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Naproxen 500mg Tablets

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1.


NAME OF THE MEDICINAL PRODUCT

Naproxen 500mg Tablets

2 QUALITATIVE AND QUANTITATIVE COMPOSITION

Each tablet contains naproxen 500mg.

For excipients, see 6.1

3.    PHARMACEUTICAL FORM

Tablet

Capsule shaped, yellow, uncoated tablet embossed N500 on one side.

4.    CLINICAL PARTICULARS

4.1.    Therapeutic indications

Adults

For the treatment of rheumatoid arthritis, osteoarthrosis (degenerative arthritis), ankylosing spondylitis, acute gout, acute musculoskeletal disorders (such as sprains and strains, direct trauma, lumbosacral pain, cervical spondylitis, tenosynovitis and fibrositis) and dysmenorrhoea.

Children

For the treatment of juvenile rheumatoid arthritis.

4.2    Posology and method of administration

For oral administration.

To be taken preferably with or after food.

Undesirable effects may be minimised by using the lowest effective dose for the shortest duration necessary to control symptoms (see section 4.4).

Adults

Rheumatoid arthritis, osteoarthritis and ankylosing spondylitis

500mg to 1000mg per day taken in two doses at 12 hour intervals or alternatively, as a single administration. In the following cases a loading dose of 750mg or 1000mg per day for the acute phase is recommended:

a)    In patients reporting severe night-time pain/or morning stiffness.

b)    In patients being switched to Naproxen from a high dose of another anti-rheumatic compound.

c)    In osteoarthrosis where pain is the predominant symptom.

Acute gout

750mg at once, then 250mg every eight hours Acute musculoskeletal disorders and dysmenorrhoea

500mg initially, followed by 250mg at 6-8 hour intervals as needed with a maximum daily dose after the first day of 1250mg.

Elderly

The unbound plasma fraction of naproxen is increased in the elderly, although total plasma concentration is unchanged (see section 4.4 for effects of reduced elimination in the elderly). The elderly are at increased risk of the serious consequences of adverse reactions. If an NSAID is considered necessary, the lowest dose should be used and the patient should be monitored regularly for GI bleeding during NSAID therapy.

Children (over 5 years)

Juvenile rheumatoid arthritis

10mg/kg/day taken in 2 doses at 12-hour intervals. Naproxen is not recommended for use in any other indication in children under 16 years of age.

Renal/Hepatic Impairment

A lower dose should be considered in patients with renal or hepatic impairment. Naproxen is contraindicated in patients with creatinine clearance less than 30 ml/minute because accumulation of naproxen metabolites has been observed in patients with severe renal failure and in those on dialysis (see section 4.3).

Treatment should be reviewed at regular intervals and discontinued if no benefit is seen or intolerance occurs.

4.3 Contraindications

Naproxen should not be administered to patients with:

•    History of, or active, peptic ulceration

•    Active gastrointestinal bleeding (two or more distinct episodes of proven ulceration or bleeding); history of gastrointestinal bleeding or perforation on a NSAID in the past

•    Hypersensitivity to naproxen, naproxen sodium formulations or any of the excipients. Since the potential exists for cross-sensitivity reactions, Naproxen should not be given to patients in whom aspirin or other non-steroidal anti-inflammatory/analgesic drugs induce the syndrome of asthma, rhinitis, nasal polyps, urticaria or angioedema. These reactions have the potential of being fatal. Severe anaphylactic-like reactions to naproxen have been reported in such patients.

•    Severe renal, hepatic or cardiac failure

Naproxen is contraindicated during the last trimester of pregnancy (see section 4.6). These reactions have the potential of being fatal.

4.4 Special warnings and special precautions for use

Undesirable effects may be minimised by using the lowest effective dose for the shortest duration necessary to control symptoms (see section 4.2 and GI and cardiovascular risks below). Patients treated with NSAIDs long-term should undergo regular medical supervision to monitor for adverse events.

The antipyretic and anti-inflammatory activities of naproxen may reduce fever and inflammation, thereby diminishing their utility as diagnostic signs.

Elevations of one or more liver function tests may occur. Hepatic abnormalities may be the result of hypersensitivity rather than direct toxicity. Severe hepatic reactions, including jaundice and hepatitis (some cases have been fatal) have been reported. Cross reactivity may occur.

