!"<ref name="latimes2016"/> The journalists who covered the investigation argued that Purdue Pharma has insisted on a 12-hour duration of action for nearly all patients, despite evidence to the contrary, to protect the reputation of OxyContin as a 12-hour drug and the willingness of [[health insurance]] and [[managed care]] companies to cover OxyContin despite its high cost relative to generic opiates such as morphine.<ref name="latimes2016"/>

Purdue sales representatives were instructed to encourage doctors to write prescriptions for larger 12-hour doses instead of more frequent dosing. An August 1996 memo to Purdue sales representatives in Tennessee entitled "$$$$$$$$$$$$$ It's Bonus Time in the Neighborhood!" reminded the representatives that their commissions would dramatically increase if they were successful in convincing doctors to prescribe larger doses. ''Los Angeles Times'' journalists argue using interviews from opioid addiction experts that such high doses of OxyContin spaced 12 hours apart create a combination of agony during opiate withdrawal (lower lows) and a [[schedule of reinforcement]] that relieves this agony fostering addiction.<ref name="latimes2016"/>

==Chemistry==
{{See also|List of opioids}}

Oxycodone's chemical name is derived from [[codeine]]. The chemical structures are very similar, differing only in that

* Oxycodone has a [[hydroxy group]] at carbon-14 (codeine has just a hydrogen in its place)
* Oxycodone has a 7,8-dihydro feature. Codeine has a [[double bond]] between those two carbons; and
* Oxycodone has a [[carbonyl group]] (as in [[ketone]]s) in place of the hydroxyl group of codeine.

It is also similar to [[hydrocodone]], differing only in that it has a hydroxyl group at carbon-14.<ref name=AHFS/>

===Biosynthesis===
In terms of biosynthesis, oxycodone has been found naturally in nectar extracts from the orchid family ''[[Epipactis helleborine]]''; together along with another opioid: 3-<nowiki/>{2-<nowiki/>{3-<nowiki/>{3-benzyloxypropyl}-3-indol, 7,8-didehydro- 4,5-epoxy-3,6-d-morphinan.<ref>[https://www.erowid.org/references/texts/show/8710docid7639 "Why do pollinators become 'sluggish'? Nectar chemical constituents from Epipactis helleborine L. Crantz Orchidaceae".] {{Webarchive|url=https://web.archive.org/web/20201108121426/https://www.erowid.org/references/texts/show/8710docid7639 |date=8 November 2020 }} Applied Ecology & Environmental Research. 2005;3(2):29–38. Jakubska A, Przado D, Steininger M, Aniol-Kwiatkowska A, Kadej M.</ref>

Thodey ''et al.'', 2014 introduces a [[microbe|microbial]] compound manufacturing system for compounds including oxycodone.<ref name="engineeringsecondary" /> The Thodey platform produces both natural and [[semisynthetic]] opioids including this one.<ref name="engineeringsecondary" /> This system uses ''[[Saccharomyces cerevisiae]]'' with [[transgene]]s from ''[[Papaver somniferum]]'' (the opium poppy) and ''[[Pseudomonas putida]]'' to turn a [[thebaine]] input into other opiates and opioids.<ref name="engineeringsecondary">
   {{Unbulleted list citebundle
      |{{*}} {{cite journal | vauthors = O'Connor SE | title = Engineering of Secondary Metabolism | journal = Annual Review of Genetics | volume = 49 | issue = 1 | pages = 71–94 | year = 2015 | pmid = 26393965 | doi = 10.1146/annurev-genet-120213-092053 | publisher = [[Annual Reviews (publisher)|Annual Reviews]] | doi-access = free }}
      |{{*}} {{cite journal | year=2015 | publisher=[[Faculty Opinions Ltd]] | journal=[[Faculty Opinions]] | vauthors = Deng Z, Liu T | title=Faculty Opinions recommendation of A microbial biomanufacturing platform for natural and semisynthetic opioids | doi=10.3410/f.718541729.793511628 | s2cid=222595431 | doi-access=free }}
      |{{*}} {{cite journal | vauthors = Thodey K, Galanie S, Smolke CD | title = A microbial biomanufacturing platform for natural and semisynthetic opioids | journal = Nature Chemical Biology | volume = 10 | issue = 10 | pages = 837–844 | date = October 2014 | pmid = 25151135 | pmc = 4167936 | doi = 10.1038/nchembio.1613 | publisher = [[Nature Portfolio]] | s2cid = 38478470 }}
   }}
</ref>

===Detection in biological fluids===
Oxycodone and/or its major metabolites may be measured in blood or urine to monitor for [[Clearance (medicine)|clearance]], non-medical use, confirm a diagnosis of poisoning or assist in a medicolegal death investigation. Many commercial opiate screening tests cross-react appreciably with oxycodone and its metabolites, but chromatographic techniques can easily distinguish oxycodone from other opiates.<ref>{{cite book | vauthors = Baselt R | date = 2017 | title = Disposition of Toxic Drugs and Chemicals in Man | edition = 11th | publisher = Biomedical Publications | location = Foster City, CA | pages = 1604–1607 }}</ref>

==History==
[[Martin Freund]] and (Jakob) [[Edmund Speyer]] of the [[Johann Wolfgang Goethe University Frankfurt am Main|University of Frankfurt]] in Germany published the first synthesis of oxycodone from [[thebaine]] in 1916.<ref>{{cite journal | vauthors = Freund M, Speyer E |title=Über die Umwandlung von Thebain in Oxycodeinon und dessen Derivate |journal=Journal für Praktische Chemie |date=24 November 1916 |volume=94 |issue=1 |pages=135–178 |doi=10.1002/prac.19160940112 |url=https://zenodo.org/record/1428060 }}</ref><ref name="Oxysynthesis2005">{{cite book |url=https://archive.org/details/drugdiscoveryhis00snea |title=Drug discovery: a history |vauthors=Sneader W |publisher=Wiley |year=2005 |isbn=978-0-471-89980-8 |location=Hoboken, NJ |page=[https://archive.org/details/drugdiscoveryhis00snea/page/n132 119] |url-access=limited}}</ref> When Freund died, in 1920, Speyer wrote his obituary for the [[German Chemical Society]].<ref>{{cite journal |title=Martin Freund |journal=Berichte der Deutschen Chemischen Gesellschaft (A and B Series) |date=7 May 1921 |volume=54 |issue=5 |pages=A53–A79 |doi=10.1002/cber.19210540533}}</ref> Speyer, born to a Jewish family in Frankfurt am Main in 1878, became a victim of the [[Holocaust]]. He died on 5 May 1942, the second day of deportations from the [[Lodz Ghetto]]; his death was noted in the ghetto's chronicle.<ref>{{cite book |title=The Holocaust: a history of the Jews of Europe during the Second World War |year=1986 |url=https://archive.org/details/holocausthistory0000gilb |url-access=registration |publisher=Holt, Rinehart, and Winston |isbn=0-03-062416-9 |pages=[https://archive.org/details/holocausthistory0000gilb/page/346 346] |edition=1st American |access-date=3 June 2020}}</ref>

