Available forms
Oxycodone is available in a variety of formulations for by mouth or under the tongue:
Immediate-release oxycodone (OxyFast, OxyIR, OxyNorm, Roxicodone)
Controlled-release oxycodone (OxyContin, Xtampza ER) – 10-12 hour duration
Oxycodone tamper-resistant (OxyContin OTR)
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)
Controlled-release oxycodone with naloxone (Targin, Targiniq, Targinact) – 10-12 hour duration
Controlled-release oxycodone with naltrexone (Troxyca) – 10-12 hour duration
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. In Spain, the Netherlands and the United Kingdom, oxycodone is approved for intravenous (IV) and 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. Side effects
Most common side effects of oxycodone include reduced sensitivity to pain, delayed gastric emptying, euphoria, anxiolysis, feelings of relaxation, and respiratory depression. Common side effects of oxycodone include constipation (23%), nausea (23%), vomiting (12%), somnolence (23%), dizziness (13%), itching (13%), dry mouth (6%), and sweating (5%). Less common side effects (experienced by less than 5% of patients) include loss of appetite, nervousness, abdominal pain, diarrhea, urinary retention, dyspnea, and hiccups. Most side effects generally become less intense over time, although issues related to constipation are likely to continue for the duration of use.
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. 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. 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. 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. 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. Further research by this group indicated the drug appears to be a high-affinity κ2b-opioid receptor agonist. However, this conclusion has been disputed, primarily on the basis that oxycodone produces effects that are typical of MOR agonists. In 2006, research by a Japanese group suggested the effect of oxycodone is mediated by different receptors in different situations. Specifically in diabetic mice, the KOR appears to be involved in the antinociceptive effects of oxycodone, while in nondiabetic mice, the μ1-opioid receptor seems to be primarily responsible for these effects. Pharmacokinetics
Instant-release absorption profile
Oxycodone can be administered orally, intranasally, via intravenous, intramuscular, or subcutaneous injection, or rectally.