This information is intended for use by health professionals

1. Name of the medicinal product


2. Qualitative and quantitative composition

Each tablet contains 8mg Codeine Phosphate BP and 500mg Paracetamol PhEur.

For the full list of excipients, see section 6.1.

3. Pharmaceutical form

White, circular, flat bevelled-edge uncoated tablets impressed 'C' and the identifying letters 'CH' on either side of a central division line on one face.

4. Clinical particulars
4.1 Therapeutic indications

1) Co-codamol is indicated in adults and children older than 12 years of age for the treatment of acute moderate pain which is not considered to be relieved by other analgesics such as paracetamol or ibuprofen (alone).

2) As an antipyretic.

4.2 Posology and method of administration

Prior to starting treatment with opioids, a discussion should be held with patients to put in place a strategy for ending treatment with codeine phosphate in order to minimise the risk of addiction and drug withdrawal syndrome (see section 4.4).


Co-codamol should be used at the lowest effective dose for the shortest period of time. This dose may be taken, up to 4 times a day at intervals of not less than 6 hours.


Two tablets, to be taken with a glass of water, not more frequently than every 4 to six hours, up to a maximum of 8 tablets in any 24 hour period.

Children aged 16-18 years:

One to two tablets every 6 hours when necessary up to a maximum of 8 tablets in 24 hours.

Children aged 12 years to 15 years:

One tablet every 6 hours when necessary up to a maximum dose of 4 tablets in any 24 hours.

Do not take for more than 3 days without consulting your doctor.

Paediatric population:

Children aged less than 12 years:

Co-codamol should not be used in children below the age of 12 years because of the risk of opioid toxicity due to the variable and unpredictable metabolism of codeine to morphine (see sections 4.3 and 4.4).

Children aged 12 years to 18 years:

Co-codamol is not recommended for use in children aged 12 years to 18 years with compromised respiratory function for the symptomatic treatment of colds (see section 4.4).

Elderly: Dosage should be reduced in the elderly where there is impairment of hepatic function.

Method of administration

For oral administration.

4.3 Contraindications

• Hypersensitivity to paracetamol, codeine phosphate or to any of the excipients listed in section 6.1.

• In children below the age of 12 years for the symptomatic treatment of colds due to an increased risk of developing serious and life-threatening adverse reactions.

• in all paediatric patients (0-18 years of age) who undergo tonsillectomy and/or adenoidectomy for obstructive sleep apnoea syndrome due to an increased risk of developing serious and lifethreatening adverse reactions (see section 4.4)

• Diarrhoea caused by poisoning until the toxic material has been eliminated, or diarrhoea associated with pseudomembraneous colitis

• Respiratory depression

• Obstructive airways disease

• In women during breastfeeding (see section 4.6)

• In patients for whom it is known they are CYP2D6 ultra-rapid metabolisers

4.4 Special warnings and precautions for use

Paediatric population

Not recommended for children under 12 years of age.

Care is advised in the administration of paracetamol to patients with severe renal or severe hepatic impairment. The hazard of overdose is greater in those with non-cirrhotic alcoholic liver disease.

The recommended dose should not be exceeded.

This medicine should not be taken with any other paracetamol-containing products. If symptoms persist, the patient should be advised to consult their doctor. The patient should be advised to seek immediate medical advice in the event of an overdose, even if they feel well, because of the risk of delayed, serious liver damage.

Use with caution in patients with convulsive disorders.

The risk-benefit of continued use should be assessed regularly by the prescriber.

The leaflet will state in a prominent position in the 'before taking' section:

• Do not take for longer than your doctor tells you to.

• This medicine contains paracetamol. Do not take anything else containing paracetamol while taking this medicine.

• Taking a painkiller for headaches too often or for too long can make them worse.

The label will state (To be displayed prominently on outer pack – not boxed):

• Do not take for longer than directed by your prescriber as taking codeine regularly for a long time can lead to addiction.

• Do not take anything else containing paracetamol while taking this medicine.

• Immediate medical advice should be sought in the event of an overdose, even if you feel well, because of the risk of delayed, serious liver damage.

or if leaflet present:

Talk to a doctor at once if you take too much of this medicine even if you feel well.

CYP2D6 metabolism

Codeine is metabolised by the liver enzyme CYP2D6 into morphine, its active metabolite. If a patient has a deficiency or is completely lacking this enzyme an adequate analgesic effect will not be obtained. Estimates indicate that up to 7% of the Caucasian population may have this deficiency. However, if the patient is an extensive or ultra-rapid metaboliser there is an increased risk of developing side effects of opioid toxicity even at commonly prescribed doses. These patients convert codeine into morphine rapidly resulting in higher than expected serum morphine levels.