Naproxen decreases platelet aggregation and prolongs bleeding time. This effect should be kept in mind when bleeding times are determined.

Although sodium retention has not been reported in metabolic studies, it is possible that patients with compromised cardiac function may be at greater risk when taking naproxen.

Elderly

Elderly patients are particularly susceptible to the adverse effects of NSAIDs, especially gastrointestinal bleeding and perforation, which may be fatal.

Use the lowest possible dose for the shortest amount of time. Monitor very carefully for adverse effects, particularly in the elderly, in whom prolonged therapy is not recommended.

Respiratory disorders

Bronchospasm may be precipitated in patients suffering from, or with a history of, bronchial asthma or allergic disease.

Gastrointestinal bleeding, ulceration and perforation

GI bleeding, ulceration or perforation, which can be fatal, has been reported with all NSAIDs at anytime during treatment, with or without warning symptoms or a previous history of serious GI events.

The risk of GI bleeding, ulceration or perforation is higher with increasing NSAID doses, in patients with a history of ulcer, particularly if complicated with haemorrhage or perforation (see section 4.3), and in the elderly. These patients should commence treatment on the lowest dose available. Combination therapy with protective agents (e.g. misoprostol or proton pump inhibitors) should be considered for these patients, and also for patients requiring concomitant low dose aspirin, or other drugs likely to increase gastrointestinal risk (see section 4.5).

Patients with a history of GI toxicity, particularly when elderly, should report any unusual abdominal symptoms (especially GI bleeding) particularly in the initial stages of treatment.

Caution should be advised in patients receiving concomitant medications which could increase the risk of ulceration or bleeding, such as oral corticosteroid, anticoagulants such as warfarin, selective serotonin-reuptake inhibitors or anti-platelet agents such as aspirin (see Section 4.5).

When GI bleeding or ulceration occurs in patients receiving naproxen, the treatment should be withdrawn.

NSAIDs should be given with care to patients with a history of gastrointestinal disease (ulcerative colitis, Crohn's disease) as these conditions may be exacerbated (see Section 4.8).

Renal Effects

There have been reports of impaired renal function, renal failure, acute interstitial nephritis, haematuria, proteinuria, renal papillary necrosis and occasionally nephrotic syndrome associated with naproxen.

Renal failure linked to reduced prostaglandin production

The administration of an NSAID may cause a dose dependent reduction in prostaglandin formation and precipitate renal failure. Patients at greatest risk of this reaction are those with impaired renal function, cardiac impairment, liver dysfunction, those taking diuretics and the elderly. Renal function should be monitored in these patients (see also Section 4.3).

Use in patients with impaired renal function

As naproxen is eliminated to a large extent (95%) by urinary excretion via glomerular filtration, it should be used with great caution in patients with impaired renal function and the monitoring of serum creatinine and/or creatinine clearance is advised in these patients. Naproxen is contraindicated in patients having a baseline creatinine clearance of less than 30ml/minute.

Haemodialysis does not decrease the plasma concentration of naproxen because of the high degree of protein binding.

Certain patients, specifically those whose renal blood flow is compromised, such as in extracellular volume depletion, cirrhosis of the liver, sodium restriction, congestive heart failure, and pre-existing renal disease, should have renal function assessed before and during Naproxen therapy. Some elderly patients, in whom impaired renal function may be expected, as well as patients using diuretics, may also fall within this category. A reduction in daily dosage should be considered to avoid the possibility of excessive accumulation of naproxen metabolites in these patients.

Use in patients with impaired liver function

Chronic alcoholic liver disease and probably also other forms of cirrhosis reduce the total plasma concentration of naproxen, but the plasma concentration of unbound naproxen is increased. The implication of this finding for naproxen dosing is unknown but it is prudent to use the lowest effective dose.

Haematological

Patients who have coagulation disorders or are receiving drug therapy that interferes with haemostasis should be carefully observed if naproxen-containing products are administered.

Patients at high risk of bleeding or those on full anti-coagulation therapy (e.g. dicoumarol derivatives) may be at increased risk of bleeding if given naproxen-containing products concurrently.

Anaphylactic (anaphylactoid) reactions

Hypersensitivity reactions may occur in susceptible individuals. Anaphylactic (anaphylactoid) reactions may occur both in patients with and without a history of hypersensitivity or exposure to aspirin, other non-steroidal anti-inflammatory drugs or naproxen-containing products. They may also occur in individuals with a history of angioedema, bronchospastic reactivity (e.g. asthma), rhinitis and nasal polyps.

