Oxycodone is a semisynthetic opioid synthesized from thebaine, an opioid alkaloid found in Persian poppy, and one of the many alkaloids found in opium poppy. This is a potent opioid pain medication (orally about 1.5 times stronger than morphine), generally indicated for moderate to severe pain relief. Oxycodone was developed in 1917 in Germany as one of several semi-synthetic opioids in an attempt to repair the existing opioids.
Oxycodone is available as a single-drug ingredient in direct release and controlled release. In the UK, it is available in 10 mg/mL and 50 mg/mL formulations for intramuscular or intravenous administration. Combination products are also available as direct release formulations, with non-narcotic analgesic materials such as paracetamol (acetaminophen) and nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin and ibuprofen.
Because it has euphoric effects similar to other opioids, oxycodone is one of the drugs abused in the current opioid epidemic in the United States. A deterrent-wasting combination with naloxone is available on a managed-release tablet. If injected, naloxone precipitates opioid withdrawal symptoms and inhibits drug effects. However, there are concerns about the effectiveness of misuse prevention measures.
Video Oxycodone
Medical use
Oxycodone has been used clinically since 1916, and is used to treat moderate to severe acute or chronic pain. It has been found to improve the quality of life for those who have many types of pain. Experts are divided on the use for chronic pain unrelated to cancer, since most opioids have great potential for dependence and are also suspected of creating paradoxic pain sensitivity.
Oxycodone is available as a controlled release tablet, which is intended to be taken every 12 hours. A review in 2006 found that controlled release oxycodone was comparable to oxycodone, morphine and hydromorphon released directly in moderate to severe cancer pain management, with fewer side effects than morphine. The authors conclude that the controlled release form is a valid alternative to morphine and first-line treatment for cancer pain. In 2014, the European Association for Palliative Care recommends oral oxycodone as a second-line alternative to oral morphine for cancer pain.
In the US, extended release oxycodone is approved for use in children as young as 11 years. Approved indications are to relieve cancer pain, traumatic pain, or severe pain from major surgery, in opioid-treated children, who can tolerate at least 20 mg per day of oxycodone; this provides an alternative to Duragesic (fentanyl) the only other extended-release opioid analgesic approved for children.
Administration
In the United States, oxycodone is only approved for oral use, available as a tablet and oral solution. In Spain, the Netherlands and the UK, oxycodone is also approved for intravenous (IV) and intramuscular (IM) use. When first introduced in Germany during World War I, both IV administration and IM oxycodone were commonly used for post operative pain management of Central Powers soldiers.
Maps Oxycodone
Side effects
Serious side effects of oxycodone include reduced sensitivity to pain (beyond the pain of drugs taken to reduce), 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.
In high doses, overdose, or in some people are intolerant of opioids, oxycodone may cause shallow breathing, slowing heartbeat, cold/sweating skin, stop breathing, low blood pressure, limited pupils, circulatory collapse, respiratory arrest, and Dead.
Oxycodone overdose has also been described to cause high-dose spinal cord infarction and ischemic damage to the brain, due to prolonged hypoxia from suppressed breathing.
Oxycodone in combination with naloxone in a released-release tablet has been formulated to prevent deter and reduce "opioid-induced constipation".
Dependency, addiction, and withdrawal
The risk of experiencing severe withdrawal symptoms is high if a patient has been physically dependent and stops oxycodone abruptly. Medically, when the drug has been drunk regularly for long periods of time, the drug is gradually withdrawn rather than suddenly. People who regularly use oxycodone in recreation or at higher doses than those prescribed have a higher risk for severe withdrawal symptoms. Oxycodone withdrawal symptoms, such as other opioids, may include "anxiety, panic attacks, nausea, insomnia, muscle aches, muscle weakness, fever, and other flu-like symptoms".
Withdrawal symptoms have also been reported in newborns whose mothers have injected or orally taken oxycodone during pregnancy.
Hormone imbalance
Like other opioids, the chronic use of oxycodone (especially with higher doses) often leads to hypogonadism or concomitant hormonal imbalance.
Interactions
Oxycodone is metabolized by the CYP3A4 and CYP2D6 enzymes, and its opening can therefore be altered by the inhibitors and inducers of this enzyme. (For a list of CYP3A4 and CYP2D6 inhibitors and inducers, see here and here, respectively.) Natural genetic variations in this enzyme may also affect oxycodone cleansing, which may be related to wide inter-individual variability in half-life and potential.