The first clinical use of the drug was documented in 1917, the year after it was first developed.<ref name=Oxysynthesis2005/><ref name="sunshine1996"/> It was first introduced to the U.S. market in May 1939. In early 1928, [[Merck Group|Merck]] introduced a combination product containing [[Hyoscine hydrobromide|scopolamine]], oxycodone, and [[ephedrine]] under the German initials for the ingredients SEE, which was later renamed Scophedal (SCOpolamine, ePHEDrine, and eukodAL) in 1942. It was last manufactured in 1987 but can be [[Compounded drug|compounded]]. This combination is essentially an oxycodone [[Analogue (chemical)|analogue]] of the morphine-based "[[twilight sleep]]", with ephedrine added to reduce circulatory and respiratory effects.<ref name="ReferenceA">{{cite journal | vauthors = Defalque RJ, Wright AJ | title = Scophedal (SEE) was it a fad or a miracle drug? | journal = Bulletin of Anesthesia History | volume = 21 | issue = 4 | pages = 12–14 | date = October 2003 | pmid = 17494237 | doi = 10.1016/S1522-8649(03)50051-8 }}</ref> The drug became known as the "Miracle Drug of the 1930s" in Continental Europe and elsewhere and it was the [[Wehrmacht]]'s choice for a battlefield analgesic for a time. The drug was expressly designed to provide what the patent application and package insert referred to as "very deep analgesia and profound and intense euphoria" as well as tranquillisation and [[anterograde amnesia]] useful for surgery and battlefield wounding cases. Oxycodone was allegedly chosen over other common opiates for this product because it had been shown to produce less sedation at equianalgesic doses compared to morphine, hydromorphone (Dilaudid), and hydrocodone (Dicodid).<ref>William S Burroughs 1952 letter to Allen Ginsburg concerning Eukodal, in Collected Correspondance, pp 141–2</ref>

During [[Operation Himmler]], Skophedal was also reportedly injected in massive overdose into the prisoners dressed in Polish Army uniforms in the [[Gleiwitz incident|staged incident on 1 September 1939]] which opened the Second World War.<ref name="ReferenceA"/><ref>Merck 1930 package insert for Skophedal (German)</ref>

The personal notes of [[Adolf Hitler]]'s physician, [[Theodor Morell]], indicate Hitler received repeated injections of "Eukodal" (oxycodone; produced by Merck) and Scophedal, as well as Dolantin ([[pethidine]]) codeine, and [[morphine]] less frequently; oxycodone could not be obtained after late January 1945.<ref>{{Cite web |url= http://www.dw.com/en/a-fresh-light-on-the-nazis-wartime-drug-addiction/a-18703678 |title=A fresh light on the Nazis' wartime drug addiction |vauthors= Breitenbach D |date=9 September 2015 |website=Deutsche Welle |location=Bonn |access-date=24 April 2016 |archive-date=25 April 2016 |archive-url= https://web.archive.org/web/20160425040250/http://www.dw.com/en/a-fresh-light-on-the-nazis-wartime-drug-addiction/a-18703678 |url-status=live }}</ref><ref>{{cite book | vauthors = Ohler N, Whiteside S |title=Blitzed: drugs in the Third Reich |year=2017 |publisher=Houghton Mifflin Harcourt |location=Boston |isbn=978-1-328-66379-5 |edition=First U.S. |page = 194 }}</ref>

In the United States, the [[Controlled Substances Act|Controlled Substances Act (CSA)]] was passed by the United States Congress and signed into law by President [[Richard Nixon]] on 27 October 1970.<ref>{{USStatute|91|513|84|1236|1970|10|27}}, codified at {{usc|21|801}}et. seq.</ref> The passing of the CSA resulted in all products containing oxycodone to be classified as a [[Schedule II Controlled Substance|Schedule II controlled substance]].<ref>{{Cite journal | vauthors = Sapienza FL |date= June 2006 |title=Abuse deterrent formulations and the Controlled Substances Act (CSA) |url=https://www.sciencedirect.com/science/article/pii/S0376871606000561 |journal=Drug and Alcohol Dependence |series=Drug Formulation and Abuse Liability |volume=83 |pages=S23–S30 |doi=10.1016/j.drugalcdep.2005.11.028 |pmid=16529882 |issn=0376-8716 |quote=The CSA as enacted in 1970 provides examples of specifically listed substances in one schedule and formulations containing them in different schedules. The CSA also provides a mechanism to exempt certain formulations and products from regulations. ... Each of these substances is in Schedule II of the CSA. However, formulations/products containing limited amounts of these substances in combination with an isoquinoline alkaloid or one or more active non-narcotic ingredients in recognized therapeutic amounts were included in Schedule III or V of the CSA (Public Law 91-513, Section 202). ... It is interesting to note that no criteria were established for the differential control of the Schedule II opioid oxycodone and its combination products. Thus, oxycodone and all marketed single entity and combination products are in Schedule II.}}</ref><!-- Oxycodone is not listed by name in the CSA of 1970: https://www.govinfo.gov/content/pkg/STATUTE-84/pdf/STATUTE-84-Pg1236.pdf. Either a medical or legal source is needed to explain how and when it was scheduled. -->

[[Purdue Pharma]], a privately held company based in Stamford, Connecticut, developed the prescription painkiller OxyContin.  It was approved by the FDA in 1995 after no long-term studies and no assessment of its addictive capabilities.<ref>{{cite web |title=Confirmation Hearing for FDA Commissioner Nominee |date=14 December 2021 |url= https://archive.org/details/CSPAN3_20211214_150000_Confirmation_Hearing_for_FDA_Commissioner_Nominee |publisher=[[C-SPAN]] |access-date=12 December 2022}}</ref> David Kessler, [[Commissioner of Food and Drugs|FDA commissioner]] at the time, later said of the approval of OxyContin:  "No doubt it was a mistake. It was certainly one of the worst medical mistakes, a major mistake."<ref>{{cite news | vauthors = Mitchell J |title=How the FDA helped pave the way for an opioid epidemic |url= https://www.clarionledger.com/story/news/2018/01/26/opioid-epidemic-how-fda-helped-pave-way/950561001/ |access-date=12 December 2022 |work= Clarion Ledger |location= Jackson MS |date=26 January 2018}}</ref> Upon its release in 1995, OxyContin was hailed as a medical breakthrough, a long-lasting narcotic that could help patients with moderate to severe pain. The drug became a blockbuster and has reportedly generated some US$35 billion in revenue for Purdue.<ref name="eop">{{cite magazine |url=https://www.newyorker.com/magazine/2017/10/30/the-family-that-built-an-empire-of-pain |title=The Family That Built an Empire of Pain |vauthors= Keefe PR |author-link=Patrick Radden Keefe |date=23 October 2017 |magazine=[[The New Yorker]] |access-date=2 February 2019 |archive-date=22 January 2018 |archive-url= https://web.archive.org/web/20180122073308/https://www.newyorker.com/magazine/2017/10/30/the-family-that-built-an-empire-of-pain |url-status=live }}</ref>

==Opioid epidemic==
<!-- This Anchor tag serves to provide a permanent target for incoming section links. Please do not move it out of the section heading, even though it disrupts edit summary generation (you can manually fix the edit summary before saving your changes). Please do not modify it, even if you modify the section title. It is always best to anchor an old section header that has been changed so that links to it won't be broken. See [[Template:Anchor]] for details. (This text: [[Template:Anchor comment]]) -->
{{See also|Opioid epidemic}}
Oxycodone, like other opioid analgesics, tends to induce feelings of euphoria, relaxation and reduced anxiety in those who are occasional users.<ref>{{cite web|title=OxyContin: Pain Relief vs. Abuse|url=http://www.webmd.com/pain-management/features/oxycontin-pain-relief-vs-abuse|access-date=11 February 2018|archive-date=24 October 2017|archive-url=https://web.archive.org/web/20171024093615/https://www.webmd.com/pain-management/features/oxycontin-pain-relief-vs-abuse|url-status=live}}</ref> These effects make it one of the most commonly abused pharmaceutical drugs in the United States.<ref>{{cite web|date=28 April 2014|title=Top 10 Most Commonly Abused Prescription Medications|url=http://newlifehouse.com/top-10-commonly-abused-prescription-medications/|url-status=dead|archive-url=https://web.archive.org/web/20180102052056/https://newlifehouse.com/top-10-commonly-abused-prescription-medications/|archive-date=2 January 2018|access-date=11 February 2018}}</ref> The abuse of Oxycodone, as well as related opioids more broadly, is not unique to the United States and is a common drug of abuse globally.<ref>{{Cite web |title=Opioid overdose |url=https://www.who.int/news-room/fact-sheets/detail/opioid-overdose |access-date=11 November 2023 |website=World Health Organization }}</ref><ref>{{Cite web |title=WHO Expert Committee on Drug Dependence: forty-third report |url=https://www.who.int/publications-detail-redirect/9789240023024 |access-date=11 November 2023 |website=World Health Organization }}</ref>