Anaphylactoid reactions, like anaphylaxis, may have a fatal outcome.

Steroids

If steroid dosage is reduced or eliminated during therapy, the steroid dosage should be reduced slowly and the patients must be observed closely for any evidence of adverse effects, including adrenal insufficiency and exacerbation of symptoms of arthritis.

Ocular effects

Studies have not shown changes in the eye attributable to naproxen administration. In rare cases, adverse ocular disorders including papillitis, retrobulbar optic neuritis and papilloedema, have been reported in users of NSAIDs including naproxen, although a cause-and-effect relationship cannot be established; accordingly, patients who develop visual disturbances during treatment with naproxen-containing products should have an ophthalmological examination.

Cardiovascular and cerebrovascular effects

Appropriate monitoring and advice are required for patients with a history of hypertension and/or mild to moderate congestive heart failure as fluid retention and oedema have been reported in association with NSAID therapy.

Clinical trial and epidemiological data suggest that use of coxibs and some NSAIDs (particularly at high doses and in long term treatment) may be associated with a small increased risk of arterial thrombotic events (for example myocardial infarction or stroke). Although data suggest that the use of naproxen (1000mg daily) may be associated with a lower risk, some risk cannot be excluded.

Patients with uncontrolled hypertension, congestive heart failure, established ischaemic heart disease, peripheral arterial disease, and/or cerebrovascular disease should only be treated with naproxen after careful consideration. Similar consideration should be made before initiating longer-term treatment of patients with risk factors for cardiovascular events (e.g. hypertension, hyperlipidaemia, diabetes mellitus, smoking).

SLE and mixed connective tissue disease

In patients with systemic lupus erythematosus (SLE) and mixed connective tissue disorders there may be an increased risk of aseptic meningitis (see Section 4.8).

Dermatological

Serious skin reactions, some of them fatal, including exfoliative dermatitis, Stevens-Johnson syndrome, and toxic epidermal necrolysis, have been reported very rarely in association with the use of NSAIDs (see 4.8). Patients appear to be at highest risk for these reactions early in the course of therapy: the onset of the reactions occurring in the majority of cases within the first month of treatment. Naproxen should be discontinued at the first appearance of skin rash, mucosal lesions, or any other sign of hypersensitivity.

Precautions related to fertility

The use of naproxen, as with any drug known to inhibit cyclooxygenase/prostaglandin synthesis, may impair fertility and is not recommended in women attempting to conceive. In women who have difficulty conceiving or are undergoing investigation of infertility, withdrawal of naproxen should be considered.

Combination with other NSAIDs

The combination of naproxen-containing products and other NSAIDs, including cyclooxygenase-2 selective inhibitors, is not recommended, because of the cumulative risks of inducing serious NSAID-related adverse events.

Excipients associated with intolerance

This medicine contains the excipient lactose monohydrate. Patients with rare hereditary problems of fructose intolerance, glucose-galactose malabsorption or sucrase-isomaltase insufficiency should not take this medicine.

4.5 Interactions with other medicinal products and other forms of interaction

Concomitant administration of antacids or cholestyramine can delay absorption of naproxen, but does not affect its extent. Similarly, administration with food delays rate of absorption of naproxen, but does not affect its extent.

It is considered unsafe to take NSAIDs in combination with anticoagulants such as warfarin or heparin, as NSAIDs can enhance the effects of anticoagulants (see section 4.4).

Other analgesics including cyclooxygenase-2 selective inhibitors: Avoid concomitant use of two or more NSAIDs (including aspirin) as this may increase adverse effects (see section 4.4).

Due to the high plasma protein binding of naproxen, patients simultaneously receiving hydantoins, anticoagulants, other NSAIDs, aspirin or a highly protein-bound sulphonamide should be observed for signs of overdosage of these drugs. Adjustment of dose of the hydantoin, anticoagulant or sulphonamide may be required.

The natriuretic effect of frusemide has been reported to be inhibited by some drugs of this class. Caution is advised as this may lead to a decreased diuretic effect. Diuretics may increase the risk of NSAID nephrotoxicity.

Inhibition of renal lithium clearance leading to increase in plasma lithium concentrations has also been reported.