Ritonavir or lopinavir/ritonavir greatly increase plasma oxycodone concentrations in healthy human volunteers because of inhibition of CYP3A4 and CYP2D6. Rifampicin greatly reduces plasma oxycodone concentration due to strong induction of CYP3A4. There is also a case report of phosphenytoin, a CYP3A4 inducer, which dramatically reduces the effects of oxycodone analgesics in patients with chronic pain. Drug doses or adjustments may be required in each case.
Pharmacodynamics
Oxycodone is a highly selective agonist of -opioid receptor (MOR), with low affinity for the -opioid receptors (DOR) and the -opioid receptors (KOR). After the oxycodone binds to MOR, the protein complex G is released, which inhibits the release of neurotransmitters by cells by reducing the amount of cAMP produced, closing the calcium channel, and opening the potassium channel.
Similarly for most other opioids, oxycodone increases the secretion of prolactin, but its effect on testosterone levels is unknown. Unlike morphine, oxycodone has no immunosuppressive activity (measured by natural killer cell activity and interleukin 2 production in vitro ); this clinical relevance has not been clarified.
Controversy
In 1997, a group of Australian researchers proposed (based on studies in mice) that oxycodone acts on the -opioid receptor, unlike morphine, which acts on the -opioid receptors. Further research by this group suggests that the drug appears to be a agonist -opioid agonist << sub> 2b . However, this conclusion has been disputed, especially on the grounds that oxycodone produces a distinctive effect of? -opioid agonist.
In 2006, research by Japanese groups suggested the effects of oxycodone mediated by different receptors in different situations. Particularly in diabetic mice, the -opioid receptors appear to be involved in the antinociceptive oxycodone effect, while in nondiabetic mice, the
Pharmacokinetics
Absorption
After the oral dose of oxycodone (instant-release), the onset of action is 10-30 minutes, and peak plasma plasma levels are achieved in about 30-60 minutes; Conversely, after the dose of OxyContin (oral controlled release formulation), plasma oxycodone peak levels occur about three hours. The duration of instant-release oxycodone is 3 to 6 hours, although this may vary depending on the individual.
Distribution
Oxycodone in the blood is distributed to skeletal muscles, liver, intestinal tract, lungs, spleen, and brain. Conventional oral preparations begin to relieve pain within 10-15 minutes on an empty stomach; Instead, OxyContin begins to relieve pain within an hour.
Metabolism
The oxycodone metabolism in humans is very large (about 95%) and complex, with many small lanes and metabolites produced. About 10% (range 8-14%) of the dosage of oxycodone excreted is essentially unchanged (unconjugated or conjugated) in the urine. The main metabolites of oxycodone are noroxycodone (70%), noroxymorphone ("relatively high concentration"), and oxymorphone (5%). Direct oxycodone metabolism in humans is as follows:
- N-demethylation to noroxycodone mainly via CYP3A4
- O-demethylation to oxymorphone mainly via CYP2D6
- 6-ketoreduction to 6? - and 6? -oxycodol
- N-oxidation to oxycodone-N-oxide
In humans, N-demethylation oxycodone to noroxycodone by CYP3A4 is the main metabolic pathway, accounting for 45% Ã, Â ± 21% of oxycodone dose, while O-demethylation oxycodone becomes oxymorphone by CYP2D6 and 6-ketoreduction oxycodone to 6 -oxycodols representing pathways a relatively small metabolism, accounting for 11% Ã, Â ± 6% and 8% Ã, Â ± 6% of oxycodone dose, respectively.
Some of the oxycodone direct metabolites are then conjugated with glucuronic acid and excreted in the urine. 6? -Oxycodol and 6? -oxycodol is further metabolized by N-demethylation to nor-6? -oxycodol and nor-6? -oxycodol, respectively, and with N-oxidation being 6? -oxycodol-N-oxide and 6? -oxycodol-N-oxide (which may subsequently also be glucuronate), each separately. Oxymorphone is also further metabolized, as follows:
- 3-glucuronidation to oxymorphone-3-glucuronide mainly through UGT2B7
- 6-ketoreduction to 6? -oxymorphol and 6? -oxymorphol
- N-demethylation to noroxymorphone
The first line of the above three accounts for 40% of oxymorphone metabolism makes oxymorphone-3-glucuronide the main metabolite of oxymorphone, while the last two lines account for less than 10% of oxymorphone metabolism. After N-demethylation of the oxymorphone, noroxymorphone is further glucuronidated to noroxymorphone-3-glucuronide.
