How Long Does Oxycontin Stay In Your System

Other Medications – Other medications may make it more difficult to break down oxycodone, leading to respiratory depression, dangerous drug interactions, and other serious problems. It’s best to avoid taking oxycodone when also taking the following:

Macrolide antibiotics Azole antifungal agents Protease inhibitors

A patient will stop feeling the effects of oxycodone before it is fully eliminated, so healthcare providers have them take a tablet every four to six hours or 12 hours for controlled and extended-release forms. It’s possible to still detect oxycodone in the hair, saliva, and urine even after the blood is fully clear within 24 hours.

Urine: Up to three days after the last oxycodone dose Saliva: Up to four days after the last oxycodone dose Hair: Up to 90 days after the last oxycodone dose

What is the duration of effect of OxyContin?

Mechanism of Action – Oxycodone is a semisynthetic opioid with agonistic properties on mu, kappa, and delta-type opioid receptors, with the strongest affinity being for mu-type receptors. Upon binding to these G-protein coupled receptors, oxycodone stimulates the exchange of GDP on the G-alpha subunit for GTP, resulting in the inhibition of adenylate cyclase and a decrease in intracellular cAMP.

This signal cascade leads to a consequent inhibition of the nociceptive neurotransmitters acetylcholine, dopamine, GABA, noradrenaline, and substance P and the hormones glucagon, insulin, somatostatin, and vasopressin. As with other opioids, oxycodone causes hyperpolarization and reduced excitability of neurons in the central nervous system (CNS).

This generalized CNS depression results from the agonistic effect on kappa-type receptors, leading to N-type voltage-gated calcium channel closure. In contrast, stimulation of the mu and delta-type receptors opens calcium-dependent inward-rectifying potassium channels.

The onset of action is 10 to 30 minutes for the immediate-release formulation and about 1 hour for controlled-release. Duration range is from 3 to 6 hours for immediate-release or 12 hours in controlled-release formulations. The plasma half-life is 3 to 5 hours, and stable plasma levels are reached within 24 to 36 hours. Oxycodone is metabolized by the hepatic enzymes CYP3A4 and CYP2D6, producing the metabolites noroxycodone and oxymorphone, respectively. These metabolites get excreted from the body via the kidneys.

How long does a 20 mg OxyContin last?

My Account Area – 1. Name of the medicinal product OxyContin 5 mg, 10 mg, 15 mg, 20 mg, 30 mg, 40 mg, 60 mg, 80 mg, 120 mg prolonged release tablets 2. Qualitative and quantitative composition Each 5 mg tablet contains 4.5 mg of oxycodone as 5 mg of oxycodone hydrochloride.

Each 10 mg tablet contains 9.0 mg of oxycodone as 10 mg of oxycodone hydrochloride. Each 15 mg tablet contains 13.5 mg of oxycodone as 15 mg of oxycodone hydrochloride. Each 20 mg tablet contains 18.0 mg of oxycodone as 20 mg of oxycodone hydrochloride. Each 30 mg tablet contains 27 mg of oxycodone as 30 mg of oxycodone hydrochloride.

Each 40 mg tablet contains 36.0 mg of oxycodone as 40 mg of oxycodone hydrochloride. Each 60 mg tablet contains 54 mg of oxycodone as 60 mg of oxycodone hydrochloride. Each 80 mg tablet contains 72.0 mg of oxycodone as 80 mg of oxycodone hydrochloride.

Each 120 mg tablet contains108 mg of oxycodone as 120 mg of oxycodone hydrochloride. Excipient with known effect: Contains lactose monohydrate. For the full list of excipients, see Section 6.1.3. Pharmaceutical form Prolonged release tablet. The 5 mg tablets are light blue, round, convex tablets marked OC on one side and 5 on the other.

The 10 mg tablets are white, round, convex tablets marked OC on one side and 10 on the other. The 15 mg tablets are grey, round, convex tablets marked OC on one side and 15 on the other. The 20 mg tablets are pink, round, convex tablets marked OC on one side and 20 on the other.

The 30 mg tablets are brown, round, convex tablets marked OC on one side and 30 on the other. The 40 mg tablets are yellow, round, convex tablets marked OC on one side and 40 on the other. The 60 mg tablets are red, round, convex tablets marked OC on one side and 60 on the other. The 80 mg tablets are green, round, convex tablets marked OC on one side and 80 on the other.

The 120 mg tablets are purple, round, convex tablets marked OC on one side and 120 on the other.4. Clinical particulars 4.1 Therapeutic indications For the treatment of moderate to severe pain in patients with cancer and post-operative pain. For the treatment of severe pain requiring the use of a strong opioid.4.2 Posology and method of administration Adults over 18 years: OxyContin tablets should be taken at 12-hourly intervals.

The dosage is dependent on the severity of the pain, and the patient’s previous history of analgesic requirements. Prior to starting treatment with opioids, a discussion should be held with patients to put in place a strategy for ending treatment with oxycodone in order to minimise the risk of addiction and drug withdrawal syndrome (see section 4.4).

OxyContin is not intended for use as a prn analgesic. Generally, the lowest effective dose for analgesia should be selected. Increasing severity of pain will require an increased dosage of OxyContin tablets, using the different tablet strengths, either alone or in combination, to achieve pain relief.

• The correct dosage for any individual patient is that which controls the pain and is well tolerated for a full 12 hours.
• Patients should be titrated to pain relief unless unmanageable adverse drug reactions prevent this.
• If higher doses are necessary, increases should be made in 25% – 50% increments.
• The need for escape medication more than twice a day indicates that the dosage of OxyContin tablets should be increased.

The usual starting dose for opioid naïve patients or patients presenting with severe pain uncontrolled by weaker opioids is 10 mg, 12-hourly. Some patients may benefit from a starting dose of 5 mg to minimise the incidence of side effects. The dose should then be carefully titrated, as frequently as once a day if necessary, to achieve pain relief.

Conversion from oral morphine: Patients receiving oral morphine before OxyContin therapy should have their daily dose based on the following ratio: 10 mg of oral oxycodone is equivalent to 20 mg of oral morphine. It must be emphasised that this is a guide to the dose of OxyContin tablets required. Inter-patient variability requires that each patient is carefully titrated to the appropriate dose.

Transferring patients between oral and parenteral oxycodone: The dose should be based on the following ratio: 2 mg of oral oxycodone is equivalent to 1 mg of parenteral oxycodone. It must be emphasised that this is a guide to the dose required. Inter-patient variability requires that each patient is carefully titrated to the appropriate dose.

1. Elderly patients: A dose adjustment is not usually necessary in elderly patients.
2. Controlled pharmacokinetic studies in elderly patients (aged over 65 years) have shown that, compared with younger adults, the clearance of oxycodone is only slightly reduced.
3. No untoward adverse drug reactions were seen based on age, therefore adult doses and dosage intervals are appropriate.

Paediatric population OxyContin should not be used in patients under 18 years of age. Patients with renal or hepatic impairment: The plasma concentration in this population may be increased. The dose initiation should follow a conservative approach in these patients.

• The recommended adult starting dose should be reduced by 50% (for example a total daily dose of 10 mg orally in opioid naïve patients), and each patient should be titrated to adequate pain control according to their clinical situation.
• Use in non-malignant pain: Opioids are not first-line therapy for chronic non-malignant pain, nor are they recommended as the only treatment.

Types of chronic pain which have been shown to be alleviated by strong opioids include chronic osteoarthritic pain and intervertebral disc disease. The need for continued treatment in non-malignant pain should be assessed at regular intervals. Method of administration OxyContin tablets are for oral use.

1. OxyContin tablets must be swallowed whole and not broken, chewed or crushed.
2. Duration of treatment Oxycodone should not be used for longer than necessary.
3. Discontinuation of treatment When a patient no longer requires therapy with oxycodone, it may be advisable to taper the dose gradually to prevent symptoms of withdrawal.4.3 Contraindications Hypersensitivity to oxycodone or to any of the excipients listed in section 6.1.

Oxycodone must not be used in any situation where opioids are contraindicated: severe respiratory depression with hypoxia, paralytic ileus, acute abdomen, delayed gastric emptying, severe chronic obstructive lung disease, cor pulmonale, severe bronchial asthma, elevated carbon dioxide levels in the blood, moderate to severe hepatic impairment, chronic constipation.

Patients with rare hereditary problems of galactose intolerance, total lactase deficiency or glucose-galactose malabsorption should not take this medicine.4.4 Special warnings and precautions for use Caution must be exercised when administering oxycodone to the debilitated elderly, patients with severely impaired pulmonary function, patients with impaired hepatic or renal function, patients with myxoedema, hypothyroidism, Addison’s disease, toxic psychosis, prostate hypertrophy, adrenocortical insufficiency, alcoholism, delirium tremens, diseases of the biliary tract, pancreatitis, inflammatory bowel disorders, hypotension, hypovolaemia raised intracranial pressure, intracranial lesions, head injury (due to risk of increased intracranial pressure), reduced level of consciousness of uncertain origin, sleep apnoea or patients taking benzodiazepines, other CNS depressants (including alcohol) or MAO inhibitors (see section 4.5).

The primary risk of opioid excess is respiratory depression. Sleep related breathing disorders Opioids can cause sleep-related breathing disorders including central sleep apnoea (CSA) and sleep-related hypoxemia. Opioid use increases the risk of CSA in a dose-dependent fashion.

Opioids may also cause worsening of pre-existing sleep apnoea (see section 4.8). Concomitant use of oxycodone and sedative medicines such as benzodiazepines or related drugs may result in sedation, respiratory depression, coma and death. Because of these risks, concomitant prescribing with these sedative medicines should be reserved for patients for whom alternative treatment options are not possible.

If a decision is made to prescribe oxycodone concomitantly with sedative medicines, the lowest effective dose should be used, and the duration of treatment should be as short as possible (see also general dose recommendation in section 4.2). The patient should be followed closely for signs and symptoms of respiratory depression and sedation.

• In this respect, it is strongly recommended to inform patients and their caregivers to be aware of these symptoms (see section 4.5).
• OxyContin tablets must be administered with caution in patients taking MAOIs or who have received MAOIs within the previous two weeks.
• OxyContin tablets should not be used where there is a possibility of paralytic ileus occurring.

Should paralytic ileus be suspected or occur during use, OxyContin tablets should be discontinued immediately. OxyContin tablets are not recommended for pre-operative use or within the first 12-24 hours post-operatively. As with all opioid preparations, oxycodone products should be used with caution following abdominal surgery as opioids are known to impair intestinal motility and should not be used until the physician is assured of normal bowel function.

Patients about to undergo additional pain relieving procedures (e.g. surgery, plexus blockade) should not receive OxyContin tablets for 12 hours prior to the intervention. If further treatment with OxyContin tablets is indicated then the dosage should be adjusted to the new post-operative requirement.

OxyContin 60 mg, 80 mg and 120 mg tablets should not be used in patients not previously exposed to opioids. These tablet strengths may cause fatal respiratory depression when administered to opioid naïve patients. For appropriate patients who suffer with chronic non-malignant pain, opioids should be used as part of a comprehensive treatment programme involving other medications and treatment modalities.

A crucial part of the assessment of a patient with chronic non-malignant pain is the patient’s addiction and substance abuse history. If opioid treatment is considered appropriate for the patient, then the main aim of treatment is not to minimise the dose of opioid but rather to achieve a dose which provides adequate pain relief with a minimum of side effects.

There must be frequent contact between physician and patient so that dosage adjustments can be made. It is strongly recommended that the physician defines treatment outcomes in accordance with pain management guidelines. The physician and patient can then agree to discontinue treatment if these objectives are not met.

1. Drug dependence, tolerance and potential for abuse Opioid Use Disorder (abuse and dependence) Tolerance and physical and/or psychological dependence may develop upon repeated administration of opioids such as oxycodone.
2. Iatrogenic addiction following therapeutic use of opioids is known to occur.
3. Repeated use of OxyContin tablets may lead to Opioid Use Disorder (OUD).

Abuse or intentional misuse of OxyContin tablets may result in overdose and/or death. The risk of developing OUD is increased in patients with a personal or a family history (parents or siblings) of substance use disorders (including alcohol use disorder), in current tobacco users or in patients with a personal history of other mental health disorders (e.g.

• Major depression, anxiety and personality disorders).
• Patients will require monitoring for signs of drug-seeking behaviour (e.g.
• Too early requests for refills).
• This includes the review of concomitant opioids and psycho-active drugs (like benzodiazepines).
• For patients with signs and symptoms of OUD, consultation with an addiction specialist should be considered.

A comprehensive patient history should be taken to document concomitant medications, including over-the-counter medicines and medicines obtained on-line, and past and present medical and psychiatric conditions. Tolerance Patients may find that treatment is less effective with chronic use and express a need to increase the dose to obtain the same level of pain control as initially experienced.

Patients may also supplement their treatment with additional pain relievers. These could be signs that the patient is developing tolerance. The risks of developing tolerance should be explained to the patient. Overuse or misuse may result in overdose and/or death. It is important that patients only use medicines that are prescribed for them at the dose they have been prescribed and do not give this medicine to anyone else.

Patients should be closely monitored for signs of misuse, abuse or addiction. The clinical need for analgesic treatment should be reviewed regularly. Drug withdrawal syndrome Prior to starting treatment with any opioids, a discussion should be held with patients to put in place a withdrawal strategy for ending treatment with oxycodone.