===United States===
{{See also|Opioid epidemic in the United States}}

Oxycodone is the most widely recreationally used opioid in America. In the United States, more than 12 million people use opioid drugs recreationally.<ref name="Girioin">{{cite news|date=11 September 2013|title=FDA to require stricter labeling for pain drugs|pages=A1 and A9|newspaper=Los Angeles Times|vauthors=Girioin L, Haely M}}</ref> The [[U.S. Department of Health and Human Services]] estimates that about 11 million people in the U.S. consume oxycodone in a non-medical way annually.<ref>[http://www.sfchronicle.com/news/article/Now-a-counselor-she-went-from-stoned-to-straight-6605620.php Now a counselor, she went from stoned to straight], [[San Francisco Chronicle]], 2 November. 2015.</ref>

Opioids were responsible for 49,000 of the 72,000 [[drug overdose]] deaths in the U.S. in 2017.<ref name="NIDA-deaths">{{cite web|date=29 January 2019|title=Overdose Death Rates|url=http://www.drugabuse.gov/related-topics/trends-statistics/overdose-death-rates|access-date=11 May 2019|website=www.drugabuse.gov|archive-date=28 November 2015|archive-url=https://web.archive.org/web/20151128091723/http://www.drugabuse.gov/related-topics/trends-statistics/overdose-death-rates|url-status=live}}</ref> In 2007, about 42,800 emergency room visits occurred due to "episodes" involving oxycodone.<ref>{{Cite web|title=Oxycontin and Addiction|url=http://consumer.healthday.com/encyclopedia/substance-abuse-38/drug-abuse-news-210/oxycontin-and-addiction-648264.html|access-date=24 April 2016|website=consumer.healthday.com|archive-date=15 April 2016|archive-url=https://web.archive.org/web/20160415210939/http://consumer.healthday.com/encyclopedia/substance-abuse-38/drug-abuse-news-210/oxycontin-and-addiction-648264.html|url-status=dead}}</ref>  In 2008, recreational use of oxycodone and hydrocodone was involved in 14,800 deaths. Some of the cases were due to overdoses of the acetaminophen component, resulting in fatal liver damage.<ref>[https://web.archive.org/web/20120105112147/http://www.cdc.gov/HomeandRecreationalSafety/pdf/PolicyImpact-PrescriptionPainkillerOD.pdf Policy Impact: Prescription Pain Killer Overdoses] Centers for Disease Control and Prevention. Retrieved 24 December 2013.</ref>

In September 2013, the [[Food and Drug Administration|FDA]] released new labeling guidelines for long-acting and extended-release opioids requiring manufacturers to remove moderate pain as indication for use, instead stating the drug is for "pain severe enough to require daily, around-the-clock, long term opioid treatment".<ref>{{cite web|title=ER/LA Opioid Analgesic Class Labeling Changes and Postmarket Requirements|url=https://www.fda.gov/downloads/Drugs/DrugSafety/InformationbyDrugClass/UCM367697.pdf|access-date=12 September 2013|publisher=FDA|archive-date=18 September 2013|archive-url=https://web.archive.org/web/20130918062419/http://www.fda.gov/downloads/Drugs/DrugSafety/InformationbyDrugClass/UCM367697.pdf|url-status=live}}</ref> The updated labeling will not restrict physicians from prescribing opioids for moderate pain, as needed.<ref name="Girioin" />

Reformulated OxyContin is causing some recreational users to change to [[heroin]], which is cheaper and easier to obtain.<ref>[http://www.pharmaceutical-journal.com/news-and-analysis/news/reformulated-oxycontin-reduces-abuse-but-many-addicts-have-switched-to-heroin/20068119.article Reformulated OxyContin reduces abuse but many addicts have switched to heroin] {{Webarchive|url=https://web.archive.org/web/20171120051037/http://www.pharmaceutical-journal.com/news-and-analysis/news/reformulated-oxycontin-reduces-abuse-but-many-addicts-have-switched-to-heroin/20068119.article |date=20 November 2017 }}, The Pharmaceutical Journal, 16 March 2015.</ref>

====Lawsuits====
In October 2017, ''[[The New Yorker]]'' published a story on [[Mortimer Sackler]] and [[Purdue Pharma]] regarding their ties to the production and manipulation of the oxycodone markets.<ref name="eop" /> The article links Raymond and Arthur Sackler's business practices with the rise of direct pharmaceutical marketing and eventually to the rise of addiction to oxycodone in the United States. The article implies that the [[Sackler family]] bears some responsibility for the [[opioid epidemic in the United States]].<ref name="NewYorker_Keefe_20171023">{{Cite magazine|vauthors=Keefe PR|date=23 October 2017|title=The Family That Built an Empire of Pain|magazine=[[The New Yorker]]|url=https://www.newyorker.com/magazine/2017/10/30/the-family-that-built-an-empire-of-pain|access-date=18 November 2017|issn=0028-792X|archive-date=22 January 2018|archive-url=https://web.archive.org/web/20180122073308/https://www.newyorker.com/magazine/2017/10/30/the-family-that-built-an-empire-of-pain|url-status=live}}</ref> In 2019, ''[[The New York Times]]'' ran a piece confirming that [[Richard Sackler]], the son of Raymond Sackler, told company officials in 2008 to "measure our performance by Rx's by strength, giving higher measures to higher strengths".<ref>{{Cite news|vauthors=Meier B|date=31 January 2019|title=Sackler Scion's Email Reveals Push for High-Dose OxyContin, New Lawsuit Disclosures Claim|work=The New York Times|url=https://www.nytimes.com/2019/01/31/health/opioids-purdue-pharma-sackler.html|access-date=3 February 2019|issn=0362-4331|archive-date=2 February 2019|archive-url=https://web.archive.org/web/20190202180610/https://www.nytimes.com/2019/01/31/health/opioids-purdue-pharma-sackler.html|url-status=live}}</ref> This was verified with documents tied to a lawsuit – which was filed by the Massachusetts attorney general, [[Maura Healey]] – claiming that Purdue Pharma and members of the Sackler family knew that high doses of OxyContin over long periods would increase the risk of serious side effects, including addiction.<ref>{{cite news|vauthors=Bebinger M, Willmsen C|date=15 January 2019|title=Mass. AG Implicates Family Behind Purdue Pharma In Opioid Deaths|work=WBUR Boston|url=https://www.wbur.org/commonhealth/2019/01/15/healey-purdue-oxycontin-sacklers-unredacted-complaint|access-date=19 September 2019|archive-date=16 October 2019|archive-url=https://web.archive.org/web/20191016135025/https://www.wbur.org/commonhealth/2019/01/15/healey-purdue-oxycontin-sacklers-unredacted-complaint|url-status=live}}</ref> Despite Purdue Pharma's proposal for a US$12 billion settlement of the lawsuit, the attorneys general of 23 states, including Massachusetts, rejected the settlement offer in September 2019.<ref>{{cite news|vauthors=DeCosta-Klipa N|date=17 September 2019|title=Maura Healey explains why she refused to join the Purdue Pharma settlement|work=Boston.com|publisher=Boston Globe Media Partners, LLC|url=https://www.boston.com/news/politics/2019/09/17/maura-healey-purdue-settlement|access-date=19 September 2019|archive-date=17 October 2019|archive-url=https://web.archive.org/web/20191017195611/https://www.boston.com/news/politics/2019/09/17/maura-healey-purdue-settlement|url-status=live}}</ref>

