Medically reviewed by Militian Inessa Mesropovna, PharmD. Last updated on 2020-04-05
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AZARGA 10 mg/mL + 5 mg/mL eye drops, suspension
One ml of suspension contains 10 mg brinzolamide and 5 mg timolol (as timolol maleate).
Excipient(s) with known effect:
One ml of suspension contains 0.10 mg benzalkonium chloride.
Eye drops, suspension (eye drops)
White to off-white uniform suspension, pH 7.2 (approximately).
Decrease of intraocular pressure (IOP) in adult patients with open-angle glaucoma or ocular hypertension for whom monotherapy provides insufficient IOP reduction.
Use in adults, including the elderly
The dose is one drop of AZARGA in the conjunctival sac of the affected eye(s) twice daily.
When using nasolacrimal occlusion or closing the eyelids, the systemic absorption is reduced. This may result in a decrease in systemic side effects and an increase in local activity.
If a dose is missed, treatment should be continued with the next dose as planned. The dose should not exceed one drop in the affected eye (s) twice daily.
When substituting another ophthalmic antiglaucoma medicinal product with AZARGA, the other medicinal product should be discontinued and AZARGA should be started the following day.
The safety and efficacy of AZARGA in children and adolescents aged 0 to 18 years have not yet been established. No data are available.
Hepatic and renal impairment
No studies have been conducted with AZARGA or with timolol 5 mg/ml eye drops in patients with hepatic or renal impairment. No dosage adjustment is necessary in patients with hepatic impairment or in patients with mild to moderate renal impairment.
AZARGA has not been studied in patients with severe renal impairment (creatinine clearance <30 ml/min) or in patients with hyperchloraemic acidosis. Since brinzolamide and its main metabolite are excreted predominantly by the kidney, AZARGA is therefore contraindicated in patients with severe renal impairment.
AZARGA should be used with caution in patients with severe hepatic impairment.
Method of administration
For ocular use.
Patients should be instructed to shake the bottle well before use. After cap is removed, if tamper evident snap collar is loose, remove before using product.
To prevent contamination of the dropper tip and the suspension, care must be taken not to touch the eyelids, surrounding areas or other surfaces with the dropper tip of the bottle. Instruct patients to keep the bottle tightly closed when not in use.
If more than one topical ophthalmic medicinal product is being used, the medicinal products must be administered at least 5 minutes apart. Eye ointments should be administered last.
- Hypersensitivity to other beta-blockers.
- Hypersensitivity to sulphonamides.
- Reactive airway disease including bronchial asthma or a history of bronchial asthma, or severe chronic obstructive pulmonary disease.
- Sinus bradycardia, sick sinus syndrome, sino-atrial block, second or third degree atrioventricular block not controlled with pace-maker. Overt cardiac failure, cardiogenic shock.
- Severe allergic rhinitis
- Hyperchloraemic acidosis.
- Severe renal impairment.
- Brinzolamide and timolol are absorbed systemically.
- Hypersensitivity reactions common to all sulphonamide derivates can occur in patients receiving AZARGA as it is absorbed systemically.
In patients with cardiovascular diseases (e.g. coronary heart disease, Prinzmetal's angina and cardiac failure) and hypotension, therapy with beta-blockers should be critically assessed and the therapy with other active substances should be considered. Patients with cardiovascular diseases should be watched for signs of deterioration of these diseases and of adverse reactions.
Due to its negative effect on conduction time, beta-blockers should only be given with caution to patients with first degree heart block.
Patients with severe peripheral circulatory disturbance/disorders (i.e. severe forms of Raynaud's disease or Raynaud's syndrome) should be treated with caution.
Beta-blockers may also mask the signs of hyperthyroidism.
Beta-adrenergic blocking medicinal products have been reported to potentiate muscle weakness consistent with certain myasthenic symptoms (e.g. diplopia, ptosis and generalised weakness).
Respiratory reactions, including death due to bronchospasm in patients with asthma have been reported following administration of some ophthalmic beta-blockers. AZARGA should be used with caution, in patients with mild/moderate chronic obstructive pulmonary disease (COPD) and only if the potential benefit outweighs the potential risk.
Beta-blockers should be administered with caution in patients subject to spontaneous hypoglycaemia or to patients with labile diabetes, as beta-blockers may mask the signs and symptoms of acute hypoglycaemia.