Drug withdrawal syndrome may occur upon abrupt cessation of therapy or dose reduction. When a patient no longer requires therapy, it is advisable to taper the dose gradually to minimise symptoms of withdrawal. Tapering from a high dose may take weeks to months. The opioid drug withdrawal syndrome is characterised by some or all of the following: restlessness, lacrimation, rhinorrhoea, yawning, perspiration, chills, myalgia, mydriasis and palpitations.

Other symptoms may also develop including irritability, agitation, anxiety, hyperkinesia, tremor, weakness, insomnia, anorexia, abdominal cramps, nausea, vomiting, diarrhoea, increased blood pressure, increased respiratory rate or heart rate. If women take this drug during pregnancy there is a risk that their newborn infants will experience neonatal withdrawal syndrome.

1. Hyperalgesia Hyperalgesia may be diagnosed if the patient on long-term opioid therapy presents with increased pain.
2. This might be qualitatively and anatomically distinct from pain related to disease progression or to breakthrough pain resulting from development of opioid tolerance.
3. Pain associated with hyperalgesia tends to be more diffuse than the pre-existing pain and less defined in quality.

Symptoms of hyperalgesia may resolve with a reduction of opioid dose. OxyContin tablets must be swallowed whole, and not broken, chewed or crushed. The administration of broken, chewed, or crushed OxyContin tablets leads to a rapid release and absorption of a potentially fatal dose of oxycodone (see Section 4.9).

1. Concomitant use of alcohol and OxyContin may increase the undesirable effects of OxyContin ; concomitant use should be avoided.
2. Abuse of oral dosage forms by parenteral administration can be expected to result in serious adverse events, such as local tissue necrosis, infection, pulmonary granulomas, increased risk of endocarditis, and valvular heart injury, which may be fatal.

Empty matrix (tablets) may be seen in the stools. Opioids such as oxycodone hydrochloride may influence the hypothalamic-pituitary-adrenal or – gonadal axes. Some changes that can be seen include an increase in serum prolactin, and decreases in plasma cortisol and testosterone.

Clinical symptoms may manifest from these hormonal changes.4.5 Interaction with other medicinal products and other forms of interaction The concomitant use of opioids with sedative medicines such as benzodiazepines or related drugs increases the risk of sedation, respiratory depression, coma and death because of additive CNS depressant effect.

The dose and duration of concomitant use should be limited (see section 4.4). Drugs which affect the CNS include, but are not limited to: other opioids, gabapentinoids such as pregabalin, anxiolytics, hypnotics and sedatives (including benzodiazepines), antipsychotics, antidepressants, phenothiazines, anaesthetics, muscle relaxants, antihypertensives and alcohol.

1. Concomitant administration of oxycodone with serotonin agents, such as a Selective Serotonin Re-uptake Inhibitor (SSRI) or a Serotonin Norepinephrine Re-uptake Inhibitor (SNRI) may cause serotonin toxicity.
2. The symptoms of serotonin toxicity may include mental-status changes (e.g., agitation, hallucinations, coma), autonomic instability (e.g., tachycardia, labile blood pressure, hyperthermia), neuromuscular abnormalities (e.g., hyperreflexia, incoordination, rigidity), and/or gastrointestinal symptoms (e.g., nausea, vomiting, diarrhoea).

Oxycodone should be used with caution and the dosage may need to be reduced in patients using these medications. Concomitant administration of oxycodone with anticholinergics or medicines with anticholinergic activity (e.g. tricyclic anti-depressants, antihistamines, antipsychotics, muscle relaxants, anti-Parkinson drugs) may result in increased anticholinergic adverse effects.

Oxycodone should be used with caution and the dosage may need to be reduced in patients using these medications. MAO inhibitors are known to interact with narcotic analgesics. MAO inhibitors cause CNS excitation or depression associated with hypertensive or hypotensive crisis (see section 4.4). Co-administration with monoamine oxidase inhibitors or within two weeks of discontinuation of their use should be avoided.

Alcohol may enhance the pharmacodynamic effects of OxyContin ; concomitant use should be avoided. Oxycodone is metabolised mainly by CYP3A4, with a contribution from CYP2D6. The activities of these metabolic pathways may be inhibited or induced by various co-administered drugs or dietary elements.

Oxycodone doses may need to be adjusted accordingly. CYP3A4 inhibitors, such as macrolide antibiotics (e.g. clarithromycin, erythromycin and telithromycin), azole-antifungals (e.g. ketoconazole, voriconazole, itraconazole, and posaconazole), protease inhibitors (e.g. boceprevir, ritonavir, indinavir, nelfinavir and saquinavir), cimetidine and grapefruit juice may cause a reduced clearance of oxycodone that could cause an increase of the plasma concentrations of oxycodone.

Therefore the oxycodone dose may need to be adjusted accordingly. Some specific examples are provided below: • Itraconazole, a potent CYP3A4 inhibitor, administered 200 mg orally for five days, increased the AUC of oral oxycodone. On average, the AUC was approximately 2.4 times higher (range 1.5 – 3.4).

1. Voriconazole, a CYP3A4 inhibitor, administered 200 mg twice-daily for four days (400 mg given as first two doses), increased the AUC of oral oxycodone.
2. On average, the AUC was approximately 3.6 times higher (range 2.7 – 5.6).
3. Telithromycin, a CYP3A4 inhibitor, administered 800 mg orally for four days, increased the AUC of oral oxycodone.

On average, the AUC was approximately 1.8 times higher (range 1.3 – 2.3). • Grapefruit Juice, a CYP3A4 inhibitor, administered as 200 ml three times a day for five days, increased the AUC of oral oxycodone. On average, the AUC was approximately 1.7 times higher (range 1.1 – 2.1).

1. CYP3A4 inducers, such as rifampicin, carbamazepine, phenytoin and St John’s Wort may induce the metabolism of oxycodone and cause an increased clearance of oxycodone that could cause a reduction of the plasma concentrations of oxycodone.
2. The oxycodone dose may need to be adjusted accordingly.
3. Some specific examples are provided below: • St John’s Wort, a CYP3A4 inducer, administered as 300 mg three times a day for fifteen days, reduced the AUC of oral oxycodone.

On average, the AUC was approximately 50% lower (range 37-57%). • Rifampicin, a CYP3A4 inducer, administered as 600 mg once-daily for seven days, reduced the AUC of oral oxycodone. On average, the AUC was approximately 86% lower Drugs that inhibit CYP2D6 activity, such as paroxetine and quinidine, may cause decreased clearance of oxycodone which could lead to an increase in oxycodone plasma concentrations.

Concurrent administration of quinidine resulted in an increase in oxycodone Cmax by 11%, AUC by 13%, and t½ elim. by 14%. Also, an increase in noroxycodone level was observed, (Cmax by 50%; AUC by 85%, and t½ elim. by 42%). The pharmacodynamic effects of oxycodone were not altered.4.6 Fertility, pregnancy and lactation Pregnancy OxyContin tablets are not recommended for use in pregnancy nor during labour.

There are limited data from the use of oxycodone in pregnant women. Regular use in pregnancy may cause drug dependence in the foetus, leading to withdrawal symptoms in the neonate. If opioid use is required for a prolonged period in pregnant women, advise the patient of the risk of neonatal opioid withdrawal syndrome and ensure that appropriate treatment will be available.

Administration during labour may depress respiration in the neonate and an antidote for the child should be readily available. Breastfeeding Administration to nursing women is not recommended as oxycodone may be secreted in breast milk and may cause respiratory depression in the infant.4.7 Effects on ability to drive and use machines Oxycodone may impair the ability to drive and use machines.

Oxycodone may modify patients’ reactions to a varying extent depending on the dosage and individual susceptibility. Therefore, patients should not drive or operate machinery if affected. This medicine can impair cognitive function and can affect a patient’s ability to drive safely.

This class of medicine is in the list of drugs included in regulations under 5a of the Road Traffic Act 1988. When prescribing this medicine, patients should be told: • The medicine is likely to affect your ability to drive. • Do not drive until you know how the medicine affects you. • It is an offence to drive while you have this medicine in your body over a specified limit unless you have a defence (called the ‘statutory defence’).

• This defence applies when:

o The medicine has been prescribed to treat a medical or dental problem; and o You have taken it according to the instructions given by the prescriber and in the information provided with the medicine.

Please note that it is still an offence to drive if you are unfit because of the medicine (i.e. your ability to drive is being affected).” Details regarding a new driving offence concerning driving after drugs have been taken in the UK may be found here: https://www.gov.uk/drug-driving-law 4.8 Undesirable effects Adverse drug reactions are typical of full opioid agonists.

Term	Frequency
Very common	≥ 1/10
Common	≥ 1/100 to <1/10
Uncommon	≥ 1/1,000 to <1/100
Rare	≥1/10,000 to <1/1,000
Very rare	<1/10,000
Frequency not known	Cannot be estimated from the available data

Immune system disorders: Uncommon : hypersensitivity. Frequency not known: anaphylactic reaction, anaphylactoid reaction. Metabolism and nutrition disorders: Common : decreased appetite. Uncommon : dehydration. Psychiatric disorders: Common : anxiety, confusional state, depression, insomnia, nervousness, abnormal thinking, abnormal dreams.

• Uncommon : agitation, affect lability, euphoric mood, hallucinations, decreased libido, disorientation, mood altered, restlessness, dysphoria.
• Frequency not known : aggression, drug dependence (see section 4.4).
• Nervous system disorders: Very common : somnolence, dizziness, headache.
• Common : tremor, lethargy, sedation.

Uncommon : amnesia, convulsion, hypertonia, hypoaesthesia, involuntary muscle contractions, speech disorder, syncope, paraesthesia, dysgeusia, hypotonia. Frequency not known : hyperalgesia. Eye disorders: Uncommon : visual impairment, miosis. Ear and labyrinth disorders: Uncommon : vertigo.

1. Cardiac disorders: Uncommon : palpitations (in the context of withdrawal syndrome), supraventricular tachycardia.
2. Vascular disorders: Uncommon : vasodilatation, facial flushing.
3. Rare: hypotension, orthostatic hypotension.
4. Respiratory, thoracic and mediastinal disorders: Common : dyspnoea, bronchospasm, cough decreased.

Uncommon : respiratory depression, hiccups. Not known: central sleep apnoea syndrome. Gastrointestinal disorders: Very common : constipation, nausea, vomiting. Common : abdominal pain, diarrhoea, dry mouth, dyspepsia. Uncommon : dysphagia, flatulence, eructation, ileus, gastritis.

• Frequency not known : dental caries.
• Hepato-biliary disorders: Uncommon : increased hepatic enzymes, biliary colic.
• Frequency not known : cholestasis.
• Skin and subcutaneous tissue disorders: Very common : pruritus.
• Common : rash, hyperhidrosis.
• Uncommon : dry skin, exfoliative dermatitis.
• Rare : urticaria.

Renal and urinary disorders: Uncommon : urinary retention, ureteral spasm. Reproductive system and breast disorders: Uncommon : erectile dysfunction, hypogonadism. Frequency not known : amenorrhoea. General disorders and administration site conditions: Common : asthenia, fatigue.

Uncommon : drug withdrawal syndrome, malaise, oedema, peripheral oedema, drug tolerance, thirst, pyrexia, chills. Frequency not known: drug withdrawal syndrome neonatal. Reporting of suspected adverse reactions Reporting suspected adverse reactions after authorisation of the medicinal product is important.

It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at: www.mhra.gov.uk/yellowcard or search for MHRA Yellow Card in the Google Play or Apple App Store.4.9 Overdose Acute overdose with oxycodone can be manifested by miosis, respiratory depression, hypotension and hallucinations.

1. Circulatory failure and somnolence progressing to stupor or deepening coma, hypotonia, bradycardia, pulmonary oedema and death may occur in more severe cases.
2. Patients should be informed of the signs and symptoms of overdose and to ensure that family and friends are also aware of these signs and to seek immediate medical help if they occur.

The effects of overdosage will be potentiated by the simultaneous ingestion of alcohol or other psychotropic drugs. Treatment of oxycodone overdosage : primary attention should be given to the establishment of a patent airway and institution of assisted or controlled ventilation.

The pure opioid antagonists such as naloxone are specific antidotes against symptoms from opioid overdose. Other supportive measures should be employed as needed. In the case of massive overdosage, administer naloxone intravenously (0.4 to 2 mg for an adult and 0.01 mg/kg body weight for children) if the patient is in a coma or respiratory depression is present.

Repeat the dose at 2 minute intervals if there is no response. If repeated doses are required an infusion of 60% of the initial dose per hour is a useful starting point. A solution of 10 mg made up in 50 ml dextrose will produce 200 micrograms/ml for infusion using an IV pump (dose adjusted to the clinical response).

1. Infusions are not a substitute for frequent review of the patient’s clinical state.
2. Intramuscular naloxone is an alternative in the event that IV access is not possible.
3. As the duration of action of naloxone is relatively short, the patient must be carefully monitored until spontaneous respiration is reliably re-established.

Naloxone is a competitive antagonist and large doses (4 mg) may be required in seriously poisoned patients. For less severe overdosage, administer naloxone 0.2 mg intravenously followed by increments of 0.1 mg every 2 minutes if required. The patient should be observed for at least 6 hours after the last dose of naloxone.

Naloxone should not be administered in the absence of clinically significant respiratory or circulatory depression secondary to oxycodone overdosage. Naloxone should be administered cautiously to persons who are known, or suspected, to be physically dependent on oxycodone. In such cases, an abrupt or complete reversal of opioid effects may precipitate pain and an acute withdrawal syndrome.