Naproxen and other NSAIDs can reduce the anti-hypertensive effect of antihypertensives and may increase the risk of renal impairment associated with use of ACE inhibitors.

Probenecid given concurrently increases naproxen plasma levels and extends its plasma half-life considerably.

Caution is advised where methotrexate is administered concurrently because of possible enhancement of its toxicity, since naproxen among other NSAIDs has been reported to reduce the tubular secretion of methotrexate in an animal model.

Cardiac glycosides: Naproxen may exacerbate cardiac failure, reduce GFR and increase plasma glycoside levels.

As with all NSAIDs caution is advised when ciclosporin is co-administered because of the increased risk of nephrotoxicity.

Naproxen should not be used for 8-12 days after mifepristone administration as Naproxen can reduce the effects of mifepristone.

Corticosteroids: Increased risk of gastrointestinal ulceration or GI bleeding (see section 4.4).

Quinolone antibiotics: Animal data indicate that NSAIDs can increase the risk of convulsions associated with quinolone antibiotics. Patients taking NSAIDs and quinolones may have an increased risk of developing convulsions.

There is an increased risk of gastrointestinal bleeding (see section 4.4) when antiplatelet agents and selective serotonin reuptake inhibitors (SSRIs) are combined with NSAIDs.

There is a possible risk of nephrotoxicity when NSAIDs are given with tacrolimus.

There is an increased risk of haematological toxicity when NSAIDs are given with zidovudine. There is evidence of an increased risk of haemarthroses and haematoma in HIV(+) haemophiliacs receiving concurrent treatment with zidovudine and ibuprofen.

It is suggested that Naproxen therapy be temporarily discontinued 48 hours before adrenal function tests are performed because naproxen may artifactually interfere with some tests for 17-ketogenic steroids. Similarly, naproxen may interfere with some assays of urinary 5-hydroxyindoleacetic acid.

Phenytoin:    Naproxen may enhance the effects of phenytoin

Penicillamine:    Increased risk of nephrotoxicity

Sulphonylureas:    Naproxen may enhance effects of the sulphonylureas

Potassium sparing diuretics and drosperinone: Increased risk of hyperkalaemia Baclofen:    Naproxen possibly reduces excretion of baclofen

Erlotinib:    Increased risk of bleeding

Pentoxifylline:    Increased risk of bleeding

Other analgesics:    Avoid concomitant use of two or more NSAIDs.

4.6 Pregnancy and lactation

Pregnancy

Inhibition of prostaglandin synthesis may adversely affect the pregnancy and/or the embryo/foetal development. Data from epidemiological studies suggest an increased risk of miscarriage and of cardiac malformation and gastroschisis after use of a prostaglandin synthesis inhibitor in early pregnancy. The absolute risk for cardiovascular malformation was increased from less than 1%, up to approximately 1.5%. The risk is believed to increase with dose and duration of therapy. In animals, administration of a prostaglandin synthesis inhibitor has been shown to result in increased pre- and post-implantation loss and embryo-foetal lethality. In addition, increased incidences of various malformations, including cardiovascular, have been reported in animals given a prostaglandin synthesis inhibitor during the organogenetic period. During the first and second trimester of pregnancy, naproxen should not be given unless clearly necessary. If naproxen is used by a woman attempting to conceive, or during the first and second trimester of pregnancy, the dose should be kept as low and duration of treatment as short as possible.

During the third trimester of pregnancy, all prostaglandin synthesis inhibitors may expose the foetus to:

o cardiopulmonary toxicity (with premature closure of the ductus arteriosus and pulmonary hypertension)

o renal dysfunction, which may progress to renal failure with oligo-hydroamniosis; the mother and the neonate, at the end of pregnancy, to:

o possible prolongation of bleeding time, an anti-aggregating effect which may occur even at very low doses;

o inhibition of uterine contractions resulting in delayed or prolonged labour.

Consequently, naproxen is contraindicated during the third trimester of pregnancy.

Labour and delivery

Naproxen containing products are not recommended in labour and delivery because, through its prostaglandin synthesis inhibitory effect, naproxen may adversely affect foetal circulation and inhibit contractions, with an increased bleeding tendency in both mother and child.

Nursing mothers

Naproxen has been found in the milk of lactating women. The use of naproxen should be avoided in patients who are breast-feeding.

See section 4.4 regarding female fertility.