AZARGA contains brinzolamide, a sulphonamide. The same types of adverse reactions that are attributable to sulphonamides may occur with topical administration. Acid-base disturbances have been reported with oral carbonic anhydrase inhibitors. This medicinal product should be used with caution in patients with risk of renal impairment because of the possible risk of metabolic acidosis. If signs of serious reactions or hypersensitivity occur, discontinue the use of this medicinal product.
Oral carbonic anhydrase inhibitors may impair the ability to perform tasks requiring mental alertness and/or physical coordination. AZARGA is absorbed systemically and therefore this may occur with topical administration.
While taking beta-blockers, patients with a history of atopy or a history of severe anaphylactic reaction to a variety of allergens may be more reactive to repeated challenge with such allergens and unresponsive to the usual doses of adrenaline used to treat anaphylactic reactions.
Choroidal detachment has been reported with administration of aqueous suppressant therapy (e.g. timolol, acetazolamide) after filtration procedures.
Beta-blocking ophthalmological preparations may block systemic beta-agonist effects e.g. of adrenaline. The anaesthesiologist should be informed when the patient is receiving timolol.
The effect on intra-ocular pressure or the known effects of systemic beta-blockade may be potentiated when timolol is given to the patients already receiving a systemic beta-blocking agent. The response of these patients should be closely observed. The use of two topical beta-adrenergic blocking agents or two local carbonic anhydrase inhibitors is not recommended.
There is potential for an additive effect on the known systemic effects of carbonic anhydrase inhibition in patients receiving an oral carbonic anhydrase inhibitor and AZARGA. The concomitant administration of AZARGA and oral carbonic anhydrase inhibitors has not been studied and is not recommended.
There is limited experience with AZARGA in the treatment of patients with pseudoexfoliative glaucoma or pigmentary glaucoma. Caution should be utilised in treating these patients and close monitoring of IOP is recommended.
AZARGA has not been studied in patients with narrow-angle glaucoma and its use is not recommended in these patients.
Ophthalmic beta-blockers may induce dryness of eyes. Patients with corneal diseases should be treated with caution.
The possible role of brinzolamide on corneal endothelial function has not been investigated in patients with compromised corneas (particularly in patients with low endothelial cell count). Specifically, patients wearing contact lenses have not been studied and careful monitoring of these patients when using brinzolamide is recommended, since carbonic anhydrase inhibitors may affect corneal hydration. This may lead to a corneal decompensation and oedema and wearing contact lenses might increase the risk for the cornea. Careful monitoring of patients with compromised corneas, such as patients with diabetes mellitus or corneal dystrophies, is recommended.
AZARGA may be used while wearing contact lenses with careful monitoring (see below under 'Benzalkonium chloride').
AZARGA contains benzalkonium chloride which may cause eye irritation and is known to discolour soft contact lenses. Contact with soft contact lenses should be avoided. Patients must be instructed to remove contact lenses prior to the application of AZARGA and wait 15 minutes after instillation of the dose before reinsertion.
Benzalkonium chloride has also been reported to cause punctate keratopathy and/or toxic ulcerative keratopathy. Close monitoring is required with frequent or prolonged use.
AZARGA should be used with caution in patients with severe hepatic impairment.
No specific drug interaction studies have been performed with AZARGA.
AZARGA contains brinzolamide, a carbonic anhydrase inhibitor and, although administered topically, is absorbed systemically. Acid-base disturbances have been reported with oral carbonic anhydrase inhibitors. The potential for interactions must be considered in patients receiving AZARGA.
There is a potential for an additive effect on the known systemic effects of carbonic anhydrase inhibition in patients receiving an oral carbonic anhydrase inhibitor and brinzolamide eye drops. The concomitant administration of eye drops containing brinzolamide and oral carbonic anhydrase inhibitors is not recommended.
The cytochrome P-450 isozymes responsible for metabolism of brinzolamide include CYP3A4 (main), CYP2A6, CYP2B6, CYP2C8 and CYP2C9. It is expected that inhibitors of CYP3A4 such as ketoconazole, itraconazole, clotrimazole, ritonavir and troleandomycin will inhibit the metabolism of brinzolamide by CYP3A4. Caution is advised if CYP3A4 inhibitors are given concomitantly. However, accumulation of brinzolamide is unlikely as renal elimination is the major route. Brinzolamide is not an inhibitor of cytochrome P-450 isozymes.