Additional/other considerations: • Consider activated charcoal (50 g for adults, 10-15 g for children), if a substantial amount has been ingested within 1 hour, provided the airway can be protected. It may be reasonable to assume that late administration of activated charcoal may be beneficial for prolonged release preparations; however, there is no evidence to support this.

• OxyContin tablets will continue to release and add to the oxycodone load for up to 12 hours after administration and the management of oxycodone overdosage should be modified accordingly. Gastric contents may therefore need to be emptied as this can be useful in removing unabsorbed drug, particularly when a prolonged release formulation has been taken.5.

Pharmacological properties 5.1 Pharmacodynamic properties Pharmacotherapeutic group: Natural opium alkaloids ATC code: N02A A05 Oxycodone is a full opioid agonist with no antagonist properties. It has an affinity for kappa, mu and delta opiate receptors in the brain and spinal cord.

• The therapeutic effect is mainly analgesic, anxiolytic and sedative.
• Gastrointestinal System Opioids may induce spasm of the sphincter of Oddi.
• Endocrine system See section 4.4.
• Other pharmacological effects In- vitro and animal studies indicate various effects of natural opioids, such as morphine, on components of the immune system; the clinical significance of these findings is unknown.

Whether oxycodone, a semisynthetic opioid, has immunological effects similar to morphine is unknown.5.2 Pharmacokinetic properties Absorption The release of oxycodone from OxyContin tablets is biphasic with an initial relatively fast release providing an early onset of analgesia followed by a more controlled release, which determines the 12 hour duration of action.

1. Release of oxycodone from OxyContin tablets is independent of pH.
2. OxyContin tablets have an oral bioavailability comparable with conventional oral oxycodone, but the former achieve maximal plasma concentrations at about 3 hours rather than about 1 to 1.5 hours.
3. Peak and trough concentrations of oxycodone from OxyContin tablets 10 mg administered 12-hourly are equivalent to those achieved from conventional oxycodone 5 mg administered 6-hourly.

All strengths of OxyContin tablets are bioequivalent in terms of both rate and extent of absorption. Distribution Following absorption, oxycodone is distributed throughout the entire body. Approximately 45% is bound to plasma protein. Metabolism Oxycodone is metabolised in the liver via CYP3A4 and CYP2D6 to noroxycodone, oxymorphone and noroxymorphone, which are subsequently glucuronidated.

Noroxycodone and noroxymorphone are the major circulating metabolites. Noroxycodone is a weak mu opioid agonist. Noroxymorphone is a potent mu opioid agonist; however, it does not cross the blood-brain barrier to a significant extent. Oxymorphone is a potent mu opioid agonist but is present at very low concentrations following oxycodone administration.

None of these metabolites are thought to contribute significantly to the analgesic effect of oxycodone. Elimination The mean apparent elimination half-life of OxyContin is 4.5 hours, which leads to steady-state being achieved in about one day. The active drug and its metabolites are excreted in urine.

• Elderly The AUC in elderly subjects is 15% greater when compared with young subjects.
• Gender Female subjects have, on average, plasma oxycodone concentrations up to 25% higher than males on a body weight adjusted basis.
• The reason for this difference is unknown.
• Patients with renal impairment Preliminary data from a study of patients with mild to moderate renal dysfunction show peak plasma oxycodone and noroxycodone concentrations approximately 50% and 20% higher, respectively and AUC values for oxycodone, noroxycodone and oxymorphone approximately 60%, 60% and 40% higher than normal subjects, respectively.

There was an increase in t ½ of elimination for oxycodone of only 1 hour. Patients with mild to moderate hepatic impairment Patients with mild to moderate hepatic dysfunction showed peak plasma oxycodone and noroxycodone concentrations approximately 50% and 20% higher, respectively, than normal subjects.

• AUC values were approximately 95% and 75% higher, respectively.
• Oxymorphone peak plasma concentrations and AUC values were lower by 15% to 50%.
• The t ½ elimination for oxycodone increased by 2.3 hours.5.3 Preclinical safety data Reproductive and Development Toxicology Oxycodone had no effect on fertility or early embryonic development in male and female rats at doses as high as 8 mg/kg/d.

Also, oxycodone did not induce any deformities in rats at doses as high as 8 mg/kg/d or in rabbits at doses as high as 125 mg/kg/d. Dose-related increases in developmental variations (increased incidences of extra (27) presacral vertebrae and extra pairs of ribs) were observed in rabbits when the data for individual foetuses were analysed.

1. However, when the same data were analysed using litters as opposed to individual foetuses, there was no dose-related increase in developmental variations although the incidence of extra presacral vertebrae remained significantly higher in the 125 mg/kg/d group compared to the control group.
2. Since this dose level was associated with severe pharmacotoxic effects in the pregnant animals, the foetal findings may have been a secondary consequence of severe maternal toxicity.

In a prenatal and postnatal development study in rats, maternal body weight and food intake parameters were reduced for doses ≥ 2 mg/kg/d compared to the control group. Body weights were lower in the F1 generation from maternal rats in the 6 mg/kg/d dosing group.

• There were no effects on physical, reflexological, or sensory developmental parameters or on behavioural and reproductive indices in the F1 pups (the NOEL for F1 pups was 2 mg/kg/d based on body weight effects seen at 6 mg/kg/d).
• There were no effects on the F2 generation at any dose in the study.
• Genotoxicity The results of in-vitro and in-vivo studies indicate that the genotoxic risk of oxycodone to humans is minimal or absent at the systemic oxycodone concentrations that are achieved therapeutically.

Oxycodone was not genotoxic in a bacterial mutagenicity assay or in an in-vivo micronucleus assay in the mouse. Oxycodone produced a positive response in the in-vitro mouse lymphoma assay in the presence of rat liver S9 metabolic activation at dose levels greater than 25 μg/mL.

Two in-vitro chromosomal aberrations assays with human lymphocytes were conducted. In the first assay, oxycodone was negative without metabolic activation but was positive with S9 metabolic activation at the 24 hour time point but not at other time points or at 48 hour after exposure. In the second assay, oxycodone did not show any clastogenicity either with or without metabolic activation at any concentration or time point.

Carcinogenicity Carcinogenicity was evaluated in a 2-year oral gavage study conducted in Sprague-Dawley rats. Oxycodone did not increase the incidence of tumours in male and female rats at doses up to 6 mg/kg/day. The doses were limited by opioid-related pharmacological effects of oxycodone.6.

• Pharmaceutical particulars 6.1 List of excipients Lactose monohydrate Povidone Ammoniomethacrylate Co-polymer Sorbic acid Glycerol triacetate Stearyl Alcohol Talc Magnesium Stearate Film coat Hypromellose (E464) Titanium Dioxide (E171) Macrogol The 5 mg tablets also contain brilliant blue (E133).
• The 10 mg tablets also contain hydroxypropylcellulose.

The 15 mg tablets also contain iron oxide (E172). The 20 mg, 30 mg, 40 mg, 60 mg and 120 mg tablets also contain polysorbate 80 (E433) and iron oxide (E172). The 80 mg tablets also contain hydroxypropylcellulose, iron oxide (E172) and indigo carmine (E132).6.2 Incompatibilities Not applicable.6.3 Shelf life Three years.6.4 Special precautions for storage Do not store above 25°C.6.5 Nature and contents of container PVC blister packs with aluminium foil backing (containing 28 or 56 tablets).6.6 Special precautions for disposal and other handling None.7.

1. Marketing authorisation holder Napp Pharmaceuticals Ltd Cambridge Science Park Milton Road Cambridge CB4 0GW 8.
2. Marketing authorisation number(s) PL 16950/0097 PL 16950/0098 PL 16950/0099 PL 16950/0100 PL 16950/0123 PL 16950/0139 PL 16950/0140 PL 16950/0141 PL 16950/0150 9.
3. Date of first authorisation/renewal of the authorisation 21 May 2002 10.

Date of revision of the text 1 April 2022

What is the elimination half-life of OxyContin?

Metabolism and Elimination Oxycodone has an elimination half-life of approximately 3 hours and is metabolised principally to noroxycodone and oxymorphone.

How long does OxyContin 80 last?

My Account Area – 1. Name of the medicinal product OxyContin 5 mg, 10 mg, 15 mg, 20 mg, 30 mg, 40 mg, 60 mg, 80 mg, 120 mg prolonged release tablets 2. Qualitative and quantitative composition Each 5 mg tablet contains 4.5 mg of oxycodone as 5 mg of oxycodone hydrochloride.

Each 10 mg tablet contains 9.0 mg of oxycodone as 10 mg of oxycodone hydrochloride. Each 15 mg tablet contains 13.5 mg of oxycodone as 15 mg of oxycodone hydrochloride. Each 20 mg tablet contains 18.0 mg of oxycodone as 20 mg of oxycodone hydrochloride. Each 30 mg tablet contains 27 mg of oxycodone as 30 mg of oxycodone hydrochloride.

Each 40 mg tablet contains 36.0 mg of oxycodone as 40 mg of oxycodone hydrochloride. Each 60 mg tablet contains 54 mg of oxycodone as 60 mg of oxycodone hydrochloride. Each 80 mg tablet contains 72.0 mg of oxycodone as 80 mg of oxycodone hydrochloride.

Each 120 mg tablet contains108 mg of oxycodone as 120 mg of oxycodone hydrochloride. Excipient with known effect: Contains lactose monohydrate. For the full list of excipients, see Section 6.1.3. Pharmaceutical form Prolonged release tablet. The 5 mg tablets are light blue, round, convex tablets marked OC on one side and 5 on the other.

The 10 mg tablets are white, round, convex tablets marked OC on one side and 10 on the other. The 15 mg tablets are grey, round, convex tablets marked OC on one side and 15 on the other. The 20 mg tablets are pink, round, convex tablets marked OC on one side and 20 on the other.

• The 30 mg tablets are brown, round, convex tablets marked OC on one side and 30 on the other.
• The 40 mg tablets are yellow, round, convex tablets marked OC on one side and 40 on the other.
• The 60 mg tablets are red, round, convex tablets marked OC on one side and 60 on the other.
• The 80 mg tablets are green, round, convex tablets marked OC on one side and 80 on the other.

The 120 mg tablets are purple, round, convex tablets marked OC on one side and 120 on the other.4. Clinical particulars 4.1 Therapeutic indications For the treatment of moderate to severe pain in patients with cancer and post-operative pain. For the treatment of severe pain requiring the use of a strong opioid.4.2 Posology and method of administration Adults over 18 years: OxyContin tablets should be taken at 12-hourly intervals.

1. The dosage is dependent on the severity of the pain, and the patient’s previous history of analgesic requirements.
2. Prior to starting treatment with opioids, a discussion should be held with patients to put in place a strategy for ending treatment with oxycodone in order to minimise the risk of addiction and drug withdrawal syndrome (see section 4.4).

OxyContin is not intended for use as a prn analgesic. Generally, the lowest effective dose for analgesia should be selected. Increasing severity of pain will require an increased dosage of OxyContin tablets, using the different tablet strengths, either alone or in combination, to achieve pain relief.

1. The correct dosage for any individual patient is that which controls the pain and is well tolerated for a full 12 hours.
2. Patients should be titrated to pain relief unless unmanageable adverse drug reactions prevent this.
3. If higher doses are necessary, increases should be made in 25% – 50% increments.
4. The need for escape medication more than twice a day indicates that the dosage of OxyContin tablets should be increased.

The usual starting dose for opioid naïve patients or patients presenting with severe pain uncontrolled by weaker opioids is 10 mg, 12-hourly. Some patients may benefit from a starting dose of 5 mg to minimise the incidence of side effects. The dose should then be carefully titrated, as frequently as once a day if necessary, to achieve pain relief.

Conversion from oral morphine: Patients receiving oral morphine before OxyContin therapy should have their daily dose based on the following ratio: 10 mg of oral oxycodone is equivalent to 20 mg of oral morphine. It must be emphasised that this is a guide to the dose of OxyContin tablets required. Inter-patient variability requires that each patient is carefully titrated to the appropriate dose.

Transferring patients between oral and parenteral oxycodone: The dose should be based on the following ratio: 2 mg of oral oxycodone is equivalent to 1 mg of parenteral oxycodone. It must be emphasised that this is a guide to the dose required. Inter-patient variability requires that each patient is carefully titrated to the appropriate dose.

1. Elderly patients: A dose adjustment is not usually necessary in elderly patients.
2. Controlled pharmacokinetic studies in elderly patients (aged over 65 years) have shown that, compared with younger adults, the clearance of oxycodone is only slightly reduced.
3. No untoward adverse drug reactions were seen based on age, therefore adult doses and dosage intervals are appropriate.

Paediatric population OxyContin should not be used in patients under 18 years of age. Patients with renal or hepatic impairment: The plasma concentration in this population may be increased. The dose initiation should follow a conservative approach in these patients.

• The recommended adult starting dose should be reduced by 50% (for example a total daily dose of 10 mg orally in opioid naïve patients), and each patient should be titrated to adequate pain control according to their clinical situation.
• Use in non-malignant pain: Opioids are not first-line therapy for chronic non-malignant pain, nor are they recommended as the only treatment.

Types of chronic pain which have been shown to be alleviated by strong opioids include chronic osteoarthritic pain and intervertebral disc disease. The need for continued treatment in non-malignant pain should be assessed at regular intervals. Method of administration OxyContin tablets are for oral use.

OxyContin tablets must be swallowed whole and not broken, chewed or crushed. Duration of treatment Oxycodone should not be used for longer than necessary. Discontinuation of treatment When a patient no longer requires therapy with oxycodone, it may be advisable to taper the dose gradually to prevent symptoms of withdrawal.4.3 Contraindications Hypersensitivity to oxycodone or to any of the excipients listed in section 6.1.