4.7 Effects on ability to drive and use machines

Some patients may experience drowsiness, dizziness, vertigo, insomnia, fatigue, visual disturbances or depression with the use of naproxen. If patients experience these or similar undesirable effects, they should not drive or operate machinery.

4.8 Undesirable effects

Gastrointestinal disorders: The most commonly observed adverse events are heartburn, nausea, vomiting, constipation, diarrhoea, flatulence, dyspepsia, abdominal discomfort and epigastric distress.

More serious reactions which may occur are gastrointestinal bleeding, which is sometimes fatal, particularly in the elderly (see section 4.4), peptic ulceration, perforation, non-peptic gastrointestinal ulceration, melaena, haematemesis, stomatitis, ulcerative stomatitis, exacerbation of ulcerative colitis and Crohn's disease (see section 4.4), oesophagitis, gastritis and pancreatitis.

Blood and lymphatic system disorders: Neutropenia, thrombocytopenia, granulocytopenia including agranulocytosis, eosinophilia, leucopenia, aplastic anaemia and haemolytic anaemia.

Immune system disorders: Hypersensitivity reactions have been reported following treatment with NSAIDs in patients with, or without, a history of previous hypersensitivity reactions to NSAIDs. These may consist of (a) non-specific allergic reactions and anaphylaxis (b) respiratory tract reactivity comprising asthma, aggravated asthma, bronchospasm or dyspnoea, or (c) assorted skin disorders, including rashes of various types, pruritus, urticaria, purpura, angio-oedema and more rarely exfoliative and bullous dermatoses (including epidermal necrolysis and erythema multiforme).

Metabolic and nutrition disorders: hyperkalaemia.

Psychiatric disorders: Insomnia, dream abnormalities, depression, confusion and hallucinations.

Nervous system disorders: Convulsions, dizziness, headache, lightheadedness, drowsiness, paraesthesia, retrobulbar optic neuritis, inability to concentrate and cognitive dysfunction have been reported. Aseptic meningitis (especially in patients with existing auto-immune disorders, such as systemic lupus erythematosus, mixed connective tissue disease), with symptoms such as stiff neck, headache, nausea, vomiting, fever or disorientation (see section 4.4).

Eye Disorders: Visual disturbances, corneal opacity, papillitis and papilloedema.

Ear and Labyrinth disorders: Tinnitus, hearing disturbances including impairment and vertigo.

Cardiac disorders: Oedema, palpitations, cardiac failure and congestive heart failure have been reported.

Clinical trial and epidemiological data suggest that use of coxibs and some NSAIDs (particularly at high doses and in long term treatment) may be associated with a small increased risk of arterial thrombotic events (for example myocardial infarction or stroke) (see section 4.4).

Vascular disorders: Hypertension, vasculitis.

Respiratory, thoracic and mediastinal disorders: Dyspnoea, asthma, eosinophilic pneumonitis and pulmonary oedema.

Hepatobiliary disorders: Jaundice, fatal hepatitis and abnormal liver function tests.

Skin and subcutaneous tissue disorders: Skin rashes including fixed drug eruption, itching (pruritus), urticaria, ecchymoses, purpura, sweating. Alopecia, erythema multiforme, Stevens Johnson syndrome, erythema nodosum, lichen planus, pustular reaction, SLE, epidermal necrolysis, very rarely toxic epidermal necrolysis, photosensitivity reactions (including cases in which skin resembles porphyria cutanea tarda “pseudoporphyria”) or epidermolysis bullosa-like reactions which may occur rarely.

If skin fragility, blistering or other symptoms suggestive of pseudoporphyria occur, treatment should be discontinued and the patient monitored.

Musculoskeletal and connective tissue disorders: Myalgia and muscle weakness.

Renal and urinary disorders: Including, but not limited to, glomerular nephritis, interstitial nephritis, nephrotic syndrome, haematuria, raised serum creatinine, renal papillary necrosis and renal failure.

Reproductive system and breast disorders: Female infertility.

General disorders and administration site conditions: Thirst, pyrexia, fatigue and malaise.

4.9 Overdose

a)    Symptoms

Symptoms include headache, heartburn, nausea, vomiting, epigastric pain, gastrointestinal bleeding, rarely diarrhoea, disorientation, excitation, drowsiness, dizziness, tinnitus, fainting, occasionally convulsions. In cases of significant poisoning acute renal failure and liver damage are possible.