There is a potential for additive effects resulting in hypotension and/or marked bradycardia when an ophthalmic beta-blocker solution is administered concomitantly with oral calcium channel blockers, beta-adrenergic blocking agents, antiarrhythmics (including amiodarone), digitalis glycosides, parasympathomimetics, guanethidine.
Beta blockers can decrease the response to adrenaline used to treat anaphylactic reactions. Special caution should be exercised in patients with a history of atopy or anaphylaxis.
The hypertensive reaction to sudden withdrawal of clonidine can be potentiated when taking beta-blockers. Caution is recommended in the concomitant use of this medicinal product with clonidine.
Potentiated systemic beta-blockade (e.g. decreased heart rate, depression) has been reported during combined treatment with CYP2D6 inhibitors (e.g. quinidine, fluoxetine, paroxetine) and timolol. Caution is recommended.
Beta-blockers may increase the hypoglycaemic effect of antidiabetic agents. Beta-blockers can mask the signs and symptoms of hypoglycaemia.
Mydriasis resulting from concomitant use of ophthalmic beta-blockers and adrenaline (epinephrine) has been reported occasionally.
There are no adequate data regarding the use of ophthalmic brinzolamide and timolol in pregnant women.
Epidemiological studies have not revealed malformative effects but show a risk for intra uterine growth retardation when beta-blockers are administered by the oral route. In addition, signs and symptoms of beta-blockade (e.g. bradycardia, hypotension, respiratory distress and hypoglycaemia) have been observed in the neonate when beta-blockers have been administered until delivery. If AZARGA is administered until delivery, the neonate should be carefully monitored during the first days of life.
It is not known whether ophthalmic brinzolamide is excreted in human breast milk.
Beta-blockers are excreted in breast milk.
However, a risk to the suckling child cannot be excluded. A decision must be made whether to discontinue breast-feeding or to discontinue/abstain from AZARGA therapy taking into account the benefit of breast-feeding for the child and the benefit of therapy for the woman.
Studies have not been performed to evaluate the effect of topical ocular administration of Azarga on human fertility.
Non clinical data do not show any effects of either brinzolamide or timolol on male or female fertility following oral dosing. No effects on male or female fertility are anticipated from the use of AZARGA.
AZARGA has minor influence on the ability to drive and use machines.
Temporary blurred vision or other visual disturbances may affect the ability to drive or use machines. If blurred vision occurs at instillation, the patient must wait until the vision clears before driving or using machines.
Carbonic anhydrase inhibitors may impair the ability to perform tasks requiring mental alertness and/or physical coordination.
Summary of the safety profile
In clinical trials, the most common adverse reactions were blurred vision, eye irritation and eye pain, occurring in approximately 2% to 7% of patients.
Tabulated summary of adverse reactions
The following adverse reactions have been reported during clinical studies and post-marketing surveillance with AZARGA and the individual components brinzolamide and timolol. They are classified according to the following convention: very common (>1/10), common>1/100 to <1/10), uncommon (>1/1,000 to <1/100), rare (>1/10,000 to <1/1000), very rare (<1/10,000), or not known (cannot be estimated from the available data). Within each frequency grouping, adverse reactions are presented in order of decreasing seriousness.