Contribution of metabolite activity
Some oxycodone metabolites have also been found to be active as MOR agonists, some of which have a higher affinity for (as well as higher efficacy in) MOR in comparison. Oxymorphone has a 3 to 5 fold higher affinity for MOR than oxycodone, while noroxycodone and noroxymorphone have a third of and a 3-fold higher affinity for MOR, respectively, and MOR activation is 5-10 times less with noroxycodone but 2-fold higher with noroxymorphone relative to oxycodone. Noroxycodone, noroxymorphone, and oxymorphone also have a longer half-life than oxycodone.
However, despite greater in vitro activity of some of its metabolites, it has been determined that oxycodone alone is responsible for 83.0% and 94.8% of its analgesic effects after oral and intravenous administration respectively. Oxymorphone only plays a minor role, responsible for 15.8% and 4.5% of the analytic effects of oxycodone after oral and intravenous administration. Despite the CYP2D6 genotype and administrative route results in the differential rate of oxymorphone formation, unchanged parent compounds remain a major contributor to the overall analgesic effect of oxycodone. In contrast to oxycodone and oxymorphone, noroxycodone and noroxymorphone, while also powerful MOR agonists, poorly cross the blood-brain barrier into the central nervous system, and for this reason, only a small amount of analgesics in comparison. Accordingly, while higher CYP2D6 activity increases the oxycodone effect (due to increased conversion to oxymorphone), higher CYP3A4 activity has the opposite effect, and reduced oxycodone effects (due to increased metabolism to noroxycodone and noroxymorphone).
Variations
Oxycodone is metabolized by the cytochrome P450 enzyme system in the liver, making it susceptible to drug interactions. Some people are rapid metabolites, producing a reduced analgesic effect, but increasing side effects, while others are slow metabolites, resulting in increased toxicity without improved analgesia. The dose of oxycodone should be reduced in patients with reduced liver function.
Elimination
Oxycodone and its metabolites are mainly excreted in urine and sweat; therefore, accumulates in patients with renal impairment.
Bioavailability
Oxycodone may be administered orally, intranasally, by intravenous, intramuscular, or subcutaneous, or rectal injection. Bioavailability of oral oxycodone averaged 60-87%, with rectal administration yielding the same results; intranasal varies between individuals with an average of 46%.
Morphine Equality
Taken orally, 20 mg of immediate release oxycodone is equivalent to 30 mg of morphine. Extended release of oxycodone is considered twice as strong as oral morphine.
Chemistry
Oxycodone's chemical name comes from codeine. The chemical structure is very similar, just different in that
- Oxycodone has a hydroxy group on carbon-14 (codeine only has hydrogen in place)
- Oxycodone features a 7.8-dihydro. Codeine has a double bond between two carbon; and
- Oxycodone has a carbonyl group (as in ketones) instead of a hydroxyl codeine group.
It is also similar to a hydrocodon, different simply because it has a hydroxyl group on carbon-14.
Oxycodone is marketed as a variety of salts, most commonly as a hydrochloride salt. The free base conversion ratios of various salts are: hydrochloride (0.896), bitartrate (0.667), tartrate (0.750), camphosulphonate (0.576), pectinate (0.588), phenylpriopionate (0.678), sulfate (0.887), phosphate (0.763), and terephthalate (0.792). Hydrochloride salts are the basis of most American oxycodone products while bitartrate, tartrate, pectinate, terephthalate and phosphate salts are also available in European products. Methyiodide and hydroiodide are mentioned in older European publications.
Biosynthesis
In terms of biosynthesis, oxycodone has been found naturally in nectar extracts from the orchid family helleborine epipactis ; along with other opioids: 3- {2- {3- {3-benzyloxypropyl} -3-indole, 7,8-didehydro- 4,5-epoxy-3,6-d-morphinan.
Detection in biological fluid
Oxycodone and/or its main metabolites can be measured in blood or urine to monitor cleansing, abuse, confirm the diagnosis of poisoning, or assist in investigating medicolegal death. Many commercial opiate screening tests react with the oxycodone and its metabolites, but chromatographic techniques can easily differentiate oxycodone from other opiates.
History
Freund and Speyer of the University of Frankfurt in Germany first synthesized oxycodone from Thebaine in 1916, a few years after the German pharmaceutical company Bayer halted the mass production of heroin due to its harmful use, harmful use, and dependence. It is hoped that drugs derived from thebaine will retain the analgesic effects of morphine and heroin with less dependency. Unfortunately, this is ultimately not found to be the case.