===Australia===
The non-medical use of oxycodone existed from the early 1970s, but by 2015, 91% of a national sample of injecting drug users in Australia had reported using oxycodone, and 27% had injected it in the last six months.<ref>{{cite book|url=http://ndarc.med.unsw.edu.au/NDARCWeb.nsf/resources/DRUG_TRENDS_1_NAT/$file/DT001.PDF |title=Australian drug trends 2007. Findings from the Illicit Drug Reporting System (IDRS)|vauthors=Black E|publisher=National Drug and Alcohol Research Centre, University of New South Wales|year=2008|isbn=978-0-7334-2625-4|location=Sydney|archive-url= https://web.archive.org/web/20080721045101/http://ndarc.med.unsw.edu.au/NDARCWeb.nsf/resources/DRUG_TRENDS_1_NAT/$file/DT001.PDF |archive-date=21 July 2008|url-status=dead}}</ref>

===Canada===
Opioid-related deaths in Ontario had increased by 242% from 1969 to 2014.<ref name="The_Star_2014">{{cite web|vauthors=Boyle T|title=Opioid deaths soaring, study finds Opioid-related deaths in Ontario jumped by a whopping 242 per cent over two decades, according to a study by ICES and St. Mike's|date=7 July 2014|url=https://www.thestar.com/life/health_wellness/2014/07/07/opioid_deaths_soaring_study_finds.html|work=The Star|location=Toronto, Ontario|access-date=23 January 2015|archive-date=23 January 2015|archive-url=https://web.archive.org/web/20150123191050/http://www.thestar.com/life/health_wellness/2014/07/07/opioid_deaths_soaring_study_finds.html|url-status=live}}</ref> By 2009 in Ontario there were more deaths from oxycodone overdoses than from cocaine overdoses.<ref name="The_Star_2009">{{cite web|vauthors=Donovan K|title=Oxycodone found to be more deadly than heroin|date=10 February 2009|url=https://www.thestar.com/life/health_wellness/2009/02/10/oxycodone_found_to_be_more_deadly_than_heroin.html|work=The Star|location=Toronto, Ontario|access-date=23 January 2015|archive-date=23 January 2015|archive-url=https://web.archive.org/web/20150123191054/http://www.thestar.com/life/health_wellness/2009/02/10/oxycodone_found_to_be_more_deadly_than_heroin.html|url-status=live}}</ref> Deaths from opioid pain relievers had increased from 13.7 deaths per million residents in 1991 to 27.2 deaths per million residents in 2004.<ref>{{cite news|title=Study finds huge rise in oxycodone deaths|publisher=[[CTV News]]|url=https://www.ctvnews.ca/study-finds-huge-rise-in-oxycodone-deaths-1.461899|access-date=7 December 2009|archive-date=28 June 2012|archive-url=https://web.archive.org/web/20120628112202/http://www.ctvnews.ca/study-finds-huge-rise-in-oxycodone-deaths-1.461899|url-status=live}}</ref> The non-medical use of oxycodone in Canada became a problem. Areas where oxycodone is most problematic are [[Atlantic Canada]] and [[Ontario]], where its non-medical use is prevalent in rural towns and in many smaller to medium-sized cities.<ref name="Oxyabuse">{{cite web|title=OxyContin Fact Sheet|url=http://www.ccsa.ca/2006%20CCSA%20Documents/ccsa-003642-2006.pdf|archive-url=https://web.archive.org/web/20081117203212/http://www.ccsa.ca/2006%20CCSA%20Documents/ccsa-003642-2006.pdf|archive-date=17 November 2008|access-date=10 May 2012|website=ccsa.ca|url-status=dead}}</ref> Oxycodone is also widely available across [[Western Canada]], but [[methamphetamine]] and [[heroin]] are more serious problems in larger cities, while oxycodone is more common in rural towns. Oxycodone is diverted through [[doctor shopping]], prescription forgery, pharmacy theft, and overprescription.<ref name="Oxyabuse" /><ref>{{cite web|date=11 January 2010|title=Health Canada – Misuse and Abuse of Oxycodone-based Prescription Drugs|url=http://www.hc-sc.gc.ca/hc-ps/pubs/precurs/oxycodone/fs-fi/index-eng.php|archive-url=https://web.archive.org/web/20111126013544/http://www.hc-sc.gc.ca/hc-ps/pubs/precurs/oxycodone/fs-fi/index-eng.php|archive-date=26 November 2011|access-date=10 May 2012|website=Hc-sc.gc.ca}}</ref>

The recent formulations of oxycodone, particularly Purdue Pharma's crush-, chew-, injection- and dissolve-resistant OxyNEO<ref>{{cite news| vauthors = Kirkey S |date=23 May 2012|title=OxyNEO another prescription for disaster?|newspaper=Globe and Mail|location=Toronto, Ontario}}</ref> which replaced the banned OxyContin product in Canada in early 2012, have led to a decline in the recreational use of this opiate but have increased the recreational use of the more potent drug fentanyl.<ref>{{cite web|vauthors=Criger E|date=17 August 2015|title=Death of OxyContin behind rise of fentanyl?|url=https://toronto.citynews.ca/2015/08/17/death-of-oxycontin-behind-rise-of-fentanyl/|access-date=7 February 2019|website=CityNews|publisher=Rogers Digital Media|archive-date=9 February 2019|archive-url=https://web.archive.org/web/20190209180023/https://toronto.citynews.ca/2015/08/17/death-of-oxycontin-behind-rise-of-fentanyl/|url-status=live}}</ref> According to a Canadian Centre on Substance Abuse study quoted in [[Maclean's]] magazine, there were at least 655 fentanyl-related deaths in Canada in a five-year period.<ref>{{cite web|vauthors=Gatehouse J, Macdonald N|date=22 June 2015|title=Fentanyl: The King of all Opiates, and a Killer Drug Crisis|url=http://www.macleans.ca/society/health/fentanyl-the-king-of-all-opiates-and-a-killer-drug-crisis/|access-date=15 December 2015|website=Maclean's|publisher=Rogers Media|archive-date=15 December 2015|archive-url=https://web.archive.org/web/20151215045912/http://www.macleans.ca/society/health/fentanyl-the-king-of-all-opiates-and-a-killer-drug-crisis/|url-status=live}}</ref>