System Organ Classification
MedDRA Preferred Term (v. 18.0)
Infections and infestations
Not known: nasopharyngitis3, pharyngitis3, sinusitis3, rhinitis3
Blood and lymphatic system disorders
Uncommon: white blood cell count decreased1
Not known: decreased red blood cell count3, increased blood chloride3
Immune system disorders
Not known: anaphylaxis2, anaphylactic shock1, systemic allergic reactions including angioedema, 2 localised and generalised rash2, hypersensitivity1, urticaria2, pruritus2
Metabolism and nutrition disorders
Not known: hypoglycaemia2
Not known: depression1, memory loss2, apathy3, depressed mood3, decreased libido3, nightmare2,3, nervousness3
Nervous system disorders
Not known: cerebral ischaemia2, cerebrovascular accident2, syncope2, increases in the signs and symptoms of myasthenia gravis2, somnolence3, motor dysfunction3, amnesia3, memory impairment3, paraesthesia2,3, tremor3, hypoaesthesia3, ageusia3, dizziness1, headache1
Common: punctate keratitis1, blurred vision1, eye pain1, eye irritation1
Uncommon: keratitis1,2,3, dry eye1, vital dye staining cornea present1, eye discharge1, eye pruritus1, foreign body sensation in eyes1, ocular hyperaemia1, conjunctival hyperaemia1
Rare: corneal erosion1, anterior chamber flare1, photophobia1, lacrimation increased1, scleral hyperaemia1, erythema of eyelid1, eyelid margin crusting1
Not known: increased optic nerve cup/disc ratio3, choroidal detachment following filtration surgery2 (see section 4.4 Special warnings and precautions for use), keratopathy3, corneal epithelium defect3, corneal epithelium disorder3, increased intraocular pressure3, eye deposit3, corneal staining3, corneal oedema3, decreased corneal sensitivity2, conjunctivitis3, meibomianitis3, diplopia2, 3, glare3, photopsia3, reduced visual acuity3, visual impairment1, pterygium3, ocular discomfort3, keratoconjunctivitis sicca3, hypoaesthesia of the eye3, scleral pigmentation3, subconjunctival cyst3, visual disturbance3, eye swelling3, eye allergy3, madarosis3, eyelid disorder3, eyelid oedema1, ptosis2
Ear and labyrinth disorders
Not known: vertigo3, tinnitus3
Common: heart rate decreased1
Not known: cardiac arrest2, cardiac failure2, congestive heart failure2, atrioventricular block2, cardio-respiratory distress3, angina pectoris3, bradycardia2,3, irregular heart rate3, arrhythmia2,3, palpitations2,3, tachycardia3, increased heart rate3, chest pain2, oedema2
Uncommon: decreased blood pressure1
Not known: hypotension2, hypertension3, blood pressure increased1, Raynaud's phenomenon2, cold hands and feet2
Respiratory, thoracic and mediastinal disorders
Rare: oropharyngeal pain1, rhinorrhoea1
Not known: bronchospasm2 (predominantly in patients with pre-existing bronchospastic disease), dyspnoea1, asthma3, epistaxis1, bronchial hyperactivity3, throat irritation3, nasal congestion3, upper respiratory tract congestion3, postnasal drip3, sneezing3, nasal dryness3
Not known: vomiting2,3, abdominal pain upper1, abdominal pain2, diarrhoea1, dry mouth1, nausea1, oesophagitis3, dyspepsia2,3, abdominal discomfort3, stomach discomfort3, frequent bowel movements3, gastrointestinal disorder3, oral hypoaesthesia3, oral paraesthesia3, flatulence3
Not known: abnormal liver function test3
Skin and subcutaneous tissue disorders
Not known: urticaria3, maculo-papular rash3, generalised pruritus3, skin tightness3, dermatitis3, alopecia1, psoriasiform rash or exacerbation of psoriasis2, rash1, erythema1
Musculoskeletal and connective tissue disorders
Not known: myalgia1, muscle spasms3, arthralgia3, back pain3, pain in extremity3
Renal and urinary disorders
Uncommon: blood urine present1
Not known: renal pain3, pollakiuria3
Reproductive system and breast disorders
Not known: erectile dysfunction3, sexual dysfunction2, decreased libido2
General disorders and administration site conditions
Not known: chest pain1, pain3, fatigue1, asthenia2,3, chest discomfort3, feeling jittery3, irritability3, peripheral oedema3, medication residue3
Uncommon: blood potassium increase1, blood lactate dehydrogenase increased1
1 adverse reactions observed for Azarga
2 additional adverse reactions observed with timolol monotherapy
3 additional adverse reactions observed with brinzolamide monotherapy
Description of selected adverse reactions
Dysgeusia (bitter or unusual taste in the mouth following instillation) was a frequently reported systemic adverse reaction associated with the use of AZARGA during clinical trials. It is likely to be caused by passage of the eye drops in the nasopharynx via the nasolacrimal canal and is attributable to brinzolamide. Nasolacrimal occlusion or gently closing the eyelid after instillation may help reduce the occurrence of this effect.