The first clinical use of this drug was documented in 1917, the year after it was first developed. It was first introduced to the US market in May 1939. In early 1928, Merck introduced a combination product containing scopolamine, oxycodone, and ephedrine under the German initials for the VIEW ingredients, later renamed < b> Scophedal (SCOpolamine ePHEDrine and eukodal). This combination is essentially an oxycodone analogue of morphine-based Â'twilight bed, with ephedrine added to reduce circulation and respiratory effects.
Personal notes from doctor Adolf Hitler, Dr. Theodor Morell, suggesting Hitler received repeated "eukodal" (oxycodone) injections.
In the early 1970s, the United States government classified oxycodone as a drug of schedule II.
Purdue Pharma - a private company based in Stamford, Connecticut, developed the OxyContin prescription painkiller. After its release in 1995, OxyContin was hailed as a medical breakthrough, a long-lasting narcotic that can help patients suffering from moderate to severe pain. The drug became a blockbuster, and is reported to have generated about thirty-five billion dollars in revenue for Purdue.
Society and culture
Legal status
General
Oxycodone is subject to international conventions on narcotic drugs. In addition, oxycodone is subject to different national laws in each country. 1931 Convention to Limit the Establishment and Regulation of Drug-Drugs Distribution of the League of Nations includes oxycodone. The 1961 Convention on Drugs of the United Nations, which supersedes the 1931 Convention, categorizes oxycodone in Schedule I. The global restriction on drug Schedule I includes "exclusively limiting [ing] for medical and scientific purposes of production, manufacture, export, import, distribution, trade, use and possession "of these drugs; "requires medical prescriptions for the supply or dispensation of these [drugs] to individuals"; and "prevent the accumulation" of these drugs "beyond what is required for normal business behavior".
Australia
Oxycodone is on Schedule I (originated from the Narcotic Drug Single Convention) of the 1967 Commonwealth Drug Act. In addition, in Schedule 8 of the Australian Standard for Scheduling Drug and Poison Uniforms ("Standard Poison"), it means "controlled drugs... which should be available for use but requires [s] restricting the manufacture, supply, distribution, ownership and use to reduce abuse, misuse and physical or psychological dependence ".
Canada
Oxycodone is a substance controlled under Schedule I of the Controlled Drugs and Substances Act (CDSA).
Canadian legislative changes
In February 2012, Ontario passed a law to allow the expansion of an existing drug tracer system for publicly funded drugs to include those who were personally insured. This database will serve to identify and monitor patients attempts to find prescriptions from many doctors or take from several pharmacies. Other provinces have proposed similar laws, while some, such as Nova Scotia, have laws that apply to monitor prescription drug use. These changes coincide with other changes in Ontario law to target abuse of painkillers and high addiction rates for drugs such as oxycodone. On February 29, 2012, Ontario passed a delisting of oxycodone legislation from the provincial public drug benefit program. This is the first for any province to remove the drug based on its addictive properties. The new law prohibits prescriptions for OxyNeo except for certain patients under the Extraordinary Access Program including palliative care and in other special circumstances. The prescribed patient oxycodone will receive coverage for an additional year for OxyNeo, and after that, it will be disallowed unless specified under an exceptional access program.
Much of the legislative activity stems from Purdue Pharma's decision in 2011 to initiate the modification of the Oxycontin composition to make it more difficult to destroy due to grunting or injecting. The new formulation, OxyNeo, is meant to be a precaution in this regard and maintain its effectiveness as a painkiller. Since introducing the Narcotics and Awareness Law, Ontario has committed to focusing on drug addiction, particularly in monitoring and identification of opioid prescription problems, as well as the education of patients, doctors, and pharmacists. This law, introduced in 2010, is committed to the establishment of an integrated database to meet this objective. Both the general public and the medical have received legislation positively, though concerns about the consequences of legal changes have been disclosed. Since legislation is largely regulated by province, many speculate that a national strategy is needed to prevent smuggling across provincial borders from jurisdictions with more restrictive restrictions.
By 2015, OxyNEO Purdue Pharma's anti-abuse and six generic versions of OxyContin have been on the approved list in Canada for recipes since 2012. In June 2015, federal Health Minister Rona Ambrose announced that in three years all oxycodone products sold in Canada must hold tamper. Some experts warn that manufacturers of generic products may not have the technology to achieve that goal, perhaps giving Purdue Pharma a monopoly over this opiate.