Oxycodone must not be used in any situation where opioids are contraindicated: severe respiratory depression with hypoxia, paralytic ileus, acute abdomen, delayed gastric emptying, severe chronic obstructive lung disease, cor pulmonale, severe bronchial asthma, elevated carbon dioxide levels in the blood, moderate to severe hepatic impairment, chronic constipation.

Patients with rare hereditary problems of galactose intolerance, total lactase deficiency or glucose-galactose malabsorption should not take this medicine.4.4 Special warnings and precautions for use Caution must be exercised when administering oxycodone to the debilitated elderly, patients with severely impaired pulmonary function, patients with impaired hepatic or renal function, patients with myxoedema, hypothyroidism, Addison’s disease, toxic psychosis, prostate hypertrophy, adrenocortical insufficiency, alcoholism, delirium tremens, diseases of the biliary tract, pancreatitis, inflammatory bowel disorders, hypotension, hypovolaemia raised intracranial pressure, intracranial lesions, head injury (due to risk of increased intracranial pressure), reduced level of consciousness of uncertain origin, sleep apnoea or patients taking benzodiazepines, other CNS depressants (including alcohol) or MAO inhibitors (see section 4.5).

The primary risk of opioid excess is respiratory depression. Sleep related breathing disorders Opioids can cause sleep-related breathing disorders including central sleep apnoea (CSA) and sleep-related hypoxemia. Opioid use increases the risk of CSA in a dose-dependent fashion.

Opioids may also cause worsening of pre-existing sleep apnoea (see section 4.8). Concomitant use of oxycodone and sedative medicines such as benzodiazepines or related drugs may result in sedation, respiratory depression, coma and death. Because of these risks, concomitant prescribing with these sedative medicines should be reserved for patients for whom alternative treatment options are not possible.

If a decision is made to prescribe oxycodone concomitantly with sedative medicines, the lowest effective dose should be used, and the duration of treatment should be as short as possible (see also general dose recommendation in section 4.2). The patient should be followed closely for signs and symptoms of respiratory depression and sedation.

• In this respect, it is strongly recommended to inform patients and their caregivers to be aware of these symptoms (see section 4.5).
• OxyContin tablets must be administered with caution in patients taking MAOIs or who have received MAOIs within the previous two weeks.
• OxyContin tablets should not be used where there is a possibility of paralytic ileus occurring.

Should paralytic ileus be suspected or occur during use, OxyContin tablets should be discontinued immediately. OxyContin tablets are not recommended for pre-operative use or within the first 12-24 hours post-operatively. As with all opioid preparations, oxycodone products should be used with caution following abdominal surgery as opioids are known to impair intestinal motility and should not be used until the physician is assured of normal bowel function.

Patients about to undergo additional pain relieving procedures (e.g. surgery, plexus blockade) should not receive OxyContin tablets for 12 hours prior to the intervention. If further treatment with OxyContin tablets is indicated then the dosage should be adjusted to the new post-operative requirement.

OxyContin 60 mg, 80 mg and 120 mg tablets should not be used in patients not previously exposed to opioids. These tablet strengths may cause fatal respiratory depression when administered to opioid naïve patients. For appropriate patients who suffer with chronic non-malignant pain, opioids should be used as part of a comprehensive treatment programme involving other medications and treatment modalities.

A crucial part of the assessment of a patient with chronic non-malignant pain is the patient’s addiction and substance abuse history. If opioid treatment is considered appropriate for the patient, then the main aim of treatment is not to minimise the dose of opioid but rather to achieve a dose which provides adequate pain relief with a minimum of side effects.

There must be frequent contact between physician and patient so that dosage adjustments can be made. It is strongly recommended that the physician defines treatment outcomes in accordance with pain management guidelines. The physician and patient can then agree to discontinue treatment if these objectives are not met.

Drug dependence, tolerance and potential for abuse Opioid Use Disorder (abuse and dependence) Tolerance and physical and/or psychological dependence may develop upon repeated administration of opioids such as oxycodone. Iatrogenic addiction following therapeutic use of opioids is known to occur. Repeated use of OxyContin tablets may lead to Opioid Use Disorder (OUD).

Abuse or intentional misuse of OxyContin tablets may result in overdose and/or death. The risk of developing OUD is increased in patients with a personal or a family history (parents or siblings) of substance use disorders (including alcohol use disorder), in current tobacco users or in patients with a personal history of other mental health disorders (e.g.

major depression, anxiety and personality disorders). Patients will require monitoring for signs of drug-seeking behaviour (e.g. too early requests for refills). This includes the review of concomitant opioids and psycho-active drugs (like benzodiazepines). For patients with signs and symptoms of OUD, consultation with an addiction specialist should be considered.

A comprehensive patient history should be taken to document concomitant medications, including over-the-counter medicines and medicines obtained on-line, and past and present medical and psychiatric conditions. Tolerance Patients may find that treatment is less effective with chronic use and express a need to increase the dose to obtain the same level of pain control as initially experienced.

• Patients may also supplement their treatment with additional pain relievers.
• These could be signs that the patient is developing tolerance.
• The risks of developing tolerance should be explained to the patient.
• Overuse or misuse may result in overdose and/or death.
• It is important that patients only use medicines that are prescribed for them at the dose they have been prescribed and do not give this medicine to anyone else.

Patients should be closely monitored for signs of misuse, abuse or addiction. The clinical need for analgesic treatment should be reviewed regularly. Drug withdrawal syndrome Prior to starting treatment with any opioids, a discussion should be held with patients to put in place a withdrawal strategy for ending treatment with oxycodone.

Drug withdrawal syndrome may occur upon abrupt cessation of therapy or dose reduction. When a patient no longer requires therapy, it is advisable to taper the dose gradually to minimise symptoms of withdrawal. Tapering from a high dose may take weeks to months. The opioid drug withdrawal syndrome is characterised by some or all of the following: restlessness, lacrimation, rhinorrhoea, yawning, perspiration, chills, myalgia, mydriasis and palpitations.

Other symptoms may also develop including irritability, agitation, anxiety, hyperkinesia, tremor, weakness, insomnia, anorexia, abdominal cramps, nausea, vomiting, diarrhoea, increased blood pressure, increased respiratory rate or heart rate. If women take this drug during pregnancy there is a risk that their newborn infants will experience neonatal withdrawal syndrome.

• Hyperalgesia Hyperalgesia may be diagnosed if the patient on long-term opioid therapy presents with increased pain.
• This might be qualitatively and anatomically distinct from pain related to disease progression or to breakthrough pain resulting from development of opioid tolerance.
• Pain associated with hyperalgesia tends to be more diffuse than the pre-existing pain and less defined in quality.

Symptoms of hyperalgesia may resolve with a reduction of opioid dose. OxyContin tablets must be swallowed whole, and not broken, chewed or crushed. The administration of broken, chewed, or crushed OxyContin tablets leads to a rapid release and absorption of a potentially fatal dose of oxycodone (see Section 4.9).

Concomitant use of alcohol and OxyContin may increase the undesirable effects of OxyContin ; concomitant use should be avoided. Abuse of oral dosage forms by parenteral administration can be expected to result in serious adverse events, such as local tissue necrosis, infection, pulmonary granulomas, increased risk of endocarditis, and valvular heart injury, which may be fatal.

Empty matrix (tablets) may be seen in the stools. Opioids such as oxycodone hydrochloride may influence the hypothalamic-pituitary-adrenal or – gonadal axes. Some changes that can be seen include an increase in serum prolactin, and decreases in plasma cortisol and testosterone.

Clinical symptoms may manifest from these hormonal changes.4.5 Interaction with other medicinal products and other forms of interaction The concomitant use of opioids with sedative medicines such as benzodiazepines or related drugs increases the risk of sedation, respiratory depression, coma and death because of additive CNS depressant effect.

The dose and duration of concomitant use should be limited (see section 4.4). Drugs which affect the CNS include, but are not limited to: other opioids, gabapentinoids such as pregabalin, anxiolytics, hypnotics and sedatives (including benzodiazepines), antipsychotics, antidepressants, phenothiazines, anaesthetics, muscle relaxants, antihypertensives and alcohol.

Concomitant administration of oxycodone with serotonin agents, such as a Selective Serotonin Re-uptake Inhibitor (SSRI) or a Serotonin Norepinephrine Re-uptake Inhibitor (SNRI) may cause serotonin toxicity. The symptoms of serotonin toxicity may include mental-status changes (e.g., agitation, hallucinations, coma), autonomic instability (e.g., tachycardia, labile blood pressure, hyperthermia), neuromuscular abnormalities (e.g., hyperreflexia, incoordination, rigidity), and/or gastrointestinal symptoms (e.g., nausea, vomiting, diarrhoea).

Oxycodone should be used with caution and the dosage may need to be reduced in patients using these medications. Concomitant administration of oxycodone with anticholinergics or medicines with anticholinergic activity (e.g. tricyclic anti-depressants, antihistamines, antipsychotics, muscle relaxants, anti-Parkinson drugs) may result in increased anticholinergic adverse effects.

Oxycodone should be used with caution and the dosage may need to be reduced in patients using these medications. MAO inhibitors are known to interact with narcotic analgesics. MAO inhibitors cause CNS excitation or depression associated with hypertensive or hypotensive crisis (see section 4.4). Co-administration with monoamine oxidase inhibitors or within two weeks of discontinuation of their use should be avoided.

Alcohol may enhance the pharmacodynamic effects of OxyContin ; concomitant use should be avoided. Oxycodone is metabolised mainly by CYP3A4, with a contribution from CYP2D6. The activities of these metabolic pathways may be inhibited or induced by various co-administered drugs or dietary elements.

Oxycodone doses may need to be adjusted accordingly. CYP3A4 inhibitors, such as macrolide antibiotics (e.g. clarithromycin, erythromycin and telithromycin), azole-antifungals (e.g. ketoconazole, voriconazole, itraconazole, and posaconazole), protease inhibitors (e.g. boceprevir, ritonavir, indinavir, nelfinavir and saquinavir), cimetidine and grapefruit juice may cause a reduced clearance of oxycodone that could cause an increase of the plasma concentrations of oxycodone.

Therefore the oxycodone dose may need to be adjusted accordingly. Some specific examples are provided below: • Itraconazole, a potent CYP3A4 inhibitor, administered 200 mg orally for five days, increased the AUC of oral oxycodone. On average, the AUC was approximately 2.4 times higher (range 1.5 – 3.4).

Voriconazole, a CYP3A4 inhibitor, administered 200 mg twice-daily for four days (400 mg given as first two doses), increased the AUC of oral oxycodone. On average, the AUC was approximately 3.6 times higher (range 2.7 – 5.6). • Telithromycin, a CYP3A4 inhibitor, administered 800 mg orally for four days, increased the AUC of oral oxycodone.

On average, the AUC was approximately 1.8 times higher (range 1.3 – 2.3). • Grapefruit Juice, a CYP3A4 inhibitor, administered as 200 ml three times a day for five days, increased the AUC of oral oxycodone. On average, the AUC was approximately 1.7 times higher (range 1.1 – 2.1).

CYP3A4 inducers, such as rifampicin, carbamazepine, phenytoin and St John’s Wort may induce the metabolism of oxycodone and cause an increased clearance of oxycodone that could cause a reduction of the plasma concentrations of oxycodone. The oxycodone dose may need to be adjusted accordingly. Some specific examples are provided below: • St John’s Wort, a CYP3A4 inducer, administered as 300 mg three times a day for fifteen days, reduced the AUC of oral oxycodone.

On average, the AUC was approximately 50% lower (range 37-57%). • Rifampicin, a CYP3A4 inducer, administered as 600 mg once-daily for seven days, reduced the AUC of oral oxycodone. On average, the AUC was approximately 86% lower Drugs that inhibit CYP2D6 activity, such as paroxetine and quinidine, may cause decreased clearance of oxycodone which could lead to an increase in oxycodone plasma concentrations.

• Concurrent administration of quinidine resulted in an increase in oxycodone Cmax by 11%, AUC by 13%, and t½ elim. by 14%.
• Also, an increase in noroxycodone level was observed, (Cmax by 50%; AUC by 85%, and t½ elim. by 42%).
• The pharmacodynamic effects of oxycodone were not altered.4.6 Fertility, pregnancy and lactation Pregnancy OxyContin tablets are not recommended for use in pregnancy nor during labour.

There are limited data from the use of oxycodone in pregnant women. Regular use in pregnancy may cause drug dependence in the foetus, leading to withdrawal symptoms in the neonate. If opioid use is required for a prolonged period in pregnant women, advise the patient of the risk of neonatal opioid withdrawal syndrome and ensure that appropriate treatment will be available.

• Administration during labour may depress respiration in the neonate and an antidote for the child should be readily available.
• Breastfeeding Administration to nursing women is not recommended as oxycodone may be secreted in breast milk and may cause respiratory depression in the infant.4.7 Effects on ability to drive and use machines Oxycodone may impair the ability to drive and use machines.

Oxycodone may modify patients’ reactions to a varying extent depending on the dosage and individual susceptibility. Therefore, patients should not drive or operate machinery if affected. This medicine can impair cognitive function and can affect a patient’s ability to drive safely.

• This class of medicine is in the list of drugs included in regulations under 5a of the Road Traffic Act 1988.
• When prescribing this medicine, patients should be told: • The medicine is likely to affect your ability to drive.
• Do not drive until you know how the medicine affects you.
• It is an offence to drive while you have this medicine in your body over a specified limit unless you have a defence (called the ‘statutory defence’).