In Alberta, the Blood Tribe police claimed that from the fall of 2014 through January 2015, oxycodone pills or a lethal fake variation referred to as Oxy 80s<ref name="Southwick">{{cite news| vauthors = Southwick R |date=2 December 2015|title=Fentanyl brings tragedy to Blood Tribe|newspaper=Calgary Herald|location=Calgary, Alberta|url=https://calgaryherald.com/news/crime/fentanyl-brings-tragedy-to-blood-tribe|url-status=dead|access-date=15 December 2015|archive-url=https://web.archive.org/web/20151222143028/http://calgaryherald.com/news/crime/fentanyl-brings-tragedy-to-blood-tribe|archive-date=22 December 2015}}</ref> containing [[fentanyl]] made in illegal labs by members of organized crime were responsible for ten deaths on the [[Blood Indian Reserve No. 148|Blood Reserve]], which is located southwest of [[Lethbridge]], [[Alberta]].<ref name="Calgary_Herald_2015">{{citation|title=Police believe organized crime is flooding the Blood Tribe reserve with an illegal drug that has been linked to 10 deaths|date=23 January 2015|url=https://calgaryherald.com/storyline/police-believe-organized-crime-is-behind-flooding-the-blood-tribe-reserve-with-an-illegal-drug-that-has-been-linked-to-10-deaths|archive-url=https://web.archive.org/web/20160124073724/http://calgaryherald.com/storyline/police-believe-organized-crime-is-behind-flooding-the-blood-tribe-reserve-with-an-illegal-drug-that-has-been-linked-to-10-deaths|location=Alberta|publisher=Calgary Herald|access-date=23 January 2015|archive-date=24 January 2016|url-status=dead}}</ref> Province-wide, approximately 120 Albertans died from fentanyl-related overdoses in 2014.<ref name="Southwick" />

===United Kingdom===
Prescriptions of Oxycodone rose in Scotland by 430% between 2002 and 2008, prompting fears of usage problems that would mirror those of the United States.<ref>{{cite news|vauthors=Gordon T|date=30 March 2008|title=Huge rise in Scots misuse of painkiller|work=Sunday Times (London)|url=https://www.thetimes.co.uk/article/huge-rise-in-scots-misuse-of-painkiller-q5bl8rlpb6b|access-date=12 April 2022|archive-date=10 October 2022|archive-url=https://web.archive.org/web/20221010053102/https://www.thetimes.co.uk/article/huge-rise-in-scots-misuse-of-painkiller-q5bl8rlpb6b|url-status=live}}</ref> The first known death due to overdose in the UK occurred in 2002.<ref>{{cite news|vauthors=Thompson T|date=24 March 2002|title=Epidemic fear as 'hillbilly heroin' hits the streets|work=Society Guardian|url=https://www.theguardian.com/society/2002/mar/24/drugsandalcohol|access-date=16 April 2009|archive-date=26 August 2013|archive-url=https://web.archive.org/web/20130826005512/http://www.theguardian.com/society/2002/mar/24/drugsandalcohol|url-status=live}}</ref>

==={{anchor|OxyContin}}Preventive measures===
In August 2010, [[Purdue Pharma]] reformulated their long-acting oxycodone line, marketed as OxyContin, using a polymer, Intac,<ref>{{cite web |date=2010 |title=New Abuse Deterrent Formulation Technology for Immediate-Release Opioids |url=http://www.grunenthal.com/cms/cda/file/Drug+Development+%26+Delivery+October+2013+Vol+13+No+8.pdf?fileID=273800346&cacheFix=1383822554000&__k=3870fc7ab9c0252c7a9c8547fb47de75 |url-status=dead |archive-url=https://web.archive.org/web/20151222103656/http://www.grunenthal.com/cms/cda/file/Drug+Development+%26+Delivery+October+2013+Vol+13+No+8.pdf?fileID=273800346&cacheFix=1383822554000&__k=3870fc7ab9c0252c7a9c8547fb47de75 |archive-date=22 December 2015 |access-date=15 December 2015 |website=Grünenthal Group |publisher=Grünenthal Group Worldwide}}</ref> to make the pills more difficult to crush or dissolve in water<ref>{{cite web|vauthors=Diep F|date=13 May 2013|title=How Do You Make a Painkiller Addiction-Proof|url=https://www.popsci.com/science/article/2013-05/science-un-crushable-oxycontin|access-date=30 January 2019|website=Popular Science|publisher=Bonnier Corporation|archive-date=14 December 2019|archive-url=https://web.archive.org/web/20191214154207/https://www.popsci.com/science/article/2013-05/science-un-crushable-oxycontin/|url-status=live}}</ref> to reduce non-medical use of OxyContin.<ref>{{Cite conference|vauthors=Coplan P|year=2012|title=Findings from Purdue's Post-Marketing Epidemiology Studies of Reformulated OxyContin's Effects|url=http://www.nascsa.org/Conference2012/Presentations/Coplan.pdf|conference=NASCSA 2012 Conference|location=Scottsdale, Arizona|archive-url=https://web.archive.org/web/20130614115419/http://www.nascsa.org/Conference2012/Presentations/Coplan.pdf|archive-date=14 June 2013|conference-url=https://web.archive.org/web/20130512052124/http://www.nascsa.org/conference2012.htm|url-status=dead|accessdate=23 May 2013}}</ref> The FDA approved relabeling the reformulated version as abuse-resistant in April 2013.<ref>{{cite web|title=Press Announcements; FDA approves abuse-deterrent labeling for reformulated OxyContin|url=https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm348252.htm|url-status=dead|archive-url=https://web.archive.org/web/20130520025104/http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm348252.htm|archive-date=20 May 2013|access-date=23 May 2013|publisher=US Government – FDA}}</ref>

[[Pfizer]] manufactures a preparation of short-acting oxycodone, marketed as Oxecta, which contains inactive ingredients, referred to as tamper-resistant Aversion Technology.<ref>{{cite web|title=Pfizer and Acura Announce FDA Approval of Oxectatm (Oxycodone HCL, USP) CII|url=http://press.pfizer.com/press-release/pfizer-and-acura-announce-fda-approval-oxectatm-oxycodone-hcl-usp-cii|url-status=dead|archive-url=https://web.archive.org/web/20151222111749/http://press.pfizer.com/press-release/pfizer-and-acura-announce-fda-approval-oxectatm-oxycodone-hcl-usp-cii|archive-date=22 December 2015|access-date=15 December 2015|website=Pfizer News and Media|publisher=Pfizer Inc.}}</ref> Approved by the FDA in the U.S. in June 2011, the new formulation, while not being able to deter oral recreational use, makes crushing, chewing, snorting, or injecting the opioid impractical because of a change in its chemical properties.<ref>{{cite web| vauthors = Fiore K |date=20 June 2011|title=FDA Okays New Abuse-Resistant Opioid|url=http://www.medpagetoday.com/ProductAlert/Prescriptions/27157|url-status=dead|archive-url= https://web.archive.org/web/20151222095414/http://www.medpagetoday.com/ProductAlert/Prescriptions/27157|archive-date=22 December 2015|access-date=15 December 2015|website=MedPage Today}}</ref>

==Legal status==
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.<ref>{{cite web |author=League of Nations |title=Convention for limiting the manufacture and regulating the distribution of narcotic drugs |year=1931 |url=http://treaties.un.org/doc/Treaties/1931/07/19310713%2006-44%20AM/Ch_VI_8_ap.pdf |access-date=4 April 2009 |archive-date=3 June 2012 |archive-url=https://web.archive.org/web/20120603203403/http://treaties.un.org/doc/Treaties/1931/07/19310713%2006-44%20AM/Ch_VI_8_ap.pdf |url-status=live }}</ref> The 1961 [[Single Convention on Narcotic Drugs]] of the [[United Nations]], which replaced the 1931 convention, categorized oxycodone in Schedule I.<ref name="SingleConvention">{{cite web |title=United Nations conference for the adoption of a single convention on narcotic drugs. Final act |year=1961 |url=http://treaties.un.org/doc/Treaties/1964/12/19641213%2002-14%20AM/Ch_VI_15p.pdf |access-date=4 April 2009 |url-status=dead |archive-url=https://web.archive.org/web/20110817062450/http://treaties.un.org/doc/Treaties/1964/12/19641213%2002-14%20AM/Ch_VI_15p.pdf |archive-date=17 August 2011 }}</ref> Global restrictions on Schedule I drugs include "limit[ing] exclusively to medical and scientific purposes the production, manufacture, export, import, distribution of, trade in, use and possession of" these drugs; "requir[ing] medical prescriptions for the supply or dispensation of [these] drugs to individuals"; and "prevent[ing] the accumulation" of quantities of these drugs "in excess of those required for the normal conduct of business".<ref name="SingleConvention" />