Respiratory depression and coma may occur after the ingestion of NSAIDs but are rare.

In one case of naproxen overdose, transient prolongation of the prothrombin time due to hypothrombinaemia may have been due to selective inhibition of the synthesis of vitamin-K dependent clotting factors.

A few patients have experienced seizures, but it is not known whether these were naproxen-related or not. It is not known what dose of the drug would be life-threatening.

b)    Therapeutic measure

Patients should be treated symptomatically as required. Within one hour of ingestion of a potentially toxic amount, activated charcoal should be considered. Alternatively in adults, gastric lavage should be considered within one hour of ingestion of a potentially life-threatening overdose.

Should a patient ingest a large amount of Naproxen accidentally or purposefully, the stomach may be emptied and usual supportive measures employed.

Animal studies indicate that the prompt administration of activated charcoal in adequate amounts would tend to reduce markedly the absorption of the drug.

Alternatively in adults gastric lavage should be considered within one hour of ingestion of a potentially life-threatening overdose.

Good urine output should be maintained.

Renal and liver function should be closely monitored.

Patients should be observed for at least four hours after ingestion of potentially toxic amounts. Frequent or prolonged convulsions should be treated with intravenous diazepam.

Other measures may be indicated by the patient's clinical condition.

Haemodialysis does not decrease the plasma concentration of Naproxen because of the high degree of its protein binding. However, haemodialysis may still be appropriate in a patient with renal failure who has taken Naproxen.

5 PHARMACOLOGICAL PROPERTIES

5.1 Pharmacodynamic properties

Pharmacotherapeutic group: Anti-inflammatory and antirheumatic products ATC code: M01 AE02 03

Naproxen is a non-steroidal anti-inflammatory analgesic compound with antipyretic properties as has been demonstrated in classical animal test systems. Naproxen exhibits its anti-inflammatory effect even in adrenalectomised animals, indicating that its action is not mediated through the pituitary-adrenal axis.

Naproxen inhibits prostaglandin synthetase (as do other NSAIDs). As with other NSAIDs, however, the exact mechanism of its anti-inflammatory action is not known.

5.2 Pharmacokinetic properties

Naproxen is readily absorbed from the gastro-intestinal tract. Peak plasma concentrations are attained 2 to 4 hours after ingestion. At therapeutic concentrations Naproxen is more than 99% bound to plasma proteins. The plasma half life is between 12 and 15 hours, enabling a steady state to be achieved within 3 days of initiation of therapy on a twice daily dose regimen. The degree of absorption is not significantly affected by either foods or most antacids. Approximately 95% of a dose is excreted in urine as Naproxen and 6-0-desmethyl-Naproxen and their conjugates. Less than 3% of a dose has been recovered in the faeces. Naproxen crosses the placenta and is excreted in breast milk.

Metabolism in children is similar to that in adults. Chronic alcoholic liver disease reduces the total plasma concentration of naproxen but the concentration of unbound naproxen increases. In the elderly, the unbound plasma concentration of naproxen is increased although total plasma concentration is unchanged.

5.3 Preclinical safety data

There are no pre-clinical data of relevance to the prescriber which are additional to that already included in other sections of the SmPC.

PHARMACEUTICAL PARTICULARS

6


6.1 List of excipients

Lactose, maize starch, povidone, sodium starch glycollate, magnesium stearate and quinoline yellow (E104).

6.2 Incompatibilities

Not applicable.

6.3 Shelf life

3 years.

6.4 Special precautions for storage

Do not store above 25°C.

Keep the container tightly closed. Store in the original container.

6.5 Nature and contents of container

The product is available in bottle packs of 28, 60, 100 and 250 tablets.

The containers are tamper evident containers which are made up of high density polypropylene body and low density polyethylene cap.

6.6 Special precautions for disposal

None stated

7 MARKETING AUTHORISATION HOLDER

ATHLONE PHARMACEUTICALS LIMITED BALLYMURRAY, ROSCOMMON COUNTY ROSCOMMON IRELAND

8 MARKETING AUTHORISATION NUMBER(S)

Pl 30464/0004

9    DATE OF FIRST AUTHORISATION/RENEWAL OF THE

AUTHORISATION 17/08/2007

10 DATE OF REVISION OF THE TEXT

01/08/2013