• This defence applies when:

o The medicine has been prescribed to treat a medical or dental problem; and o You have taken it according to the instructions given by the prescriber and in the information provided with the medicine.

Please note that it is still an offence to drive if you are unfit because of the medicine (i.e. your ability to drive is being affected).” Details regarding a new driving offence concerning driving after drugs have been taken in the UK may be found here: https://www.gov.uk/drug-driving-law 4.8 Undesirable effects Adverse drug reactions are typical of full opioid agonists.

Term	Frequency
Very common	≥ 1/10
Common	≥ 1/100 to <1/10
Uncommon	≥ 1/1,000 to <1/100
Rare	≥1/10,000 to <1/1,000
Very rare	<1/10,000
Frequency not known	Cannot be estimated from the available data

Immune system disorders: Uncommon : hypersensitivity. Frequency not known: anaphylactic reaction, anaphylactoid reaction. Metabolism and nutrition disorders: Common : decreased appetite. Uncommon : dehydration. Psychiatric disorders: Common : anxiety, confusional state, depression, insomnia, nervousness, abnormal thinking, abnormal dreams.

• Uncommon : agitation, affect lability, euphoric mood, hallucinations, decreased libido, disorientation, mood altered, restlessness, dysphoria.
• Frequency not known : aggression, drug dependence (see section 4.4).
• Nervous system disorders: Very common : somnolence, dizziness, headache.
• Common : tremor, lethargy, sedation.

Uncommon : amnesia, convulsion, hypertonia, hypoaesthesia, involuntary muscle contractions, speech disorder, syncope, paraesthesia, dysgeusia, hypotonia. Frequency not known : hyperalgesia. Eye disorders: Uncommon : visual impairment, miosis. Ear and labyrinth disorders: Uncommon : vertigo.

Cardiac disorders: Uncommon : palpitations (in the context of withdrawal syndrome), supraventricular tachycardia. Vascular disorders: Uncommon : vasodilatation, facial flushing. Rare: hypotension, orthostatic hypotension. Respiratory, thoracic and mediastinal disorders: Common : dyspnoea, bronchospasm, cough decreased.

Uncommon : respiratory depression, hiccups. Not known: central sleep apnoea syndrome. Gastrointestinal disorders: Very common : constipation, nausea, vomiting. Common : abdominal pain, diarrhoea, dry mouth, dyspepsia. Uncommon : dysphagia, flatulence, eructation, ileus, gastritis.

• Frequency not known : dental caries.
• Hepato-biliary disorders: Uncommon : increased hepatic enzymes, biliary colic.
• Frequency not known : cholestasis.
• Skin and subcutaneous tissue disorders: Very common : pruritus.
• Common : rash, hyperhidrosis.
• Uncommon : dry skin, exfoliative dermatitis.
• Rare : urticaria.

Renal and urinary disorders: Uncommon : urinary retention, ureteral spasm. Reproductive system and breast disorders: Uncommon : erectile dysfunction, hypogonadism. Frequency not known : amenorrhoea. General disorders and administration site conditions: Common : asthenia, fatigue.

1. Uncommon : drug withdrawal syndrome, malaise, oedema, peripheral oedema, drug tolerance, thirst, pyrexia, chills.
2. Frequency not known: drug withdrawal syndrome neonatal.
3. Reporting of suspected adverse reactions Reporting suspected adverse reactions after authorisation of the medicinal product is important.

It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at: www.mhra.gov.uk/yellowcard or search for MHRA Yellow Card in the Google Play or Apple App Store.4.9 Overdose Acute overdose with oxycodone can be manifested by miosis, respiratory depression, hypotension and hallucinations.

1. Circulatory failure and somnolence progressing to stupor or deepening coma, hypotonia, bradycardia, pulmonary oedema and death may occur in more severe cases.
2. Patients should be informed of the signs and symptoms of overdose and to ensure that family and friends are also aware of these signs and to seek immediate medical help if they occur.

The effects of overdosage will be potentiated by the simultaneous ingestion of alcohol or other psychotropic drugs. Treatment of oxycodone overdosage : primary attention should be given to the establishment of a patent airway and institution of assisted or controlled ventilation.

1. The pure opioid antagonists such as naloxone are specific antidotes against symptoms from opioid overdose.
2. Other supportive measures should be employed as needed.
3. In the case of massive overdosage, administer naloxone intravenously (0.4 to 2 mg for an adult and 0.01 mg/kg body weight for children) if the patient is in a coma or respiratory depression is present.

Repeat the dose at 2 minute intervals if there is no response. If repeated doses are required an infusion of 60% of the initial dose per hour is a useful starting point. A solution of 10 mg made up in 50 ml dextrose will produce 200 micrograms/ml for infusion using an IV pump (dose adjusted to the clinical response).

1. Infusions are not a substitute for frequent review of the patient’s clinical state.
2. Intramuscular naloxone is an alternative in the event that IV access is not possible.
3. As the duration of action of naloxone is relatively short, the patient must be carefully monitored until spontaneous respiration is reliably re-established.

Naloxone is a competitive antagonist and large doses (4 mg) may be required in seriously poisoned patients. For less severe overdosage, administer naloxone 0.2 mg intravenously followed by increments of 0.1 mg every 2 minutes if required. The patient should be observed for at least 6 hours after the last dose of naloxone.

Naloxone should not be administered in the absence of clinically significant respiratory or circulatory depression secondary to oxycodone overdosage. Naloxone should be administered cautiously to persons who are known, or suspected, to be physically dependent on oxycodone. In such cases, an abrupt or complete reversal of opioid effects may precipitate pain and an acute withdrawal syndrome.

Additional/other considerations: • Consider activated charcoal (50 g for adults, 10-15 g for children), if a substantial amount has been ingested within 1 hour, provided the airway can be protected. It may be reasonable to assume that late administration of activated charcoal may be beneficial for prolonged release preparations; however, there is no evidence to support this.

OxyContin tablets will continue to release and add to the oxycodone load for up to 12 hours after administration and the management of oxycodone overdosage should be modified accordingly. Gastric contents may therefore need to be emptied as this can be useful in removing unabsorbed drug, particularly when a prolonged release formulation has been taken.5.

Pharmacological properties 5.1 Pharmacodynamic properties Pharmacotherapeutic group: Natural opium alkaloids ATC code: N02A A05 Oxycodone is a full opioid agonist with no antagonist properties. It has an affinity for kappa, mu and delta opiate receptors in the brain and spinal cord.

1. The therapeutic effect is mainly analgesic, anxiolytic and sedative.
2. Gastrointestinal System Opioids may induce spasm of the sphincter of Oddi.
3. Endocrine system See section 4.4.
4. Other pharmacological effects In- vitro and animal studies indicate various effects of natural opioids, such as morphine, on components of the immune system; the clinical significance of these findings is unknown.

Whether oxycodone, a semisynthetic opioid, has immunological effects similar to morphine is unknown.5.2 Pharmacokinetic properties Absorption The release of oxycodone from OxyContin tablets is biphasic with an initial relatively fast release providing an early onset of analgesia followed by a more controlled release, which determines the 12 hour duration of action.

Release of oxycodone from OxyContin tablets is independent of pH. OxyContin tablets have an oral bioavailability comparable with conventional oral oxycodone, but the former achieve maximal plasma concentrations at about 3 hours rather than about 1 to 1.5 hours. Peak and trough concentrations of oxycodone from OxyContin tablets 10 mg administered 12-hourly are equivalent to those achieved from conventional oxycodone 5 mg administered 6-hourly.

All strengths of OxyContin tablets are bioequivalent in terms of both rate and extent of absorption. Distribution Following absorption, oxycodone is distributed throughout the entire body. Approximately 45% is bound to plasma protein. Metabolism Oxycodone is metabolised in the liver via CYP3A4 and CYP2D6 to noroxycodone, oxymorphone and noroxymorphone, which are subsequently glucuronidated.

Noroxycodone and noroxymorphone are the major circulating metabolites. Noroxycodone is a weak mu opioid agonist. Noroxymorphone is a potent mu opioid agonist; however, it does not cross the blood-brain barrier to a significant extent. Oxymorphone is a potent mu opioid agonist but is present at very low concentrations following oxycodone administration.

None of these metabolites are thought to contribute significantly to the analgesic effect of oxycodone. Elimination The mean apparent elimination half-life of OxyContin is 4.5 hours, which leads to steady-state being achieved in about one day. The active drug and its metabolites are excreted in urine.

Elderly The AUC in elderly subjects is 15% greater when compared with young subjects. Gender Female subjects have, on average, plasma oxycodone concentrations up to 25% higher than males on a body weight adjusted basis. The reason for this difference is unknown. Patients with renal impairment Preliminary data from a study of patients with mild to moderate renal dysfunction show peak plasma oxycodone and noroxycodone concentrations approximately 50% and 20% higher, respectively and AUC values for oxycodone, noroxycodone and oxymorphone approximately 60%, 60% and 40% higher than normal subjects, respectively.

There was an increase in t ½ of elimination for oxycodone of only 1 hour. Patients with mild to moderate hepatic impairment Patients with mild to moderate hepatic dysfunction showed peak plasma oxycodone and noroxycodone concentrations approximately 50% and 20% higher, respectively, than normal subjects.

AUC values were approximately 95% and 75% higher, respectively. Oxymorphone peak plasma concentrations and AUC values were lower by 15% to 50%. The t ½ elimination for oxycodone increased by 2.3 hours.5.3 Preclinical safety data Reproductive and Development Toxicology Oxycodone had no effect on fertility or early embryonic development in male and female rats at doses as high as 8 mg/kg/d.

Also, oxycodone did not induce any deformities in rats at doses as high as 8 mg/kg/d or in rabbits at doses as high as 125 mg/kg/d. Dose-related increases in developmental variations (increased incidences of extra (27) presacral vertebrae and extra pairs of ribs) were observed in rabbits when the data for individual foetuses were analysed.

• However, when the same data were analysed using litters as opposed to individual foetuses, there was no dose-related increase in developmental variations although the incidence of extra presacral vertebrae remained significantly higher in the 125 mg/kg/d group compared to the control group.
• Since this dose level was associated with severe pharmacotoxic effects in the pregnant animals, the foetal findings may have been a secondary consequence of severe maternal toxicity.

In a prenatal and postnatal development study in rats, maternal body weight and food intake parameters were reduced for doses ≥ 2 mg/kg/d compared to the control group. Body weights were lower in the F1 generation from maternal rats in the 6 mg/kg/d dosing group.

There were no effects on physical, reflexological, or sensory developmental parameters or on behavioural and reproductive indices in the F1 pups (the NOEL for F1 pups was 2 mg/kg/d based on body weight effects seen at 6 mg/kg/d). There were no effects on the F2 generation at any dose in the study. Genotoxicity The results of in-vitro and in-vivo studies indicate that the genotoxic risk of oxycodone to humans is minimal or absent at the systemic oxycodone concentrations that are achieved therapeutically.

Oxycodone was not genotoxic in a bacterial mutagenicity assay or in an in-vivo micronucleus assay in the mouse. Oxycodone produced a positive response in the in-vitro mouse lymphoma assay in the presence of rat liver S9 metabolic activation at dose levels greater than 25 μg/mL.

Two in-vitro chromosomal aberrations assays with human lymphocytes were conducted. In the first assay, oxycodone was negative without metabolic activation but was positive with S9 metabolic activation at the 24 hour time point but not at other time points or at 48 hour after exposure. In the second assay, oxycodone did not show any clastogenicity either with or without metabolic activation at any concentration or time point.

Carcinogenicity Carcinogenicity was evaluated in a 2-year oral gavage study conducted in Sprague-Dawley rats. Oxycodone did not increase the incidence of tumours in male and female rats at doses up to 6 mg/kg/day. The doses were limited by opioid-related pharmacological effects of oxycodone.6.

Pharmaceutical particulars 6.1 List of excipients Lactose monohydrate Povidone Ammoniomethacrylate Co-polymer Sorbic acid Glycerol triacetate Stearyl Alcohol Talc Magnesium Stearate Film coat Hypromellose (E464) Titanium Dioxide (E171) Macrogol The 5 mg tablets also contain brilliant blue (E133). The 10 mg tablets also contain hydroxypropylcellulose.

The 15 mg tablets also contain iron oxide (E172). The 20 mg, 30 mg, 40 mg, 60 mg and 120 mg tablets also contain polysorbate 80 (E433) and iron oxide (E172). The 80 mg tablets also contain hydroxypropylcellulose, iron oxide (E172) and indigo carmine (E132).6.2 Incompatibilities Not applicable.6.3 Shelf life Three years.6.4 Special precautions for storage Do not store above 25°C.6.5 Nature and contents of container PVC blister packs with aluminium foil backing (containing 28 or 56 tablets).6.6 Special precautions for disposal and other handling None.7.

• Marketing authorisation holder Napp Pharmaceuticals Ltd Cambridge Science Park Milton Road Cambridge CB4 0GW 8.
• Marketing authorisation number(s) PL 16950/0097 PL 16950/0098 PL 16950/0099 PL 16950/0100 PL 16950/0123 PL 16950/0139 PL 16950/0140 PL 16950/0141 PL 16950/0150 9.
• Date of first authorisation/renewal of the authorisation 21 May 2002 10.

Date of revision of the text 1 April 2022

Does OxyContin last 24 hours?