=== Australia ===
Oxycodone is in Schedule I (derived from the Single Convention on Narcotic Drugs) of the Commonwealth's Narcotic Drugs Act 1967.<ref>{{cite web |author=Commonwealth of Australia |title=Narcotic Drugs Act 1967 – first schedule |publisher=Australasian Legal Information Institute |url=http://www.austlii.edu.au/au/legis/cth/consol_act/nda1967160/sch1.html |access-date=6 April 2009 |archive-date=24 June 2010 |archive-url=https://web.archive.org/web/20100624044036/http://www.austlii.edu.au/au/legis/cth/consol_act/nda1967160/sch1.html |url-status=live }}</ref> 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".<ref>{{cite book |author=Australian Government. Department of Health and Aging. Therapeutic Goods Administration |title=Standard for the uniform scheduling of drugs and poisons no. 23 |url=http://www.comlaw.gov.au/ComLaw/Legislation/LegislativeInstrument1.nsf/0/3BBB39C4645284BCCA2574A6001C711F/$file/PoisonsStandard2008.pdf |publisher=Commonwealth of Australia |location=Canberra |isbn=978-1-74186-596-7 |date=June 2008 |access-date=6 April 2009 |archive-date=19 April 2009 |archive-url=https://web.archive.org/web/20090419080155/http://www.comlaw.gov.au/ComLaw/Legislation/LegislativeInstrument1.nsf/0/3BBB39C4645284BCCA2574A6001C711F/$file/PoisonsStandard2008.pdf |url-status=live }}</ref>

=== Canada ===
Oxycodone is a controlled substance under Schedule I of the [[Controlled Drugs and Substances Act]] (CDSA).<ref name="CanadaCDSA">{{cite web |last=Canada Department of Justice |title=Controlled Drugs and Substances Act (1996, c. 19) |date=27 February 2009 |url=http://laws.justice.gc.ca/en/ShowFullDoc/cs/C-38.8///en |access-date=23 March 2009 |archive-date=5 June 2011 |archive-url=https://web.archive.org/web/20110605062114/http://laws.justice.gc.ca/en/ShowFullDoc/cs/C-38.8///en |url-status=dead }}</ref>

[[File:Oxycocet.jpg|thumb|Canadian oxycodone HCL/acetaminophen 5/325 mg tablet]]

In February 2012, Ontario passed legislation to allow the expansion of an already existing drug-tracking system for publicly funded drugs to include those that are privately insured. This database will function to identify and monitor patient's attempts to seek prescriptions from multiple doctors or retrieve them from multiple pharmacies. Other provinces have proposed similar legislation, while some, such as Nova Scotia, have legislation already in effect for monitoring prescription drug use. These changes have coincided with other changes in Ontario's legislation to target the misuse of painkillers and high addiction rates to drugs such as oxycodone. As of 29 February 2012, Ontario passed legislation delisting oxycodone from the province's public drug benefit program. This was a first for any province to delist a drug based on addictive properties. The new law prohibits prescriptions for OxyNeo except to certain patients under the Exceptional Access Program including palliative care and in other extenuating circumstances. Patients already prescribed oxycodone will receive coverage for an additional year for OxyNeo, and after that, it will be disallowed unless designated under the exceptional access program.<ref>Olgilvie, Megan. [https://www.thestar.com/news/canada/article/1133247--ontario-to-delist-oxycontin-and-its-substitute-from-drug-benefit-program "Ontario delisting OxyContin and its substitute from drug benefit program"] {{Webarchive|url=https://web.archive.org/web/20120623022441/http://www.thestar.com/news/canada/article/1133247--ontario-to-delist-oxycontin-and-its-substitute-from-drug-benefit-program |date=23 June 2012 }} Toronto Star (17 February 2012)</ref>

Much of the legislative activity has stemmed from Purdue Pharma's decision in 2011 to begin a modification of Oxycontin's composition to make it more difficult to crush for snorting or injecting. The new formulation, OxyNeo, is intended to be preventive in this regard and retain its effectiveness as a painkiller. Since introducing its ''Narcotics Safety and Awareness Act'', Ontario has committed to focusing on drug addiction, particularly in the monitoring and identification of problem opioid prescriptions, as well as the education of patients, doctors, and pharmacists.<ref>[http://www.health.gov.on.ca/en/public/programs/drugs/ons/ons_legislation.aspx Narcotics Safety and Awareness Act] {{Webarchive|url=https://web.archive.org/web/20200607162003/http://health.gov.on.ca/en/public/programs/drugs/ons/ons_legislation.aspx |date=7 June 2020 }}. 2010. Ministry of Health and Long Term Care.</ref> This Act, introduced in 2010, commits to the establishment of a unified database to fulfil this intention.<ref>{{cite web |date=22 February 2012 |url=http://healthydebate.ca/2011/02/_mailpress_mailing_list_healthydebate-news/opioids | vauthors = Dhalla I, Born K |website=healthydebate.ca |title=Opioids |archive-url=https://web.archive.org/web/20150321100652/http://healthydebate.ca/2011/02/_mailpress_mailing_list_healthydebate-news/opioids |archive-date=21 March 2015 }}</ref> Both the public and medical community have received the legislation positively, though concerns about the ramifications of legal changes have been expressed. Because laws are largely provincially regulated, many speculate a national strategy is needed to prevent smuggling across provincial borders from jurisdictions with looser restrictions.<ref>{{cite web | url = http://www.huffingtonpost.ca/2012/02/20/ontario-oxycontin-rules-national-regulations_n_1288375.html | title = Ontario OxyContin Rules: New Restrictions Applauded But National Rules Needed | archive-url = https://web.archive.org/web/20200923061253/https://www.huffingtonpost.ca/2012/02/20/ontario-oxycontin-rules-national-regulations_n_1288375.html | archive-date=23 September 2020 | work = Huffington Post. Canadian Press | date = 20 February 2012 }}</ref>

In 2015, Purdue Pharma's abuse-resistant OxyNEO and six generic versions of OxyContin had been on the Canada-wide approved list for prescriptions since 2012. In June 2015, then federal Minister of Health Rona Ambrose announced that within three years, all oxycodone products sold in Canada would need to be tamper-resistant. Some experts warned that the generic product manufacturers may not have the technology to achieve that goal, possibly giving Purdue Pharma a monopoly on this opiate.<ref>{{cite news |vauthors=Weeks C, Howlett K |date=4 August 2015 |title=New oxycodone rules would give drug maker a monopoly in Canada, experts warn |url=https://www.theglobeandmail.com/news/national/new-oxycodone-rules-would-give-drug-maker-a-monoply-in-canada-experts-warn/article25820214/ |newspaper=Globe and Mail |location=Toronto, Ontario |access-date=15 December 2015 |archive-date=22 December 2015 |archive-url=https://web.archive.org/web/20151222143809/http://www.theglobeandmail.com/news/national/new-oxycodone-rules-would-give-drug-maker-a-monoply-in-canada-experts-warn/article25820214/ |url-status=live }}</ref>