General symptoms of opioid toxicity include confusion, somnolence, shallow breathing, small pupils, nausea, vomiting, constipation and lack of appetite. In severe cases this may include symptoms of circulatory and respiratory depression, which may be life-threatening and very rarely fatal. Estimates of prevalence of ultra-rapid metabolisers in different populations are summarized below:


Prevalence %



African American

3.4% to 6.5%


1.2% to 2%


3.6% to 6.5%





Northern European


Co-codamol should be used with caution in patients with:

• hepatic function impairment (avoid if severe) and those with non-cirrhotic alcoholic liver disease. The hazards of overdose are greater in those with alcoholic liver disease.

• Prolonged use of co-codamol may cause hepatic necrosis.

• renal function impairment

• hypothyroidism (risk of depression and prolonged CNS depression is increased)

• inflammatory bowel disease - risk of toxic megacolon

• Opioids should not be administered during an asthma attack

• convulsions - may be induced or exacerbated

• drug abuse, dependence (including alcoholism), enhanced instability, suicidal ideation or attempts - predisposed to drug abuse

• head injuries or conditions where intracranial pressure is raised

• gall bladder disease or gall stones - opioids may cause biliary contraction

• gastro-intestinal surgery - use with caution after recent GI surgery as opioids may alter GI motility

• prostatic hypertrophy or recent urinary tract surgery

• adrenocortical insufficiency, e.g. Addison's Disease

• hypotension and shock

• myasthenia gravis

• phaeochromocytoma - opioids may stimulate catecholamine release by inducing the release of endogenous histamine

Monitoring after prolonged use should include blood count, liver function and renal function.

Where analgesics are used long-term (>3 months) with administration every two days or more frequently, headache may develop or worsen. Headache induced by overuse of analgesics (MOH medication-overuse headache) should not be treated by dose increase. In such cases, the use of analgesics should be discontinued in consultation with the doctor.

Drug dependence, tolerance and potential for abuse

For all patients, prolonged use of this product may lead to drug dependence (addiction), even at therapeutic doses. The risks are increased in individuals with current or past history of substance misuse disorder (including alcohol misuse) or mental health disorder (e.g., major depression).

Additional support and monitoring may be necessary when prescribing for patients at risk of opioid misuse.

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.

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 codeine phosphate.

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 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.

Post-operative use in children

There have been reports in the published literature that codeine given post-operatively in children after tonsillectomy and/or adenoidectomy for obstructive sleep apnoea, led to rare, but life-threatening adverse events including death (see also section 4.3). All children received doses of codeine that were within the appropriate dose range; however there was evidence that these children were either ultrarapid or extensive metabolisers in their ability to metabolise codeine to morphine.

Children with compromised respiratory function

Codeine is not recommended for use in children in whom respiratory function might be compromised including neuromuscular disorders, severe cardiac or respiratory conditions, upper respiratory or lung infections, multiple trauma or extensive surgical procedures. These factors may worsen symptoms of morphine toxicity.

Risk from concomitant use of sedative medicines such as benzodiazepines or related drugs:

Concomitant use of Co-codamol 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 Co-codamol concomitantly with sedative medicines, the lowest effective dose should be used, and the duration of treatment should be as short as possible.

The patients 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).

Risks from concomitant use of opioids and alcohol

Concomitant use of opioids, including codeine, with alcohol may result in sedation, respiratory depression, coma and death. Concomitant use with alcohol is not recommended (see section 4.5).

Label Warnings:

The risk-benefit of continued use should be assessed regularly by the prescriber.

4.5 Interaction with other medicinal products and other forms of interaction

Paracetamol can interact with the following:

• Drugs which alter gastric emptying time (eg cimetidine, ethyl alcohol, oral steroid contraceptives). These drugs reduce or delay peak paracetamol blood levels.

• Metoclopramide or domperidone increases the speed of absorption of paracetamol.

• Colestyramine reduces paracetamol absorption.

• Drugs which interfere with the metabolism of paracetamol by competition with metabolic pathways or substrates eg anticonvulsants (phenytoin), hepatic enzyme inducers, alcohol, barbiturates, tricyclic antidepressants. A poor diet (low protein) may also have a similar effect on the risk of serious paracetamol toxicity to hepatic enzyme inducers. Patients who have taken barbiturates, tricyclic antidepressants and alcohol may show diminished ability to metabolise large doses of paracetamol, the plasma half-life of which may be prolonged.