Key facts –

Oxycodone liquid and capsules work in 30 to 60 minutes but wear off after 4 to 6 hours. Slow-release tablets can take up to 1 to 2 days to work fully but the pain relief will last longer.It’s possible to become addicted to oxycodone, but your doctor will explain how to reduce the risks of becoming addicted.If you need to take oxycodone for more than a few weeks, your treatment plan may include details of how and when to stop taking this medicine.The most common side effects of oxycodone are constipation, feeling sick and feeling sleepy.Do not have grapefruit juice while taking oxycodone. It can affect the way your body uses the oxycodone and cause more serious side effects.

Page last reviewed: 17 November 2022 Next review due: 17 November 2025

Does OxyContin make pain go away?

How does oxycodone work? – Oxycodone works directly on opioid receptors in the central nervous system and reduces feelings of pain by interrupting the way nerves signal pain between the brain and the body.

Is it safe to take 10 mg of OxyContin?

The starting dosage for patients who are not opioid tolerant is OXYCONTIN 10 mg orally every 12 hours. Use of higher starting doses in patients who are not opioid tolerant may cause fatal respiratory depression.

How strong is 325 mg of OxyContin?

Oxycodone 5/325 Dosage – As was touched on above, if you’re looking for information about the oxycodone 5/325 dosage, it’s probably actually Percocet Ⓡ dosages that you’re researching. This is because the 5/325 part of the dosage refers to a combination of two drugs.

Percocet Ⓡ dosages include oxycodone/acetaminophen 2.5 mg/325 mg, 5 mg/325 mg, 7.5 mg/325 mg and 10 mg/325 mg. If you were looking at an oxycodone dosage, such as what’s found in OxyContin Ⓡ, the doses can be higher, and they begin at 10 mg per tablet, whereas with a combination drug, 10 mg is the highest amount of oxycodone available in each tablet.

With most Percocet Ⓡ dosages you take only one tablet every six hours as needed, but there are maximum daily doses that people need to understand and follow. These maximum daily doses are important because Percocet Ⓡ contains acetaminophen, which is an over-the-counter pain reliever that’s viewed as relatively harmless when taken as instructed but can lead to liver damage, or acute liver failure.

1. The 325-mg part of the dosages listed above refers to how much acetaminophen is in a dose.
2. If you take more than the maximum daily dose of Percocet Ⓡ or other combination drugs with acetaminophen in a day, you’re putting the health of your liver at serious risk, and it can even lead to death.
3. People also might wonder if an oxycodone 5/325 dosage is strong, and the answer is that it’s a medium-strength dose.

It’s relatively small dosage-wise, and the amount of acetaminophen in all of these doses is around what’s found in an extra-strength Tylenol Ⓡ tablet.

Is OxyContin 20 mg addictive?

What are the risks ? – Individuals who abuse OxyContin risk developing tolerance for the drug, meaning they must take increasingly higher doses to achieve the same effects. Long-term abuse of the drug can lead to physical dependence and addiction. Individuals who become dependent upon or addicted to the drug may experience withdrawal symptoms if they cease using the drug.

1. Withdrawal symptoms associated with OxyContin dependency or addiction include restlessness, muscle and bone pain, insomnia, diarrhea, vomiting, cold flashes, and involuntary leg movements.
2. Individuals who take a large dose of OxyContin are at risk of severe respiratory depression that can lead to death.

Inexperienced and new users are at particular risk, because they may be unaware of what constitutes a large dose and have not developed a tolerance for the drug. In addition, OxyContin abusers who inject the drug expose themselves to additional risks, including contracting HIV (human immunodeficiency virus), hepatitis B and C, and other blood-borne viruses.

What is the reversal for OxyContin?

Naloxone Naloxone is an opioid antagonist medication that is used to reverse an opioid overdose.

Naloxone is a medication approved by the (FDA) designed to rapidly reverse opioid overdose. It is an opioid antagonist—meaning that it binds to opioid receptors and can reverse and block the effects of other opioids, such as heroin, morphine, and oxycodone. Administered when a patient is showing signs of, naloxone is a temporary treatment and its effects do not last long. Therefore, it is critical to obtain medical intervention as soon as possible after administering/receiving naloxone. The medication can be given by intranasal spray (into the nose), intramuscular (into the muscle), subcutaneous (under the skin), or intravenous injection. A practitioner should assess the need to prescribe naloxone for patients who are taking methadone or buprenorphine receiving or otherwise considered a risk for opioid overdose.

Candidates for naloxone are those who:

Take high doses of opioids for long-term management of chronic pain Receive rotating opioid medication regimens Have been discharged from emergency medical care following opioid poisoning or intoxication Take certain extended-release or long-acting opioid medication Those who have had a period of abstinence to include those recently released from incarceration.

Pregnant women can be safely given naloxone in limited doses under the supervision of a doctor. A doctor or pharmacist can show patients, their family members, or caregivers how to administer naloxone. Patients given an automatic injection device or nasal spray should keep the item available at all times. It is important to remember to replace medication when the expiration date passes and if exposed to temperatures below 39°F or above 104°F.

Naloxone is effective if opioids are misused in combination with other sedatives or stimulants. It is not effective in treating overdoses of benzodiazepines or stimulant overdoses involving cocaine and amphetamines.

How is OxyContin excreted in the body?

Approximately 72% of an oxycodone dose is excreted in the urine ; 8% as oxycodone, 47% as oxidative metabolites and 18% as reduced metabolites.

Does OxyContin keep you up?

Oxycodone use can significantly impact sleep, both in terms of quantity and quality of sleep. As an opioid pain medication, oxycodone can cause drowsiness, increasing the time a person sleeps. However, oxycodone can also disrupt the normal sleep cycle and lead to problems with both falling and staying asleep.

What is OxyContin made of?

OxyContin is a trade name product for the generic narcotic oxycodone hydrochloride, an opiate agonist. Opiate agonists provide pain relief by acting on opioid receptors in the spinal cord, brain, and possibly in the tissues directly. Opioids, natural or synthetic classes of drugs that act like morphine, are the most effective pain relievers available.

• Oxycodone is manufactured by modifying thebaine, an alkaloid found in opium.
• Oxycodone has a high abuse potential and is prescribed for moderate to high pain relief associated with injuries, bursitis, dislocation, fractures, neuralgia, arthritis, and lower back and cancer pain.
• It is also used postoperatively and for pain relief after childbirth.

Percocet, Percodan, and Tylox are other trade name oxycodone products. Oxycodone is a central nervous system depressant. Oxycodone’s action appears to work through stimulating the opioid receptors found in the central nervous system that activate responses ranging from analgesia to respiratory depression to euphoria.

People who take the drug repeatedly can develop a tolerance or resistance to the drug’s effects. Thus, a cancer patient can take a dose of oxycodone on a regular basis that would be fatal in a person never exposed to oxycodone or another opioid. Most individuals who abuse oxycodone seek to gain the euphoric effects, mitigate pain, and avoid withdrawal symptoms associated with oxycodone or heroin abstinence.

OxyContin is an oral, controlled-release oxycodone that acts for 12 hours, making it the longest lasting oxycodone on the market. Patients taking shorter acting oxycodone products, such as Percocet, may need to take the product every 4 to 6 hours. While drug doses vary by individual, the typical OxyContin dose prescribed by physicians ranges from two to four tablets per day.

Is OxyContin better than tramadol for pain?

Can I use tramadol or oxycodone with alcohol? – You should avoid taking tramadol or oxycodone with alcohol. Both tramadol and oxycodone carry an FDA Black Box Warning about taking them with other central nervous system depressants, including alcohol. It increases your risk of a potentially fatal overdose.

What kind of pain does OxyContin help?

Oxycodone is an analgesic opioid medication that is generally used for the relief of moderate-to-severe pain.

How long does OxyContin 40mg last?

My Account Area – 1. Name of the medicinal product OxyContin 5 mg, 10 mg, 15 mg, 20 mg, 30 mg, 40 mg, 60 mg, 80 mg, 120 mg prolonged release tablets 2. Qualitative and quantitative composition Each 5 mg tablet contains 4.5 mg of oxycodone as 5 mg of oxycodone hydrochloride.

1. Each 10 mg tablet contains 9.0 mg of oxycodone as 10 mg of oxycodone hydrochloride.
2. Each 15 mg tablet contains 13.5 mg of oxycodone as 15 mg of oxycodone hydrochloride.
3. Each 20 mg tablet contains 18.0 mg of oxycodone as 20 mg of oxycodone hydrochloride.
4. Each 30 mg tablet contains 27 mg of oxycodone as 30 mg of oxycodone hydrochloride.

Each 40 mg tablet contains 36.0 mg of oxycodone as 40 mg of oxycodone hydrochloride. Each 60 mg tablet contains 54 mg of oxycodone as 60 mg of oxycodone hydrochloride. Each 80 mg tablet contains 72.0 mg of oxycodone as 80 mg of oxycodone hydrochloride.

Each 120 mg tablet contains108 mg of oxycodone as 120 mg of oxycodone hydrochloride. Excipient with known effect: Contains lactose monohydrate. For the full list of excipients, see Section 6.1.3. Pharmaceutical form Prolonged release tablet. The 5 mg tablets are light blue, round, convex tablets marked OC on one side and 5 on the other.

The 10 mg tablets are white, round, convex tablets marked OC on one side and 10 on the other. The 15 mg tablets are grey, round, convex tablets marked OC on one side and 15 on the other. The 20 mg tablets are pink, round, convex tablets marked OC on one side and 20 on the other.

1. The 30 mg tablets are brown, round, convex tablets marked OC on one side and 30 on the other.
2. The 40 mg tablets are yellow, round, convex tablets marked OC on one side and 40 on the other.
3. The 60 mg tablets are red, round, convex tablets marked OC on one side and 60 on the other.
4. The 80 mg tablets are green, round, convex tablets marked OC on one side and 80 on the other.

The 120 mg tablets are purple, round, convex tablets marked OC on one side and 120 on the other.4. Clinical particulars 4.1 Therapeutic indications For the treatment of moderate to severe pain in patients with cancer and post-operative pain. For the treatment of severe pain requiring the use of a strong opioid.4.2 Posology and method of administration Adults over 18 years: OxyContin tablets should be taken at 12-hourly intervals.

1. The dosage is dependent on the severity of the pain, and the patient’s previous history of analgesic requirements.
2. Prior to starting treatment with opioids, a discussion should be held with patients to put in place a strategy for ending treatment with oxycodone in order to minimise the risk of addiction and drug withdrawal syndrome (see section 4.4).

OxyContin is not intended for use as a prn analgesic. Generally, the lowest effective dose for analgesia should be selected. Increasing severity of pain will require an increased dosage of OxyContin tablets, using the different tablet strengths, either alone or in combination, to achieve pain relief.

• The correct dosage for any individual patient is that which controls the pain and is well tolerated for a full 12 hours.
• Patients should be titrated to pain relief unless unmanageable adverse drug reactions prevent this.
• If higher doses are necessary, increases should be made in 25% – 50% increments.
• The need for escape medication more than twice a day indicates that the dosage of OxyContin tablets should be increased.

The usual starting dose for opioid naïve patients or patients presenting with severe pain uncontrolled by weaker opioids is 10 mg, 12-hourly. Some patients may benefit from a starting dose of 5 mg to minimise the incidence of side effects. The dose should then be carefully titrated, as frequently as once a day if necessary, to achieve pain relief.

Conversion from oral morphine: Patients receiving oral morphine before OxyContin therapy should have their daily dose based on the following ratio: 10 mg of oral oxycodone is equivalent to 20 mg of oral morphine. It must be emphasised that this is a guide to the dose of OxyContin tablets required. Inter-patient variability requires that each patient is carefully titrated to the appropriate dose.

Transferring patients between oral and parenteral oxycodone: The dose should be based on the following ratio: 2 mg of oral oxycodone is equivalent to 1 mg of parenteral oxycodone. It must be emphasised that this is a guide to the dose required. Inter-patient variability requires that each patient is carefully titrated to the appropriate dose.

Elderly patients: A dose adjustment is not usually necessary in elderly patients. Controlled pharmacokinetic studies in elderly patients (aged over 65 years) have shown that, compared with younger adults, the clearance of oxycodone is only slightly reduced. No untoward adverse drug reactions were seen based on age, therefore adult doses and dosage intervals are appropriate.

Paediatric population OxyContin should not be used in patients under 18 years of age. Patients with renal or hepatic impairment: The plasma concentration in this population may be increased. The dose initiation should follow a conservative approach in these patients.

The recommended adult starting dose should be reduced by 50% (for example a total daily dose of 10 mg orally in opioid naïve patients), and each patient should be titrated to adequate pain control according to their clinical situation. Use in non-malignant pain: Opioids are not first-line therapy for chronic non-malignant pain, nor are they recommended as the only treatment.

Types of chronic pain which have been shown to be alleviated by strong opioids include chronic osteoarthritic pain and intervertebral disc disease. The need for continued treatment in non-malignant pain should be assessed at regular intervals. Method of administration OxyContin tablets are for oral use.

OxyContin tablets must be swallowed whole and not broken, chewed or crushed. Duration of treatment Oxycodone should not be used for longer than necessary. Discontinuation of treatment When a patient no longer requires therapy with oxycodone, it may be advisable to taper the dose gradually to prevent symptoms of withdrawal.4.3 Contraindications Hypersensitivity to oxycodone or to any of the excipients listed in section 6.1.