Several class-action suits across Canada have been launched against the Purdue group of companies and affiliates. Claimants argue the pharmaceutical manufacturers did not meet a standard of care and were negligent in doing so. These lawsuits reference earlier judgments in the United States, which held that Purdue was liable for wrongful marketing practices and misbranding. Since 2007, the Purdue companies have paid over CAN$650 million in settling litigation or facing criminal fines.<!-- <ref>Martin, Kevin. {{usurped|1=[https://archive.today/20120709211050/http://chealth.canoe.ca/channel_health_news_details.asp?channel_id=131&relation_id=1883&news_channel_id=131&news_id=26055&rid Lawsuit attacks OxyContin use]}}. C-Health. Sun Media (8 August 2008)</ref> This article is about alcohol use disorder. -->

=== Germany ===
The drug is in Appendix III of the Narcotics Act (''[[Betäubungsmittelgesetz]]'' or BtMG).<ref name="GermanNarcoticsAct">{{cite web|author=German Federal Ministry of Justice|title=Act on the circulation of narcotics (Narcotics Act – BtMG)|date=19 January 2009|language=de|url=http://bundesrecht.juris.de/btmg_1981/BJNR106810981.html|access-date=6 April 2009|archive-date=1 March 2009|archive-url=https://web.archive.org/web/20090301050758/http://bundesrecht.juris.de/btmg_1981/BJNR106810981.html|url-status=live}}</ref> The law allows only physicians, dentists, and veterinarians to prescribe oxycodone and the federal government to regulate the prescriptions (e.g., by requiring reporting).<ref name="GermanNarcoticsAct" />

=== Hong Kong ===
Oxycodone is regulated under Part I of Schedule 1 of Hong Kong's Chapter 134 Dangerous Drugs Ordinance.<ref name="HKOrdinance">{{cite web|author=Hong Kong Special Administrative Region, People's Republic of China|title=Dangerous drugs ordinance – chapter 134|publisher=Hong Kong Legal Information Institute |url=http://www.hklii.org/hk/legis/en/ord/cur/134.txt|archive-url=https://web.archive.org/web/20071215204612/http://www.hklii.org/hk/legis/en/ord/cur/134.txt |url-status=dead|archive-date=15 December 2007|access-date=8 April 2009}}</ref>

=== Japan ===
Oxycodone is a restricted drug in Japan. Its import and export are strictly restricted to specially designated organizations having a prior permit to import it. In a high-profile case an American who was a top Toyota executive living in Tokyo, who claimed to be unaware of the law, was arrested for importing oxycodone into Japan.<ref>{{cite web|url=http://www.japantoday.com/category/crime/view/toyotas-american-pr-chief-arrested-on-suspected-drug-violation|title=Toyota's American PR chief arrested for suspected drug violation|date=19 June 2015 |access-date=11 February 2018|archive-date=24 April 2016|archive-url=https://web.archive.org/web/20160424223427/http://www.japantoday.com/category/crime/view/toyotas-american-pr-chief-arrested-on-suspected-drug-violation|url-status=live}}</ref><ref>{{cite web|url=https://www.msn.com/en-us/money/topstocks/toyota-american-exec-did-not-intend-to-break-japan-law/ar-AAbP7OC|archive-url=https://web.archive.org/web/20150619204445/http://www.msn.com/en-us/money/topstocks/toyota-american-exec-did-not-intend-to-break-japan-law/ar-AAbP7OC|url-status=dead|archive-date=19 June 2015|title=Toyota: American exec did not intend to break Japan law|website=[[MSN]]|access-date=11 February 2018}}</ref>

=== Singapore ===
Oxycodone is listed as a Class A drug in the [[Misuse of Drugs Act (Singapore)|Misuse of Drugs Act]] of Singapore, which means offences concerning the drug attract the most severe level of punishment. A conviction for unauthorized manufacture of the drug attracts a [[mandatory sentencing|minimum sentence]] of 10 years of imprisonment and [[caning in Singapore|corporal punishment]] of 5 strokes of the cane, and a maximum sentence of life imprisonment or 30 years of imprisonment and 15 strokes of the cane.<ref>{{Singapore legislation|title=Misuse of Drugs Act|cap=185|ed=2008}} (Singapore), section 6(1).</ref> The minimum and maximum penalties for unauthorized trafficking in the drug are respectively 5 years of imprisonment and 5 strokes of the cane, and 20 years of imprisonment and 15 strokes of the cane.<ref>Misuse of Drugs Act (Singapore), section 5(1).</ref>

=== United Kingdom ===
Oxycodone is a Class A drug under the [[Misuse of Drugs Act 1971]].<ref name="UKAct">{{cite web|url=http://www.homeoffice.gov.uk/documents/cdlist.pdf?view=Binary|title=List of drugs currently controlled under the Misuse of Drugs legislation|year=2009|publisher=UK. Home Office|access-date=8 April 2009|url-status=dead|archive-url=https://web.archive.org/web/20070205105239/http://www.homeoffice.gov.uk/documents/cdlist.pdf?view=Binary|archive-date=5 February 2007}}</ref> For Class A drugs, which are "considered to be the most likely to cause harm", possession without a prescription is punishable by up to seven years in prison, an unlimited fine, or both.<ref name="UKClassABC">{{cite web |url=http://www.homeoffice.gov.uk/drugs/drugs-law/Class-a-b-c/ |title=Class A, B and C drugs |publisher=UK. Home Office |access-date=8 April 2009 |url-status=dead |archive-url=https://web.archive.org/web/20070804233232/http://www.homeoffice.gov.uk/drugs/drugs-law/Class-a-b-c/ |archive-date=4 August 2007 }}</ref> Dealing of the drug illegally is punishable by up to life imprisonment, an unlimited fine, or both.<ref name="UKClassABC" /> Oxycodone is a Schedule 2 drug per the Misuse of Drugs Regulations 2001 which "provide certain exemptions from the provisions of the Misuse of Drugs Act 1971".<ref name="UKRegs">{{cite web|url=http://www.opsi.gov.uk/si/si2001/20013998.htm|title=Statutory instrument 2001 No. 3998. The Misuse of Drugs regulations 2001|publisher=UK. Office of Public Sector Information|access-date=8 April 2009|archive-date=18 April 2009|archive-url=https://web.archive.org/web/20090418213845/http://www.opsi.gov.uk/si/si2001/20013998.htm|url-status=live}}</ref>

=== United States ===
Under the Controlled Substances Act, oxycodone is a [[List of Schedule II drugs|Schedule II controlled substance]] whether by itself or part of a multi-ingredient medication.<ref>{{cite web |last1=DEA |title=Controlled substance scheduling |url=http://www.dea.gov/druginfo/ds.shtml |website=Drug information and scheduling |publisher=Drug Enforcerment Administration |access-date=23 November 2015 |archive-url=https://web.archive.org/web/20151121093241/http://www.dea.gov/druginfo/ds.shtml |archive-date=21 November 2015 |url-status=dead }}</ref> The DEA lists oxycodone both for sale and for use in manufacturing other opioids as ACSCN 9143 and in 2013 approved the following annual aggregate manufacturing quotas: 131.5 metric tons for sale, down from 153.75 in 2012, and 10.25 metric tons for conversion, unchanged from the previous year.<ref name=Examples>{{cite web |title=DEA Diversion Control CSA |url=http://www.deadiversion.usdoj.gov/schedules/ |publisher=US Dept of Justice – DEA |access-date=23 May 2013 |archive-date=16 May 2013 |archive-url=https://web.archive.org/web/20130516164501/http://www.deadiversion.usdoj.gov/schedules/ |url-status=dead }}</ref> In 2020, oxycodone possession was decriminalized in the U.S. state of [[Oregon]].<ref>{{cite news|url=https://apnews.com/article/oregon-first-decriminalizing-hard-drugs-01edca37c776c9ea8bfd4afdd7a7a33e|title=Oregon leads the way in decriminalizing hard drugs|work=The Associated Press|vauthors=Selsky A|date=4 November 2020|access-date=7 November 2020|archive-date=13 August 2021|archive-url=https://web.archive.org/web/20210813035025/https://apnews.com/article/oregon-first-decriminalizing-hard-drugs-01edca37c776c9ea8bfd4afdd7a7a33e|url-status=live}}</ref>