• The anticoagulant effect of warfarin and other coumarins may be enhanced by prolonged regular use of paracetamol with increased risk of bleeding; occasional doses have no significant effect.

• Alcohol can increase the hepatotoxicity of paracetamol overdosage and may have contributed to the acute pancreatitis reported in one patient who had taken an overdosage of paracetamol.

Codeine Phosphate can interact with the following:

• CNS depressants - enhanced sedative and/or hypotensive effect with anaesthetics, hypnotics, anxiolytics, antipsychotics, hydroxyzine, tricyclic antidepressants

• Sedative medicines such as benzodiazepines or related drugs - 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).

• Antibacterials, eg ciprofloxacin, - avoid premedication with opioids as reduced plasma ciprofloxacin concentration

• MAOIs - use only with extreme caution

• Cyclizine

• Mexiletine - delayed absorption

• Metoclopramide and domperidone - antagonise GI effects

• Cisapride - possible antagonism of GI effects

• Dopaminergics (eg selegiline) - possible risk of hyperpyrexia and CNS toxicity. This risk is greater with pethidine but with other opioids the risk is uncertain

• Ulcer healing drugs - cimetidine inhibits the metabolism of opioid analgesics.

• Anticholinergics (eg atropine) - risk of severe constipation which may lead to paralytic illness, and /or urinary retention

• Antidiarrhoeal drugs (eg loperamide, kaolin) - increased risk of severe constipation

• Antihypertensive drugs (eg guanethidine, diuretics) - enhanced hypotensive effect

• Opioid antagonists (eg buprenorphine, naltrexone, naloxone)

• Neuromuscular blocking agents - additive respiratory depressant effects.

• The concomitant use of alcohol and opioids increases the risk of sedation, respiratory depression, coma and death because of additive CNS depressant effect. Concomitant use with alcohol is not recommended (see section 4.4).

4.6 Fertility, pregnancy and lactation


A large amount of data on pregnant women indicate neither malformative, nor feto/neonatal toxicity. Epidemiological studies on neurodevelopment in children exposed to paracetamol in utero show inconclusive results. If clinically needed, paracetamol can be used during pregnancy however it should be used at the lowest effective dose for the shortest possible time and at the lowest possible frequency.

Results of one case control study suggest that there might be an increased risk of malformations of the respiratory tract in the offspring of women who consumed codeine during the first four months of pregnancy. This increase was statistically not significant. Evidence of other malformations is also reported in epidemiological studies on narcotic analgesics, including codeine.

Patients should follow the advice of their doctor regarding the use of this product.

Regular use during 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 a pregnant woman, 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.


Paracetamol is excreted in breast milk but not in a clinically significant amount. Available published data do not contraindicate breast feeding.

Codeine is contraindicated in women during breastfeeding (see section 4.3) as codeine may be secreted in breast milk and may cause respiratory depression in the infant.

4.7 Effects on ability to drive and use machines

Opioid analgesics can impair mental function and can cause blurred vision and dizziness. Patients should make sure they are not affected before driving or operating machinery.

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 under the influence of this medicine

• However, you would not be committing an offence (called 'statutory defence') if:

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 and

o It was not affecting your ability to drive safely

4.8 Undesirable effects

Regular prolonged use of codeine is known to lead to addiction and tolerance. Symptoms of restlessness and irritability may result when treatment is then stopped.

Prolonged use of a painkiller for headaches can make them worse.

The information below lists reported adverse reactions, ranked using the following frequency classification:

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), not known (cannot be estimated from the available data).

System organ class


Adverse effect

Blood and lymphatic system disorders

Not known

Methaemoglobinaemia, neutropenia, pancytopenia, leukopenia, thrombocytopenic purpura, haemolytic anaemia, agranulocytosis, thrombocytopenia.

Immune system disorders

Not known

Anaphylactic shock, angioedema, allergic reactions (may be caused by histamine release) - including hypersensitivity, rash, urticaria, mucosal lesions, difficulty breathing, increased sweating, redness or flushed face

Psychiatric disorders

Not known

Changes in mood, hallucinations, depression, trouble sleeping or nightmares, dependence, impaired mental functions, trembling, confusional state, dysphoria, euphoria.