Oxycodone must not be used in any situation where opioids are contraindicated: severe respiratory depression with hypoxia, paralytic ileus, acute abdomen, delayed gastric emptying, severe chronic obstructive lung disease, cor pulmonale, severe bronchial asthma, elevated carbon dioxide levels in the blood, moderate to severe hepatic impairment, chronic constipation.

Patients with rare hereditary problems of galactose intolerance, total lactase deficiency or glucose-galactose malabsorption should not take this medicine.4.4 Special warnings and precautions for use Caution must be exercised when administering oxycodone to the debilitated elderly, patients with severely impaired pulmonary function, patients with impaired hepatic or renal function, patients with myxoedema, hypothyroidism, Addison’s disease, toxic psychosis, prostate hypertrophy, adrenocortical insufficiency, alcoholism, delirium tremens, diseases of the biliary tract, pancreatitis, inflammatory bowel disorders, hypotension, hypovolaemia raised intracranial pressure, intracranial lesions, head injury (due to risk of increased intracranial pressure), reduced level of consciousness of uncertain origin, sleep apnoea or patients taking benzodiazepines, other CNS depressants (including alcohol) or MAO inhibitors (see section 4.5).

The primary risk of opioid excess is respiratory depression. Sleep related breathing disorders Opioids can cause sleep-related breathing disorders including central sleep apnoea (CSA) and sleep-related hypoxemia. Opioid use increases the risk of CSA in a dose-dependent fashion.

Opioids may also cause worsening of pre-existing sleep apnoea (see section 4.8). Concomitant use of oxycodone and sedative medicines such as benzodiazepines or related drugs may result in sedation, respiratory depression, coma and death. Because of these risks, concomitant prescribing with these sedative medicines should be reserved for patients for whom alternative treatment options are not possible.

If a decision is made to prescribe oxycodone concomitantly with sedative medicines, the lowest effective dose should be used, and the duration of treatment should be as short as possible (see also general dose recommendation in section 4.2). The patient should be followed closely for signs and symptoms of respiratory depression and sedation.

In this respect, it is strongly recommended to inform patients and their caregivers to be aware of these symptoms (see section 4.5). OxyContin tablets must be administered with caution in patients taking MAOIs or who have received MAOIs within the previous two weeks. OxyContin tablets should not be used where there is a possibility of paralytic ileus occurring.

Should paralytic ileus be suspected or occur during use, OxyContin tablets should be discontinued immediately. OxyContin tablets are not recommended for pre-operative use or within the first 12-24 hours post-operatively. As with all opioid preparations, oxycodone products should be used with caution following abdominal surgery as opioids are known to impair intestinal motility and should not be used until the physician is assured of normal bowel function.

1. Patients about to undergo additional pain relieving procedures (e.g.
2. Surgery, plexus blockade) should not receive OxyContin tablets for 12 hours prior to the intervention.
3. If further treatment with OxyContin tablets is indicated then the dosage should be adjusted to the new post-operative requirement.

OxyContin 60 mg, 80 mg and 120 mg tablets should not be used in patients not previously exposed to opioids. These tablet strengths may cause fatal respiratory depression when administered to opioid naïve patients. For appropriate patients who suffer with chronic non-malignant pain, opioids should be used as part of a comprehensive treatment programme involving other medications and treatment modalities.

A crucial part of the assessment of a patient with chronic non-malignant pain is the patient’s addiction and substance abuse history. If opioid treatment is considered appropriate for the patient, then the main aim of treatment is not to minimise the dose of opioid but rather to achieve a dose which provides adequate pain relief with a minimum of side effects.

There must be frequent contact between physician and patient so that dosage adjustments can be made. It is strongly recommended that the physician defines treatment outcomes in accordance with pain management guidelines. The physician and patient can then agree to discontinue treatment if these objectives are not met.

Drug dependence, tolerance and potential for abuse Opioid Use Disorder (abuse and dependence) Tolerance and physical and/or psychological dependence may develop upon repeated administration of opioids such as oxycodone. Iatrogenic addiction following therapeutic use of opioids is known to occur. Repeated use of OxyContin tablets may lead to Opioid Use Disorder (OUD).

Abuse or intentional misuse of OxyContin tablets may result in overdose and/or death. The risk of developing OUD is increased in patients with a personal or a family history (parents or siblings) of substance use disorders (including alcohol use disorder), in current tobacco users or in patients with a personal history of other mental health disorders (e.g.

• Major depression, anxiety and personality disorders).
• Patients will require monitoring for signs of drug-seeking behaviour (e.g.
• Too early requests for refills).
• This includes the review of concomitant opioids and psycho-active drugs (like benzodiazepines).
• For patients with signs and symptoms of OUD, consultation with an addiction specialist should be considered.

A comprehensive patient history should be taken to document concomitant medications, including over-the-counter medicines and medicines obtained on-line, and past and present medical and psychiatric conditions. Tolerance Patients may find that treatment is less effective with chronic use and express a need to increase the dose to obtain the same level of pain control as initially experienced.

Patients may also supplement their treatment with additional pain relievers. These could be signs that the patient is developing tolerance. The risks of developing tolerance should be explained to the patient. Overuse or misuse may result in overdose and/or death. It is important that patients only use medicines that are prescribed for them at the dose they have been prescribed and do not give this medicine to anyone else.

Patients should be closely monitored for signs of misuse, abuse or addiction. The clinical need for analgesic treatment should be reviewed regularly. Drug withdrawal syndrome Prior to starting treatment with any opioids, a discussion should be held with patients to put in place a withdrawal strategy for ending treatment with oxycodone.

• Drug withdrawal syndrome may occur upon abrupt cessation of therapy or dose reduction.
• When a patient no longer requires therapy, it is advisable to taper the dose gradually to minimise symptoms of withdrawal.
• Tapering from a high dose may take weeks to months.
• The opioid drug withdrawal syndrome is characterised by some or all of the following: restlessness, lacrimation, rhinorrhoea, yawning, perspiration, chills, myalgia, mydriasis and palpitations.

Other symptoms may also develop including irritability, agitation, anxiety, hyperkinesia, tremor, weakness, insomnia, anorexia, abdominal cramps, nausea, vomiting, diarrhoea, increased blood pressure, increased respiratory rate or heart rate. If women take this drug during pregnancy there is a risk that their newborn infants will experience neonatal withdrawal syndrome.

• Hyperalgesia Hyperalgesia may be diagnosed if the patient on long-term opioid therapy presents with increased pain.
• This might be qualitatively and anatomically distinct from pain related to disease progression or to breakthrough pain resulting from development of opioid tolerance.
• Pain associated with hyperalgesia tends to be more diffuse than the pre-existing pain and less defined in quality.

Symptoms of hyperalgesia may resolve with a reduction of opioid dose. OxyContin tablets must be swallowed whole, and not broken, chewed or crushed. The administration of broken, chewed, or crushed OxyContin tablets leads to a rapid release and absorption of a potentially fatal dose of oxycodone (see Section 4.9).

Concomitant use of alcohol and OxyContin may increase the undesirable effects of OxyContin ; concomitant use should be avoided. Abuse of oral dosage forms by parenteral administration can be expected to result in serious adverse events, such as local tissue necrosis, infection, pulmonary granulomas, increased risk of endocarditis, and valvular heart injury, which may be fatal.

Empty matrix (tablets) may be seen in the stools. Opioids such as oxycodone hydrochloride may influence the hypothalamic-pituitary-adrenal or – gonadal axes. Some changes that can be seen include an increase in serum prolactin, and decreases in plasma cortisol and testosterone.

Clinical symptoms may manifest from these hormonal changes.4.5 Interaction with other medicinal products and other forms of interaction The concomitant use of opioids with sedative medicines such as benzodiazepines or related drugs increases the risk of sedation, respiratory depression, coma and death because of additive CNS depressant effect.

The dose and duration of concomitant use should be limited (see section 4.4). Drugs which affect the CNS include, but are not limited to: other opioids, gabapentinoids such as pregabalin, anxiolytics, hypnotics and sedatives (including benzodiazepines), antipsychotics, antidepressants, phenothiazines, anaesthetics, muscle relaxants, antihypertensives and alcohol.

Concomitant administration of oxycodone with serotonin agents, such as a Selective Serotonin Re-uptake Inhibitor (SSRI) or a Serotonin Norepinephrine Re-uptake Inhibitor (SNRI) may cause serotonin toxicity. The symptoms of serotonin toxicity may include mental-status changes (e.g., agitation, hallucinations, coma), autonomic instability (e.g., tachycardia, labile blood pressure, hyperthermia), neuromuscular abnormalities (e.g., hyperreflexia, incoordination, rigidity), and/or gastrointestinal symptoms (e.g., nausea, vomiting, diarrhoea).

Oxycodone should be used with caution and the dosage may need to be reduced in patients using these medications. Concomitant administration of oxycodone with anticholinergics or medicines with anticholinergic activity (e.g. tricyclic anti-depressants, antihistamines, antipsychotics, muscle relaxants, anti-Parkinson drugs) may result in increased anticholinergic adverse effects.

• Oxycodone should be used with caution and the dosage may need to be reduced in patients using these medications.
• MAO inhibitors are known to interact with narcotic analgesics.
• MAO inhibitors cause CNS excitation or depression associated with hypertensive or hypotensive crisis (see section 4.4).
• Co-administration with monoamine oxidase inhibitors or within two weeks of discontinuation of their use should be avoided.

Alcohol may enhance the pharmacodynamic effects of OxyContin ; concomitant use should be avoided. Oxycodone is metabolised mainly by CYP3A4, with a contribution from CYP2D6. The activities of these metabolic pathways may be inhibited or induced by various co-administered drugs or dietary elements.

Oxycodone doses may need to be adjusted accordingly. CYP3A4 inhibitors, such as macrolide antibiotics (e.g. clarithromycin, erythromycin and telithromycin), azole-antifungals (e.g. ketoconazole, voriconazole, itraconazole, and posaconazole), protease inhibitors (e.g. boceprevir, ritonavir, indinavir, nelfinavir and saquinavir), cimetidine and grapefruit juice may cause a reduced clearance of oxycodone that could cause an increase of the plasma concentrations of oxycodone.

Therefore the oxycodone dose may need to be adjusted accordingly. Some specific examples are provided below: • Itraconazole, a potent CYP3A4 inhibitor, administered 200 mg orally for five days, increased the AUC of oral oxycodone. On average, the AUC was approximately 2.4 times higher (range 1.5 – 3.4).

Voriconazole, a CYP3A4 inhibitor, administered 200 mg twice-daily for four days (400 mg given as first two doses), increased the AUC of oral oxycodone. On average, the AUC was approximately 3.6 times higher (range 2.7 – 5.6). • Telithromycin, a CYP3A4 inhibitor, administered 800 mg orally for four days, increased the AUC of oral oxycodone.

On average, the AUC was approximately 1.8 times higher (range 1.3 – 2.3). • Grapefruit Juice, a CYP3A4 inhibitor, administered as 200 ml three times a day for five days, increased the AUC of oral oxycodone. On average, the AUC was approximately 1.7 times higher (range 1.1 – 2.1).

CYP3A4 inducers, such as rifampicin, carbamazepine, phenytoin and St John’s Wort may induce the metabolism of oxycodone and cause an increased clearance of oxycodone that could cause a reduction of the plasma concentrations of oxycodone. The oxycodone dose may need to be adjusted accordingly. Some specific examples are provided below: • St John’s Wort, a CYP3A4 inducer, administered as 300 mg three times a day for fifteen days, reduced the AUC of oral oxycodone.

On average, the AUC was approximately 50% lower (range 37-57%). • Rifampicin, a CYP3A4 inducer, administered as 600 mg once-daily for seven days, reduced the AUC of oral oxycodone. On average, the AUC was approximately 86% lower Drugs that inhibit CYP2D6 activity, such as paroxetine and quinidine, may cause decreased clearance of oxycodone which could lead to an increase in oxycodone plasma concentrations.

Concurrent administration of quinidine resulted in an increase in oxycodone Cmax by 11%, AUC by 13%, and t½ elim. by 14%. Also, an increase in noroxycodone level was observed, (Cmax by 50%; AUC by 85%, and t½ elim. by 42%). The pharmacodynamic effects of oxycodone were not altered.4.6 Fertility, pregnancy and lactation Pregnancy OxyContin tablets are not recommended for use in pregnancy nor during labour.

There are limited data from the use of oxycodone in pregnant women. Regular use in pregnancy may cause drug dependence in the foetus, leading to withdrawal symptoms in the neonate. If opioid use is required for a prolonged period in pregnant women, advise the patient of the risk of neonatal opioid withdrawal syndrome and ensure that appropriate treatment will be available.

Administration during labour may depress respiration in the neonate and an antidote for the child should be readily available. Breastfeeding Administration to nursing women is not recommended as oxycodone may be secreted in breast milk and may cause respiratory depression in the infant.4.7 Effects on ability to drive and use machines Oxycodone may impair the ability to drive and use machines.

Oxycodone may modify patients’ reactions to a varying extent depending on the dosage and individual susceptibility. Therefore, patients should not drive or operate machinery if affected. This medicine can impair cognitive function and can affect a patient’s ability to drive safely.

This class of medicine is in the list of drugs included in regulations under 5a of the Road Traffic Act 1988. When prescribing this medicine, patients should be told: • The medicine is likely to affect your ability to drive. • Do not drive until you know how the medicine affects you. • It is an offence to drive while you have this medicine in your body over a specified limit unless you have a defence (called the ‘statutory defence’).

• This defence applies when:

o The medicine has been prescribed to treat a medical or dental problem; and o You have taken it according to the instructions given by the prescriber and in the information provided with the medicine.