==Economics==
The [[International Narcotics Control Board]] estimated {{convert|11.5|ST}} of oxycodone were manufactured worldwide in 1998;<ref name="INCB2009"/> by 2007 this figure had grown to {{convert|75.2|ST}}.<ref name="INCB2009">{{cite book |author=International Narcotics Control Board |title=Narcotic drugs: estimated world requirements for 2009; statistics for 2007. Report E/INCB/2008/2 |publisher=United Nations |year=2009 |location=New York |isbn=978-92-1-048124-3 |url=http://www.incb.org/documents/Narcotic-Drugs/Technical-Publications/2008/Narcotics_drugs_publication2008.pdf |access-date=22 May 2013 |archive-date=30 September 2020 |archive-url=https://web.archive.org/web/20200930085535/https://www.incb.org/documents/Narcotic-Drugs/Technical-Publications/2008/Narcotics_drugs_publication2008.pdf |url-status=live }}</ref> United States accounted for 82% of consumption in 2007 at {{convert|51.6|ST}}. Canada, Germany, Australia, and France combined accounted for 13% of consumption in 2007.<ref name=INCB2009 /><ref name=UNPainpolicy>{{cite web |title=Availability of Opioid Analgesics in the World and Asia, With a special focus on: Indonesia, Philippines, Thailand |url=http://www.painpolicy.wisc.edu/publicat/monograp/philippines08.pdf |work=University of Wisconsin Pain & Policy Studies Group/World Health Organization (WHO) Collaborating Center for Policy and Communications in Cancer Care |publisher=United Nations |access-date=27 November 2011 |url-status=dead |archive-url=https://web.archive.org/web/20120426005126/http://www.painpolicy.wisc.edu/publicat/monograp/philippines08.pdf |archive-date=26 April 2012 }}</ref> In 2010, {{convert|1.3|ST}} of oxycodone were illegally manufactured using a fake pill imprint. This accounted for 0.8% of consumption. These illicit tablets were later seized by the U.S. Drug Enforcement Administration, according to the International Narcotics Control Board.<ref>[http://www.incb.org/documents/Narcotic-Drugs/Technical-Publications/2011/Part_FOURTH_Comments_NAR-Report-2011_English.pdf Narcotic Drugs: Estimated World Requirements for 2012 and Statistics for 2010]{{dead link|date=December 2017 |bot=InternetArchiveBot |fix-attempted=yes }}. International Narcotics Control Board (2011).</ref> The board also reported {{convert|122.5|ST}} manufactured in 2010. This number had decreased from a record high of {{convert|135.9|ST}} in 2009.<ref>[http://www.incb.org/documents/Narcotic-Drugs/Technical-Publications/2011/Part_FOUR_Comments_NAR-Report-2011_English.pdf Narcotic Drugs: Estimated World Requirements for 2012 and Statistics for 2010] {{Webarchive|url=https://web.archive.org/web/20200713133511/http://www.incb.org/documents/Narcotic-Drugs/Technical-Publications/2011/Part_FOUR_Comments_NAR-Report-2011_English.pdf |date=13 July 2020 }}. International Narcotics Control Board (2011).</ref>

==Names==
Expanded expressions for the compound oxycodone in the academic literature include "dihydrohydroxycodeinone",<ref name="MerckIndex">{{cite book|title=The Merck index|publisher=Merck & Co.|year=2006|isbn=978-0-911910-00-1| veditors = O'Neil MJ |edition=14th|location=Whitehouse Station, NJ}}</ref><ref name="Eddy1973">{{cite book| vauthors = Eddy NB | title=The National Research Council involvement in the opiate problem, 1928–1971|publisher=National Academy of Sciences|year=1973|location=Washington}}</ref><ref name="MayJacobson">{{cite journal | vauthors = May EL, Jacobson AE | title = The Committee on Problems of Drug Dependence: a legacy of the National Academy of Sciences. A historical account | journal = Drug and Alcohol Dependence | volume = 23 | issue = 3 | pages = 183–218 | date = June 1989 | pmid = 2666074 | doi = 10.1016/0376-8716(89)90083-5 }}</ref> "Eucodal",<ref name="Eddy1973" /><ref name="MayJacobson" /> "Eukodal",<ref name="Kalso2005"/><ref name="sunshine1996" /> "14-hydroxydihydrocodeinone",<ref name="MerckIndex" /><ref name="Eddy1973" /> and "Nucodan".<ref name="Eddy1973" /><ref name="MayJacobson" /> In a [[UNESCO]] [[Treaty|convention]], the translations of "oxycodone" are ''oxycodon'' (Dutch), ''oxycodone'' (French), ''oxicodona'' (Spanish), {{Script|Arab|الأوكسيكودون}} (Arabic), {{Script|Hant|羟考酮}} (Chinese), and {{Script|Cyrl|оксикодон}} (Russian).<ref>{{cite web|author1=United Nations Educational, Scientific|author2=Cultural Organization|year=2005|title=International convention against doping in sport|url=http://unesdoc.unesco.org/images/0014/001425/142594m.pdf|access-date=4 April 2009|archive-date=4 July 2010|archive-url=https://web.archive.org/web/20100704122051/http://unesdoc.unesco.org/images/0014/001425/142594m.pdf|url-status=live}}</ref>

The word "oxycodone" should not be confused with "[[oxandrolone]]", "[[oxazepam]]", "[[oxybutynin]]", "[[oxytocin]]", or "[[Roxanol]]".<ref name="MEDMARX">{{cite book|url=http://www.usp.org/pdf/EN/medmarx/2008MEDMARXReport.pdf|title=MEDMARX data report. A report on the relationship of drug names and medication errors in response to the Institute of Medicine's call for action|publisher=Center for the Advancement of Patient Safety, US Pharmacopeia|year=2008|veditors=Hicks RW, Becker SC, Cousins DD|location=Rockville, MD|access-date=4 April 2009}}{{dead link|date=March 2018|bot=InternetArchiveBot|fix-attempted=yes}}</ref>

Other brand names include Longtec and Shortec.<ref>{{cite web|vauthors=Postlethwaite J|title=Oxycodone Longtec Patient Leaflet|url=https://www.gwh.nhs.uk/media/168380/oxycodone_longtec_patient_leaflet_sept_14.pdf|access-date=23 March 2019|website=Great Western Hospitals NHS Foundation Trust|archive-date=23 March 2019|archive-url=https://web.archive.org/web/20190323155550/https://www.gwh.nhs.uk/media/168380/oxycodone_longtec_patient_leaflet_sept_14.pdf|url-status=dead}}</ref>

== References ==
{{Reflist}}

== Further reading ==
* {{cite journal | vauthors = Coluzzi F, Mattia C | title = Oxycodone. Pharmacological profile and clinical data in chronic pain management | journal = Minerva Anestesiologica | volume = 71 | issue = 7–8 | pages = 451–460 | date = July–August 2005 | pmid = 16012419 | url = http://www.minervamedica.it/pdf/R02Y2005/R02Y2005N07A0451.pdf | url-status = dead | archive-url = https://web.archive.org/web/20060309000726/http://www.minervamedica.it/pdf/R02Y2005/R02Y2005N07A0451.pdf | archive-date = 9 March 2006 }}

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