AZARGA contains brinzolamide which is a sulphonamide inhibitor of carbonic anhydrase with systemic absorption. Gastrointestinal, nervous system, haematological, renal and metabolic effects are generally associated with systemic carbonic anhydrase inhibitors. The same type of adverse reactions attributable to oral carbonic anhydrase inhibitors may occur with topical administration.
Timolol is absorbed into the systemic circulation.
AZARGA is not recommended for use in children and adolescents below 18 years due to a lack of data on safety and efficacy.
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 national reporting system:
Yellow Card Scheme
Website: www.mhra.gov.uk/yellowcard or search for MHRA Yellow Card in the Google Play or Apple App Store
IRL - Dublin 2;
Tel: +353 1 6764971
Fax: +353 1 6762517.
e-mail: [email protected]
In case of accidental ingestion, symptoms of overdose from beta blockade may include bradycardia, hypotension, cardiac failure and bronchospasm.
If overdose with AZARGA eye drops occurs, treatment should be symptomatic and supportive. Due to brinzolamide, electrolyte imbalance, development of an acidotic state, and possibly central nervous system effects may occur. Serum electrolyte levels (particularly potassium) and blood pH levels should be monitored. Studies have shown that timolol does not dialyse readily.
Pharmacotherapeutic group: Ophthalmologicals, Antiglaucoma preparation and miotics
ATC code: S01ED51
Mechanism of action
AZARGA contains two active substances: brinzolamide and timolol maleate. These two components decrease elevated IOP primarily by reducing aqueous humour secretion, but do so by different mechanisms of action. The combined effect of these two active substances results in additional IOP reduction compared to either compound alone.
Brinzolamide is a potent inhibitor of human carbonic anhydrase II (CA-II), the predominant iso-enzyme in the eye. Inhibition of carbonic anhydrase in the ciliary processes of the eye decreases aqueous humour secretion, presumably by slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport.
Timolol is a non-selective adrenergic-blocking agent that has no intrinsic sympathomimetic, direct myocardial depressant or membrane-stabilising activity. Tonography and fluorophotometry studies in man suggest that its predominant action is related to reduced aqueous humour formation and a slight increase in outflow facility.
In a twelve-month, controlled clinical trial in patients with open-angle glaucoma or ocular hypertension who, in the investigator's opinion could benefit from a combination therapy, and who had baseline mean IOP of 25 to 27 mmHg, the mean IOP-lowering effect of AZARGA dosed twice daily was 7 to 9 mmHg. The non-inferiority of AZARGA as compared to dorzolamide 20 mg/ml + timolol 5 mg/ml in the mean IOP reduction was demonstrated across all time-points at all visits.
In a six-month, controlled clinical study in patients with open-angle glaucoma or ocular hypertension and baseline mean IOP of 25 to 27 mmHg, the mean IOP-lowering effect of AZARGA dosed twice daily was 7 to 9 mmHg, and was up to 3 mmHg greater than that of brinzolamide 10 mg/ml dosed twice daily and up to 2 mmHg greater than that of timolol 5 mg/ml dosed twice daily. A statistically superior reduction in mean IOP was observed compared to both brinzolamide and timolol at all time-points and visits throughout the study.
In three controlled clinical trials, the ocular discomfort upon instillation of AZARGA was significantly lower than that of dorzolamide 20 mg/ml + timolol 5 mg/ml.
Following topical ocular administration, brinzolamide and timolol are absorbed through the cornea and into the systemic circulation. In a pharmacokinetic study, healthy subjects received oral brinzolamide (1 mg) twice daily for 2 weeks to shorten the time to reach steady-state prior to starting AZARGA administration. Following twice daily dosing of AZARGA for 13 weeks, red blood cell (RBC) concentrations of brinzolamide averaged 18.8 Â± 3.29 ÂµM, 18.1 Â± 2.68 ÂµM and 18.4 Â± 3.01 ÂµM at weeks 4, 10 and 15, respectively, indicating that steady-state RBC concentrations of brinzolamide were maintained
At steady state, following administration of AZARGA, the mean plasma Cmax and AUC0-12h of timolol were 27% and 28% lower (Cmax: 0.824 Â± 0.453 ng/ml; AUC0-12h: 4.71 Â± 4.29 ngÂ·h/ml), respectively, in comparison to the administration of timolol 5 mg/ml (Cmax: 1.13 Â± 0.494 ng/ml; AUC0-12h: 6.58 Â± 3.18 ngÂ·h/ml). The lower systemic exposure to timolol following AZARGA administration is not clinically relevant. Following administration of AZARGA, mean Cmax of timolol was reached at 0.79 Â± 0.45 hours.