Please note that it is still an offence to drive if you are unfit because of the medicine (i.e. your ability to drive is being affected).” Details regarding a new driving offence concerning driving after drugs have been taken in the UK may be found here: https://www.gov.uk/drug-driving-law 4.8 Undesirable effects Adverse drug reactions are typical of full opioid agonists.

Term	Frequency
Very common	≥ 1/10
Common	≥ 1/100 to <1/10
Uncommon	≥ 1/1,000 to <1/100
Rare	≥1/10,000 to <1/1,000
Very rare	<1/10,000
Frequency not known	Cannot be estimated from the available data

Immune system disorders: Uncommon : hypersensitivity. Frequency not known: anaphylactic reaction, anaphylactoid reaction. Metabolism and nutrition disorders: Common : decreased appetite. Uncommon : dehydration. Psychiatric disorders: Common : anxiety, confusional state, depression, insomnia, nervousness, abnormal thinking, abnormal dreams.

• Uncommon : agitation, affect lability, euphoric mood, hallucinations, decreased libido, disorientation, mood altered, restlessness, dysphoria.
• Frequency not known : aggression, drug dependence (see section 4.4).
• Nervous system disorders: Very common : somnolence, dizziness, headache.
• Common : tremor, lethargy, sedation.

Uncommon : amnesia, convulsion, hypertonia, hypoaesthesia, involuntary muscle contractions, speech disorder, syncope, paraesthesia, dysgeusia, hypotonia. Frequency not known : hyperalgesia. Eye disorders: Uncommon : visual impairment, miosis. Ear and labyrinth disorders: Uncommon : vertigo.

• Cardiac disorders: Uncommon : palpitations (in the context of withdrawal syndrome), supraventricular tachycardia.
• Vascular disorders: Uncommon : vasodilatation, facial flushing.
• Rare: hypotension, orthostatic hypotension.
• Respiratory, thoracic and mediastinal disorders: Common : dyspnoea, bronchospasm, cough decreased.

Uncommon : respiratory depression, hiccups. Not known: central sleep apnoea syndrome. Gastrointestinal disorders: Very common : constipation, nausea, vomiting. Common : abdominal pain, diarrhoea, dry mouth, dyspepsia. Uncommon : dysphagia, flatulence, eructation, ileus, gastritis.

1. Frequency not known : dental caries.
2. Hepato-biliary disorders: Uncommon : increased hepatic enzymes, biliary colic.
3. Frequency not known : cholestasis.
4. Skin and subcutaneous tissue disorders: Very common : pruritus.
5. Common : rash, hyperhidrosis.
6. Uncommon : dry skin, exfoliative dermatitis.
7. Rare : urticaria.

Renal and urinary disorders: Uncommon : urinary retention, ureteral spasm. Reproductive system and breast disorders: Uncommon : erectile dysfunction, hypogonadism. Frequency not known : amenorrhoea. General disorders and administration site conditions: Common : asthenia, fatigue.

1. Uncommon : drug withdrawal syndrome, malaise, oedema, peripheral oedema, drug tolerance, thirst, pyrexia, chills.
2. Frequency not known: drug withdrawal syndrome neonatal.
3. Reporting of suspected adverse reactions Reporting suspected adverse reactions after authorisation of the medicinal product is important.

It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at: www.mhra.gov.uk/yellowcard or search for MHRA Yellow Card in the Google Play or Apple App Store.4.9 Overdose Acute overdose with oxycodone can be manifested by miosis, respiratory depression, hypotension and hallucinations.

1. Circulatory failure and somnolence progressing to stupor or deepening coma, hypotonia, bradycardia, pulmonary oedema and death may occur in more severe cases.
2. Patients should be informed of the signs and symptoms of overdose and to ensure that family and friends are also aware of these signs and to seek immediate medical help if they occur.

The effects of overdosage will be potentiated by the simultaneous ingestion of alcohol or other psychotropic drugs. Treatment of oxycodone overdosage : primary attention should be given to the establishment of a patent airway and institution of assisted or controlled ventilation.

The pure opioid antagonists such as naloxone are specific antidotes against symptoms from opioid overdose. Other supportive measures should be employed as needed. In the case of massive overdosage, administer naloxone intravenously (0.4 to 2 mg for an adult and 0.01 mg/kg body weight for children) if the patient is in a coma or respiratory depression is present.

Repeat the dose at 2 minute intervals if there is no response. If repeated doses are required an infusion of 60% of the initial dose per hour is a useful starting point. A solution of 10 mg made up in 50 ml dextrose will produce 200 micrograms/ml for infusion using an IV pump (dose adjusted to the clinical response).

1. Infusions are not a substitute for frequent review of the patient’s clinical state.
2. Intramuscular naloxone is an alternative in the event that IV access is not possible.
3. As the duration of action of naloxone is relatively short, the patient must be carefully monitored until spontaneous respiration is reliably re-established.

Naloxone is a competitive antagonist and large doses (4 mg) may be required in seriously poisoned patients. For less severe overdosage, administer naloxone 0.2 mg intravenously followed by increments of 0.1 mg every 2 minutes if required. The patient should be observed for at least 6 hours after the last dose of naloxone.

Naloxone should not be administered in the absence of clinically significant respiratory or circulatory depression secondary to oxycodone overdosage. Naloxone should be administered cautiously to persons who are known, or suspected, to be physically dependent on oxycodone. In such cases, an abrupt or complete reversal of opioid effects may precipitate pain and an acute withdrawal syndrome.

Additional/other considerations: • Consider activated charcoal (50 g for adults, 10-15 g for children), if a substantial amount has been ingested within 1 hour, provided the airway can be protected. It may be reasonable to assume that late administration of activated charcoal may be beneficial for prolonged release preparations; however, there is no evidence to support this.

OxyContin tablets will continue to release and add to the oxycodone load for up to 12 hours after administration and the management of oxycodone overdosage should be modified accordingly. Gastric contents may therefore need to be emptied as this can be useful in removing unabsorbed drug, particularly when a prolonged release formulation has been taken.5.

Pharmacological properties 5.1 Pharmacodynamic properties Pharmacotherapeutic group: Natural opium alkaloids ATC code: N02A A05 Oxycodone is a full opioid agonist with no antagonist properties. It has an affinity for kappa, mu and delta opiate receptors in the brain and spinal cord.

The therapeutic effect is mainly analgesic, anxiolytic and sedative. Gastrointestinal System Opioids may induce spasm of the sphincter of Oddi. Endocrine system See section 4.4. Other pharmacological effects In- vitro and animal studies indicate various effects of natural opioids, such as morphine, on components of the immune system; the clinical significance of these findings is unknown.

Whether oxycodone, a semisynthetic opioid, has immunological effects similar to morphine is unknown.5.2 Pharmacokinetic properties Absorption The release of oxycodone from OxyContin tablets is biphasic with an initial relatively fast release providing an early onset of analgesia followed by a more controlled release, which determines the 12 hour duration of action.

Release of oxycodone from OxyContin tablets is independent of pH. OxyContin tablets have an oral bioavailability comparable with conventional oral oxycodone, but the former achieve maximal plasma concentrations at about 3 hours rather than about 1 to 1.5 hours. Peak and trough concentrations of oxycodone from OxyContin tablets 10 mg administered 12-hourly are equivalent to those achieved from conventional oxycodone 5 mg administered 6-hourly.

All strengths of OxyContin tablets are bioequivalent in terms of both rate and extent of absorption. Distribution Following absorption, oxycodone is distributed throughout the entire body. Approximately 45% is bound to plasma protein. Metabolism Oxycodone is metabolised in the liver via CYP3A4 and CYP2D6 to noroxycodone, oxymorphone and noroxymorphone, which are subsequently glucuronidated.

1. Noroxycodone and noroxymorphone are the major circulating metabolites.
2. Noroxycodone is a weak mu opioid agonist.
3. Noroxymorphone is a potent mu opioid agonist; however, it does not cross the blood-brain barrier to a significant extent.
4. Oxymorphone is a potent mu opioid agonist but is present at very low concentrations following oxycodone administration.

None of these metabolites are thought to contribute significantly to the analgesic effect of oxycodone. Elimination The mean apparent elimination half-life of OxyContin is 4.5 hours, which leads to steady-state being achieved in about one day. The active drug and its metabolites are excreted in urine.

Elderly The AUC in elderly subjects is 15% greater when compared with young subjects. Gender Female subjects have, on average, plasma oxycodone concentrations up to 25% higher than males on a body weight adjusted basis. The reason for this difference is unknown. Patients with renal impairment Preliminary data from a study of patients with mild to moderate renal dysfunction show peak plasma oxycodone and noroxycodone concentrations approximately 50% and 20% higher, respectively and AUC values for oxycodone, noroxycodone and oxymorphone approximately 60%, 60% and 40% higher than normal subjects, respectively.

There was an increase in t ½ of elimination for oxycodone of only 1 hour. Patients with mild to moderate hepatic impairment Patients with mild to moderate hepatic dysfunction showed peak plasma oxycodone and noroxycodone concentrations approximately 50% and 20% higher, respectively, than normal subjects.

1. AUC values were approximately 95% and 75% higher, respectively.
2. Oxymorphone peak plasma concentrations and AUC values were lower by 15% to 50%.
3. The t ½ elimination for oxycodone increased by 2.3 hours.5.3 Preclinical safety data Reproductive and Development Toxicology Oxycodone had no effect on fertility or early embryonic development in male and female rats at doses as high as 8 mg/kg/d.

Also, oxycodone did not induce any deformities in rats at doses as high as 8 mg/kg/d or in rabbits at doses as high as 125 mg/kg/d. Dose-related increases in developmental variations (increased incidences of extra (27) presacral vertebrae and extra pairs of ribs) were observed in rabbits when the data for individual foetuses were analysed.

• However, when the same data were analysed using litters as opposed to individual foetuses, there was no dose-related increase in developmental variations although the incidence of extra presacral vertebrae remained significantly higher in the 125 mg/kg/d group compared to the control group.
• Since this dose level was associated with severe pharmacotoxic effects in the pregnant animals, the foetal findings may have been a secondary consequence of severe maternal toxicity.

In a prenatal and postnatal development study in rats, maternal body weight and food intake parameters were reduced for doses ≥ 2 mg/kg/d compared to the control group. Body weights were lower in the F1 generation from maternal rats in the 6 mg/kg/d dosing group.

1. There were no effects on physical, reflexological, or sensory developmental parameters or on behavioural and reproductive indices in the F1 pups (the NOEL for F1 pups was 2 mg/kg/d based on body weight effects seen at 6 mg/kg/d).
2. There were no effects on the F2 generation at any dose in the study.
3. Genotoxicity The results of in-vitro and in-vivo studies indicate that the genotoxic risk of oxycodone to humans is minimal or absent at the systemic oxycodone concentrations that are achieved therapeutically.

Oxycodone was not genotoxic in a bacterial mutagenicity assay or in an in-vivo micronucleus assay in the mouse. Oxycodone produced a positive response in the in-vitro mouse lymphoma assay in the presence of rat liver S9 metabolic activation at dose levels greater than 25 μg/mL.

Two in-vitro chromosomal aberrations assays with human lymphocytes were conducted. In the first assay, oxycodone was negative without metabolic activation but was positive with S9 metabolic activation at the 24 hour time point but not at other time points or at 48 hour after exposure. In the second assay, oxycodone did not show any clastogenicity either with or without metabolic activation at any concentration or time point.

Carcinogenicity Carcinogenicity was evaluated in a 2-year oral gavage study conducted in Sprague-Dawley rats. Oxycodone did not increase the incidence of tumours in male and female rats at doses up to 6 mg/kg/day. The doses were limited by opioid-related pharmacological effects of oxycodone.6.

• Pharmaceutical particulars 6.1 List of excipients Lactose monohydrate Povidone Ammoniomethacrylate Co-polymer Sorbic acid Glycerol triacetate Stearyl Alcohol Talc Magnesium Stearate Film coat Hypromellose (E464) Titanium Dioxide (E171) Macrogol The 5 mg tablets also contain brilliant blue (E133).
• The 10 mg tablets also contain hydroxypropylcellulose.

The 15 mg tablets also contain iron oxide (E172). The 20 mg, 30 mg, 40 mg, 60 mg and 120 mg tablets also contain polysorbate 80 (E433) and iron oxide (E172). The 80 mg tablets also contain hydroxypropylcellulose, iron oxide (E172) and indigo carmine (E132).6.2 Incompatibilities Not applicable.6.3 Shelf life Three years.6.4 Special precautions for storage Do not store above 25°C.6.5 Nature and contents of container PVC blister packs with aluminium foil backing (containing 28 or 56 tablets).6.6 Special precautions for disposal and other handling None.7.

1. Marketing authorisation holder Napp Pharmaceuticals Ltd Cambridge Science Park Milton Road Cambridge CB4 0GW 8.
2. Marketing authorisation number(s) PL 16950/0097 PL 16950/0098 PL 16950/0099 PL 16950/0100 PL 16950/0123 PL 16950/0139 PL 16950/0140 PL 16950/0141 PL 16950/0150 9.
3. Date of first authorisation/renewal of the authorisation 21 May 2002 10.

Date of revision of the text 1 April 2022

What time of day is best to take OxyContin?

How to take it – You can take oxycodone at any time of day, but try to take it at the same time every day and space your doses evenly. For example, if you take oxycodone twice a day and have your first dose at 8am, take your second dose around 8pm. Take oxycodone with, or just after, a meal or snack as it’s less likely to make you feel sick.