Canadian lawsuits
Some class action lawsuits in Canada have been launched against the Purdue group of companies and affiliates. Plaintiffs argue that pharmaceutical manufacturers do not meet the standards of care and are negligent in doing so. This lawsuit refers to a previous assessment in the United States, which states that Purdue is responsible for misleading and misinterpreting marketing practices. Since 2007, Purdue company has paid more than $ 650 million to settle litigation or face criminal penalties.
German
The drug is in Appendix III of the Narcotics Act ( BetÃÆ'¤ubungsmittelgesetz or BtMG). The law only allows doctors, dentists, and veterinarians to prescribe oxycodone and the federal government to regulate prescriptions (eg, by requiring reporting).
Hong Kong
Oxycodone is governed by Part I of Schedule 1 of Chapter 134 of the Hong Kong Hazardous Drug Ordinance.
Japanese
Oxycodone is a drug in Japan. Imports and exports are severely limited to specially designated organizations that have prior permission to import them. In a famous case, an American who is a top Toyota executive living in Tokyo, who claims to be unaware of the law, was arrested for importing oxycodone into Japan.
Singapore
Oxycodone is listed as a Class A drug in Drug Abuse of Singapore Drugs, which means that the offense in relation to this drug attracts the most severe punishment rate. Confidence for unlawful drug making drew a minimum sentence of 10 years in prison and corporal punishment on 5 cane strokes, and maximum life imprisonment or 30 years in prison and 15 cane blows. The minimum and maximum penalties for illegal drug trade are each 5 years in prison and 5 cane blows, and 20 years in prison and 15 cane blows.
United Kingdom
Oxycodone is a Class A drug under the Drug Abuse Act. For Class A drugs, which "are considered most likely to cause harm", non-prescription ownership may be sentenced to up to seven years in prison, unlimited fines, or both. Overcoming drugs illegally can be sentenced to life imprisonment, unlimited fines, or both. In addition, oxycodone is a remedy of Schedule 2 per Drug Abuse 2001 Regulation that "provides certain exceptions to the provisions of the Drug Abuse Act 1971".
United States
Under the Controlled Substance Act, passed in 1971 by President Richard Nixon, oxycodone is a substance that is monitored by Schedule II whether by itself or part of a multi-ingredient drug. The DEA oxycodone list is good for sale and for use in the manufacture of other opioids as ACSCN 9143 and in 2013 approved the following annual aggregate production 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.
Use of recreation
Effects
Oxycodone, like other opioid analgesics, tends to induce feelings of euphoria, relaxation, and reduce anxiety in those who are sometimes users. This effect makes it one of the most frequently abused pharmaceutical drugs in the United States.
Preventive steps
In August 2010, Purdue Pharma reformulated their long-acting oxycodone path, marketed as OxyContin, using a polymer, Intac, to make the pill very difficult to destroy or dissolve in water to reduce the abuse of OxyContin. The FDA approved the re-formulated version re-formation as abuse-resistant in April 2013.
Pfizer produces short-acting oxycodone preparations, marketed as Oxecta, which contains inactivated ingredients, called the anti-breakdown Aversion Technology. It does not prevent oral abuse. Approved by the FDA in the US in June 2011, a new formulation makes crushing, chewing, snorting, or injecting opioids impractical due to changes in chemical properties.
Australia
The use of non-medical oxycodone has been around since the early 1970s, but by 2015, 91% of the national sample of injecting drug users in Australia have reported using oxycodone, and 27% have injected it in the past six months.
Canada
Opioid-related deaths in Ontario have increased 242% from 1969 to 2014. In 2009 in Ontario there were more deaths due to oxycodone overdose than from overdose of cocaine. Death from opioid pain relief has increased from 13.7 deaths per million people in 1991 to 27.2 deaths per million in 2004. The abuse of oxycodone in Canada is a problem. The areas where oxycodone is most problematic are the Atlantic of Canada and Ontario, where abuse is prevalent in rural towns, and in many small to medium-sized cities. Oxycodone is also widely available in Western Canada, but methamphetamine and heroin are more serious problems in large cities, while oxycodone is more common in rural towns. Oxycodone is diverted through physician spending, prescription counterfeiting, drug theft, and overprescribing.
The latest formulation of oxycodone, especially Purdue Pharma's crushing, chewing, injecting and OxyNEO-induced OxyContin replacement of forbidden products in Canada in early 2012, has led to a decrease in the misuse of opiates but has increased abuse. of the more potent drug fentanyl. According to a Canadian Abuse Substance Abuse Research Center quoted in Maclean magazine, there are at least 655 fentanyl-related deaths in Canada over a five-year period.