Drug dependence (see section 4.4)

Nervous system disorders

Not known

Vertigo, dizziness, CNS excitation (restlessness/excitement), convulsions, headache, raised intracranial pressure, light-headedness, confusion, drowsiness, seizure, somnolence.

Eye disorders

Not known

Blurred or double vision, miosis

Cardiac disorders

Not known

Bradycardia, palpitations, hypotension, toxic myocarditis

Gastrointestinal disorders

Not known

Constipation, nausea, vomiting, GI irritation, biliary spam, loss of appetite, dry mouth, paralytic ileus, toxic megacolon, acute pancreatitis

Respiratory, thoracic and mediastinal disorders

Not known

Respiratory depression

Hepatobiliary disorders

Not known

Chronic hepatic necrosis*

Skin and subcutaneous tissue disorders

Very Rare

Very rare cases of serious skin reactions have been reported, Toxic Epidermal Necrolysis (TEN), Stevens-Johnson syndrome (SJS), acute generalized exanthematous pustulosis, fixed drug eruption

Renal and urinary disorders



Not known

Ureteral spasm, antidiuretic effect, urinary retention, papillary necrosis

General disorders and administration site conditions


Drug withdrawal syndrome

Not known

Tolerance, unusual tiredness or weakness, malaise, hypothermia

* Chronic hepatic necrosis has been reported in a patient who took daily therapeutic doses of paracetamol for about a year, and liver damage has been reported after daily ingestion of excessive amounts for shorter periods. A review of a group of patients with chronic active hepatitis failed to reveal differences in the abnormalities of liver function in those who were long-term users of paracetamol, nor was the control of their disease improved after paracetamol withdrawal.


Abrupt withdrawal precipitates a withdrawal syndrome. Symptoms may include tremor, insomnia, nausea, vomiting, sweating and increase in heart rate, respiratory rate and blood pressure. NOTE - tolerance diminishes rapidly after withdrawal so a previously tolerated dose may prove fatal.

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; website: or search for MHRA Yellow Card in the Google Play or Apple App Store.

4.9 Overdose


Liver damage is possible in adults who have taken 10g or more of paracetamol. Ingestion of 5g or more of paracetamol may lead to liver damage if the patient has risk factors (see below).

Risk factors

If the patient:

• is on long term treatment with carbamazepine, phenobarbitone, phenytoin, primidone, rifampicin, St. John's Wort or other drugs that induce liver enzymes, or

• regularly consumes ethanol in excess of recommended amounts, or

• is likely to be glutathione deplete e.g. eating disorders, cystic fibrosis, HIV

infection, starvation, cachexia.


Symptoms of paracetamol overdosage in the first 24 hours are pallor, nausea, vomiting, anorexia and abdominal pain.

Liver damage may become apparent 12 to 48 hours after ingestion. Abnormalities of glucose metabolism and metabolic acidosis may occur. In severe poisoning, hepatic failure may progress to encephalopathy, haemorrhage, hypoglycaemia, cerebral oedema, gastrointestinal bleeding and death.

Acute renal failure with acute tubular necrosis, strongly suggested by loin pain, haematuria and proteinuria may develop even in the absence of severe liver damage.

Cardiac arrhythmias and pancreatitis have been reported.


Immediate treatment is essential in the management of paracetamol overdose. Despite a lack of significant early symptoms, patients should be referred to hospital urgently for immediate medical attention. Symptoms may be limited to nausea or vomiting and may not reflect the severity of overdose or the risk of organ damage. Management should be in accordance with established treatment guidelines (see BNF overdose section).

Treatment with activated charcoal should be considered if the overdose has been taken within 1 hour. Plasma paracetamol concentration should be measured at 4 hours or later after ingestion (earlier concentrations are unreliable). Treatment with N-acetylcysteine may be used up to 24 hours after ingestion of paracetamol, however, the maximum protective effect is obtained up to 8 hours post-ingestion. The effectiveness of the antidote declines sharply after this time. If required the patient should be given intravenous N-acetylcysteine, in line with the established dosage schedule. If vomiting is not a problem, oral methionine may be a suitable alternative for remote areas, outside hospital. Management of patients who present serious hepatic dysfunction beyond 24h from ingestion should be discussed with the NPIS or a liver unit.

Further measures will depend on the severity, nature and course of clinical symptoms of paracetamol intoxication and should follow standard intensive care protocols.


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 in overdosage will be potentiated by simultaneous ingestion of alcohol and psychotropic drugs.


