Leaflet ZAVESCA 100mg capsules
- Product code:
- W72068001
- Quantity:
- 84
- Indicated for:
- Gaucher disease; Niemann-Pick type C disease
- Route of administration:
- oral
- Substance:
- miglustat (enzyme inhibitor)
- ATC
- A16AX06 — Alimentary tract and metabolism | Other alimentary tract and metabolism products | Other alimentary tract and metabolism products | Various alimentary tract and metabolism products
The medication is taken orally, usually three times daily, with the dose adjusted based on the patient's weight and response to treatment. Common side effects include diarrhea, flatulence, abdominal pain, and weight loss.
Miglustat is contraindicated in patients with severe renal impairment or hypersensitivity to the active substance. Its use also requires careful monitoring of gastrointestinal function and body weight.
This medication is an important option for managing lysosomal storage disorders, helping to alleviate symptoms and slow disease progression.
General data about ZAVESCA 100mg
- Substance:
- miglustat
- Date of latest medicines list:
- 01-08-2026
- Product code:
- W72068001
- Concentration:
- 100mg
- Pharmaceutical form:
- capsules
- Quantity:
- 84
- Product type:
- Original
- Prescription status:
- P-RF — Medicines dispensed with a medical prescription that is retained by the pharmacy and cannot be renewed.
Official documents
- Added to database:
- 16/06/2009
- Source record updated:
- 09/07/2026
Contents of the package leaflet for the medicine ZAVESCA 100mg capsules
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Leaflet ZAVESCA 100mg
1. NAME OF THE MEDICINAL PRODUCT
Zavesca 100 mg capsules
2. QUALITATIVE AND QUANTITATIVE COMPOSITION
Each capsule contains 100 mg miglustat.
For the full list of excipients, see section 6.1.
3. PHARMACEUTICAL FORM
Capsule, hard
White capsules with “OGT 918” printed in black on the cap and “100” printed in black on the body.
4. CLINICAL PARTICULARS
4.1 Therapeutic indications
Zavesca is indicated for the oral treatment of adult patients with mild to moderate type 1 Gaucherdisease. Zavesca may be used only in the treatment of patients for whom enzyme replacement therapyis unsuitable (see sections 4.4 and 5.1).
Zavesca is indicated for the treatment of progressive neurological manifestations in adult patients andpaediatric patients with Niemann-Pick type C disease (see sections 4.4, and 5.1).
4.2 Posology and method of administration
Therapy should be directed by physicians who are knowledgeable in the management of Gaucherdisease or Niemann-Pick type C disease, as appropriate.
PosologyDosage in type 1 Gaucher disease
Adult
The recommended starting dose for the treatment of adult patients with type 1 Gaucher disease is100 mg three times a day.
Temporary dose reduction to 100 mg once or twice a day may be necessary in some patients becauseof diarrhoea.
Paediatric populationThe efficacy of Zavesca in children and adolescents aged 0-17 years with type 1 Gaucher disease hasnot been established. No data are available.
Dosage in Niemann-Pick type C disease
Adult
The recommended dose for the treatment of adult patients with Niemann-Pick type C disease is200 mg three times a day.
Paediatric populationThe recommended dose for the treatment of adolescent patients (12 years of age and above) with
Niemann-Pick type C disease is 200 mg three times a day.
Dosing in patients under the age of 12 years should be adjusted on the basis of body surface area asillustrated below:
Body surface area (m2) Recommended dose 1.25 200 mg three times a day 0.88 - 1.25 200 mg twice a day 0.73 - 0.88 100 mg three times a day 0.47 - 0.73 100 mg twice a day 0.47 100 mg once a day
Temporary dose reduction may be necessary in some patients because of diarrhoea.
The benefit to the patient of treatment with Zavesca should be evaluated on a regular basis (see section4.4).
There is limited experience with the use of Zavesca in Niemann-Pick type C disease patients under theage of 4 years.
Special populationsElderly
There is no experience with the use of Zavesca in patients over the age of 70.
Renal impairmentPharmacokinetic data indicate increased systemic exposure to miglustat in patients with renalimpairment. In patients with an adjusted creatinine clearance of 50-70 mL/min/1.73 m2,administration should commence at a dose of 100 mg twice daily in patients with type 1 Gaucherdisease and at a dose of 200 mg twice daily (adjusted for body surface area in patients below the ageof 12) in patients with Niemann-Pick type C disease.
In patients with an adjusted creatinine clearance of 30-50 mL/min/1.73 m2, administration shouldcommence at a dose of 100 mg once daily in patients with type 1 Gaucher disease and at a dose of100 mg twice daily (adjusted for body surface area in patients below the age of 12) in patients with
Niemann-Pick type C disease. Use in patients with severe renal impairment (creatinine clearance< 30 mL/min/1.73 m2) is not recommended (see sections 4.4 and 5.2).
Hepatic impairmentZavesca has not been evaluated in patients with hepatic impairment.
Method of administrationZavesca can be taken with or without food.
4.3 Contraindications
Hypersensitivity to the active substance or to any of the excipients listed in section 6.1.
4.4 Special warnings and precautions for use
Tremor
Approximately 37% of patients in clinical trials in type 1 Gaucher disease, and 58% of patients in aclinical trial in Niemann-Pick type C disease reported tremor on treatment. In type 1 Gaucher disease,these tremors were described as an exaggerated physiological tremor of the hands. Tremor usuallybegan within the first month of treatment, and in many cases resolved after 1 to 3 months of continuedtreatment. Dose reduction may ameliorate the tremor, usually within days, but discontinuation oftreatment may sometimes be required.