In Alberta, the Blood Police claim that from fall 2014 to January 2015, oxycodone pills or deadly fake variations known as Oxy 80 containing fentanyl made in illegal laboratories by organized crime members are responsible for ten deaths in Blood Reserve. , located in southwest Lethbridge, Alberta. The vast province, about 120 Albertans died from a fentanyl-related overdose in 2014.
United Kingdom
The abuse and diversion of oxycodone in the UK began in the early to mid 2000s. The first known death due to overdose in Britain occurred in 2002. However, recreational use remains relatively rare.
United States
In the United States, more than 12 million people use opioid drugs in recreation. In 2010, 16,652 deaths were associated with an overdose of opioids in combination with other drugs such as benzodiazepines and alcohols. In September 2013, the FDA released new labeling guidelines for long-term and extended opioid releases that require manufacturers to relieve moderate pain as an indication for use, instead stating the drug is for "severe pain to require every day, all the time, term long, opioid treatment. "The updated labeling will not limit doctors from moderate-to-opioid administration, as needed.
Oxycodone is the most widely used opioid in America. The US Department of Health and Human Services estimates that about 11 million people in the United States consume non-medical oxycodone every year. In 2007, approximately 42,800 emergency room visits occurred due to "episodes" involving oxycodone. Oxycodone transferred can be taken orally or digested through insufflation; used intravenously, or the steam is heated inhaled. In 2008, recreational use of oxycodone and hydrocodone was involved in 14,800 deaths. Some cases are caused by an overdose of the acetaminophen component, which results in fatal liver damage.
OxyContin Reformulation causes some recreational users to turn into heroin, which is cheaper and easier to obtain.
Economy
The International Narcotics Control Agency estimates that 11.5 tonnes (10.4 t) of oxycodone was produced worldwide in 1998; in 2007 this figure has grown to 75.2 short tons (68.2 t). The United States accounted for 82% of consumption in 2007 at 51.6 ton short (46.8 t). The combination of Canada, Germany, Australia, and France accounted for 13% of consumption in 2007. In 2010, 1.3 tonnes short (1.2 t) of oxycodone was produced illegally using fake pills traces. It accounts for 0.8% of consumption. This forbidden tablet was later confiscated by the US Drug Enforcement Agency, according to the International Narcotics Supervisory Agency. The board also reported a short 122.5 ton (111.1 t) produced in 2010. This number has fallen from a record high 135.9 tonnes (123.3 t) in 2009.
Name
The expression is extended to oxycodone compounds in academic literature including "dihydrohydroxycodeinone", "Eucodal", "Eukodal", "14-hydroxydihydrocodeinone", and "Nucodan". In the UNESCO convention, the translation of "oxycodone" is oxycodon (Dutch), oxycodone (French), oxicodona (Spanish), ?? ?????????? (Arabic), ??? (China), and ????????? (Russia). The word "oxycodone" should not be equated with "oxandrolone", "oxazepam", "oxybutynin", "oxytocin", or "Roxanol".
Available form
Oxycodone is available in various formulations for oral or sublingual administration:
- Oksikodon immediate release (OxyFast, OxyIR, OxyNorm, Roxicodone)
- Controlled oxycodone release (OxyContin) - 12 hour duration
- Oxycodone tamper-resistant (OxyContin OTR)
- Oxycodone release immediately with paracetamol (acetaminophen) (Percocet, Endocet, Roxicet, Tylox)
- Oksikodon immediately-relieved with aspirin (Endodan, Oxycodan, Percodan, Roxiprin)
- Oksikodon releases immediately with ibuprofen (Combunox)
- Oxycodone with controlled release with naloxone (Targin, Targiniq, Targinact) - 12 hour duration
- Oxycodone with controlled release with naltrexone (Troxyca) - 12 hour duration - pending regulatory approval
Parenteral formulations of oxycodone (brand name OxyNorm) are also available, and widely used in Europe.
See also
References
Further reading
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Coluzzi, F. & amp; Mattia, C. (July-August 2005). "Oxycodone. Pharmacological profile and clinical data in chronic pain management" (PDF) . Minerva Anestesiol . 71 (7-8): 451-60. PMID 16012419. Archived from the original (PDF) on March 9, 2006. CS1 maint: Use the author parameter (link)
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