Central nervous system depression, including respiratory depression, may develop but is unlikely to be severe unless other sedative agents have been co-ingested, including alcohol, or the overdose is very large. The pupils may be pinpoint in size; nausea and vomiting are common. Hypotension and tachycardia are possible but unlikely.


This should include general symptomatic and supportive measures including a clear airway and monitoring of vital signs until stable. Consider activated charcoal if an adult presents within one hour of ingestion of more than 350mg or a child more than 5mg/kg.

Give naloxone if coma or respiratory depression is present. Naloxone is a competitive antagonist and has a short half-life so large and repeated doses may be required in a seriously poisoned patient. Observe for at least four hours after ingestion, or eight hours if a sustained release preparation has been taken.

The opioid antagonist naloxone hydrochloride is an antidote to respiratory depression and must be administered intravenously.

Patients should be advised to first consult their healthcare professional before taking codeine if they are taking a benzodiazepine.

5. Pharmacological properties
5.1 Pharmacodynamic properties

Pharmacotherapeutic group: Anilides, Paracetamol combinations excl. psycholeptics

ATC Code: N02B E51

Paracetamol has analgesic and antipyretic properties but is has no useful anti-inflammatory properties.

Codeine phosphate is a weak analgesic and is used in the treatment of cough and diarrhoea.

Paracetamol's effects are thought to be related to inhibition of prostaglandin synthesis.

Codeine is much less potent than morphine and it is inadequate against severe pain even in the largest tolerable doses. It does not cause appreciable respiratory depression but does have antitussive and constipating effects. It differs from morphine in that for normal medical use serious dependence is not frequently associated with codeine and large doses produce excitement rather than depression. Codeine is a centrally acting weak analgesic. Codeine exerts its effect through μ opioid receptors, although codeine has low affinity for these receptors, and its analgesic effect is due to its conversion to morphine. Codeine, particularly in combination with other analgesics such as paracetamol, has been shown to be effective in acute nociceptive pain. Codeine also binds weakly to κ opioid receptors which mediates spinal analgesia, sedation and miosis.

5.2 Pharmacokinetic properties


Absorption and Distribution

Codeine and its salts are readily absorbed from the GI tract and ingestion of codeine phosphate produces peak plasma concentrations in about one hour.

Biotransformation and Excretion

It is metabolised in the liver; and codeine and its metabolites are entirely excreted almost by the kidney, mainly as conjugates with glucuronic acid. The plasma half-life is reported to be 3-4 hours after administration by mouth.


Absorption and Distribution

Paracetamol is readily absorbed from the GI tract with peak plasma concentrations occurring about 30 minutes-2 hours after ingestion.

Biotransformation and Excretion

It is metabolised in the liver and excreted in the urine, mainly as the glucuronide and sulfate conjugates. The elimination half-life varies from about 1-4 hours.

Plasma-protein binding is negligible at usual therapeutic concentrations but increases with increasing concentrations.

A minor hydroxylated metabolite which is usually produced in very small amounts by mixed-function oxidases in the liver and which is usually detoxified by conjugation with liver glutathione may accumulate following paracetamol overdosage and cause liver damage.

5.3 Preclinical safety data

There are no preclinical data of relevance to the prescriber which are additional to that already included in other sections of the SPC.

6. Pharmaceutical particulars
6.1 List of excipients

Also contains: colloidal anhydrous silica, maize starch, pregelatinsed maize starch, stearic acid, water.

6.2 Incompatibilities

None known.

6.3 Shelf life


Two years from the date of manufacture.

Shelf-life after dilution/reconstitution

Not applicable.

Shelf-life after first opening

Not applicable.

6.4 Special precautions for storage

Store below 25°C in a dry place. Protect from light.

6.5 Nature and contents of container

Child-resistant blister pack: (i) 250µm white rigid PVC (ii) 9µm soft aluminium / 35g/m2 glassine paper. Compliant with BS8404.

Pack sizes:


PE tablet container with a child-resistant PP closure. Compliant with ISO8317.

Pack sizes:


PP tablet container with a PE closure for supply to nursing homes.

Pack sizes:

100, 500, 1000.

6.6 Special precautions for disposal and other handling

Not applicable

7. Marketing authorisation holder

Name or style and permanent address of registered place of business of the holder of the Marketing Authorisation:

Accord Healthcare Limited

Sage House

319 Pinner Road

North Harrow



United Kingdom

8. Marketing authorisation number(s)

PL 20075/0702

9. Date of first authorisation/renewal of the authorisation


10. Date of revision of the text