Plasma protein binding of brinzolamide is moderate (about 60%). Brinzolamide is sequestered in RBCs due to its high affinity binding to CA-II and to a lesser extent to CA-I. Its active N-desethyl metabolite also accumulates in RBCs where it binds primarily to CA-I. The affinity of brinzolamide and metabolite to RBC and tissue CA results in low plasma concentrations.
Ocular tissue distribution data in rabbits showed that timolol can be measured in aqueous humour up to 48 hours after administration of AZARGA. At steady-state, timolol is detected in human plasma for up to 12 hours after administration of AZARGA.
The metabolic pathways for the metabolism of brinzolamide involve N-dealkylation, O-dealkylation and oxidation of its N-propyl side chain. N-desethyl brinzolamide is a major metabolite of brinzolamide formed in humans, which also binds to CA-I in the presence of brinzolamide and accumulates in RBCs. In vitro studies show that the metabolism of brinzolamide mainly involves CYP3A4 as well as at least four other isozymes (CYP2A6, CYP2B6, CYP2C8 and CYP2C9).
Timolol is metabolised by two pathways. One route yields an ethanolamine side chain on the thiadiazole ring and the other giving an ethanolic side chain on the morpholine nitrogen and a second similar side chain with a carbonyl group adjacent to the nitrogen. Timolol metabolism is mediated primarily by CYP2D6.
Brinzolamide is eliminated primarily by renal excretion (approximately 60%). About 20% of the dose has been accounted for in urine as metabolite. Brinzolamide and N-desethyl-brinzolamide are the predominant components found in the urine along with trace levels (<1%) of the N-desmethoxypropyl and O-desmethyl metabolites.
Timolol and its metabolites are primarily excreted by the kidneys. Approximately 20% of a timolol dose is excreted in the urine unchanged and the remainder excreted in urine as metabolites. The plasma t1/2 of timolol is 4.8 hours after administration of AZARGA.
Non-clinical data reveal no special hazard for humans with brinzolamide based on conventional studies of safety pharmacology, repeated dose toxicity, genotoxicity, and carcinogenic potential.
Developmental toxicity studies in rabbits with oral doses of brinzolamide of up to 6 mg/kg/day (214 times the recommended daily clinical dose of 28 Âµg/kg/day) revealed no effect on foetal development despite significant maternal toxicity. Similar studies in rats resulted in slightly reduced ossification of skull and sternebrae of foetuses of dams receiving brinzolamide at doses of 18 mg/kg/day (642 times the recommended daily clinical dose), but not 6 mg/kg/day. These findings occurred at doses that caused metabolic acidosis with decreased body weight gain in dams and decreased foetal weights. Dose-related decreases in foetal weights were observed in pups of dams receiving brinzolamide orally ranging from a slight decrease (about 5-6%) at 2 mg/kg/day to nearly 14% at 18 mg/kg/day. During lactation, the no adverse effect level in the offspring was 5 mg/kg/day.
Non-clinical data reveal no special hazard for humans with timolol based on conventional studies of safety pharmacology, repeated dose toxicity, genotoxicity, and carcinogenic potential. Reproduction toxicity studies with timolol showed delayed foetal ossification in rats with no adverse effects on postnatal development (at 50 mg/kg/day or 3500 times the daily clinical dose of 14 Î¼g/kg/day) and increased foetal resorptions in rabbits (at 90 mg/kg/day or 6400 times the daily clinical dose).
Hydrochloric acid and/or sodium hydroxide (for pH adjustment)
4 weeks after first opening
This medicinal product does not require any special storage conditions.
5 ml round opaque low density polyethylene bottles with a dispensing plug and white polypropylene screw cap (DROP-TAINER) containing 5 ml suspension.
Cartons containing 1 or 3 bottles. Not all pack sizes may be marketed.
No special requirements.
Novartis Europharm Limited
Elm Park, Merrion Road
Date of first Authorisation: 25th November 2008
Date of latest renewal: 26th August 2013
19 April 2018