Gastrointestinal disturbances
Gastrointestinal events, mainly diarrhoea, have been observed in more than 80% of patients, either atthe outset of treatment or intermittently during treatment (see section 4.8). The mechanism is mostlikely inhibition of intestinal disaccharidases such as sucrase-isomaltase in the gastrointestinal tractleading to reduced absorption of dietary disaccharides. In clinical practice, miglustat-inducedgastrointestinal events have been observed to respond to individualised diet modification (for examplereduction of sucrose, lactose and other carbohydrate intake), to taking Zavesca between meals, and/orto anti-diarrhoeal medicinal products such as loperamide. In some patients, temporary dose reductionmay be necessary. Patients with chronic diarrhoea or other persistent gastrointestinal events that do notrespond to these interventions should be investigated according to clinical practice. Zavesca has notbeen evaluated in patients with a history of significant gastrointestinal disease, including inflammatorybowel disease.
Cases of Crohn’s disease have been reported post-marketing in Niemann-Pick type C disease patientstreated with Zavesca. Gastrointestinal disturbances are common adverse events of Zavesca. Therefore,in patients with chronic diarrhoea and/or abdominal pain that do not respond to interventions or in theevent of clinical worsening, the possibility of Crohn’s disease should be considered.
Effects on spermatogenesis
Reliable contraceptive methods should be maintained while male patients are taking Zavesca and for3 months following discontinuation. Zavesca should be discontinued and reliable contraception beused for the next 3 months before attempting to conceive (see sections 4.6 and 5.3). Studies in the rathave shown that miglustat adversely affects spermatogenesis and sperm parameters, and reducesfertility (see sections 4.6 and 5.3).
Special populationsDue to limited experience, Zavesca should be used with caution in patients with renal or hepaticimpairment. There is a close relationship between renal function and clearance of miglustat, andexposure to miglustat is markedly increased in patients with severe renal impairment (see section 5.2).
At present, there is insufficient clinical experience in these patients to provide dosingrecommendations. Use of Zavesca in patients with severe renal impairment (creatinine clearance< 30 mL/min/1.73 m2) is not recommended.
Type 1 Gaucher disease
Although no direct comparisons with Enzyme Replacement Therapy (ERT) have been performed intreatment-naive patients with type 1 Gaucher disease, there is no evidence of Zavesca having anefficacy or safety advantage over ERT. ERT is the standard of care for patients who require treatmentfor type 1 Gaucher disease (see section 5.1). The efficacy and safety of Zavesca has not beenspecifically evaluated in patients with severe Gaucher disease.
Regular monitoring of vitamin B12 level is recommended because of the high prevalence ofvitamin B12 deficiency in patients with type 1 Gaucher disease.
Cases of peripheral neuropathy have been reported in patients treated with Zavesca with or withoutconcurrent conditions such as vitamin B12 deficiency and monoclonal gammopathy. Peripheralneuropathy seems to be more common in patients with type 1 Gaucher disease compared to thegeneral population. All patients should undergo baseline and repeat neurological evaluation.
In patients with type 1 Gaucher disease, monitoring of platelet counts is recommended. Mildreductions in platelet counts without association with bleeding were observed in patients with type 1
Gaucher disease who were switched from ERT to Zavesca.
Niemann-Pick type C disease
The benefit of treatment with Zavesca for neurological manifestations in patients with Niemann-Picktype C disease should be evaluated on a regular basis, e.g. every 6 months; continuation of therapyshould be re-appraised after at least 1 year of treatment with Zavesca.
Mild reductions in platelet counts without association to bleeding were observed in some patients with
Niemann-Pick type C disease treated with Zavesca. In patients included in the clinical trial, 40%-50%had platelet counts below the lower limit of normal at baseline. Monitoring of platelet counts isrecommended in these patients.
Reduced growth in the paediatric population
Reduced growth has been reported in some paediatric patients with Niemann-Pick type C disease inthe early phase of treatment with miglustat where the initial reduced weight gain may be accompaniedor followed by reduced height gain. Growth should be monitored in paediatric and adolescent patientsduring treatment with Zavesca; the benefit/risk balance should be re-assessed on an individual basisfor continuation of therapy.
SodiumThis medicinal product contains less than 1 mmol sodium (23 mg) per capsule, that is to sayessentially 'sodium-free'.
4.5 Interaction with other medicinal products and other forms of interaction
Limited data suggest that co-administration of Zavesca and enzyme replacement with imiglucerase inpatients with type 1 Gaucher disease may result in decreased exposure to miglustat (approximatereductions of 22% in Cmax and 14% in AUC were observed in a small parallel-group study). This studyalso indicated that Zavesca has no or limited effect on the pharmacokinetics of imiglucerase.
4.6 Fertility, pregnancy and lactation
There are no adequate data from the use of miglustat in pregnant women. Studies in animals haveshown maternal and embryo-foetal toxicity, including decreased embryo-foetal survival (seesection 5.3). The potential risk for humans is unknown. Miglustat crosses the placenta and should notbe used during pregnancy.
Breast-feedingIt is not known if miglustat is secreted in breast milk. Zavesca should not be taken duringbreast-feeding.
FertilityStudies in the rat have shown that miglustat adversely affects sperm parameters (motility andmorphology) thereby reducing fertility (see sections 4.4 and 5.3).
Contraception in males and femalesContraceptive measures should be used by women of child-bearing potential. Reliable contraceptivemethods should be maintained while male patients are taking Zavesca and for 3 months followingdiscontinuation (see sections 4.4 and 5.3).
4.7 Effects on ability to drive and use machines
Zavesca has negligible influence on the ability to drive and use machines. Dizziness has been reportedas a common adverse reaction, and patients suffering from dizziness should not drive or use machines.
4.8 Undesirable effects
The most common adverse reactions reported in clinical studies with Zavesca were diarrhoea,flatulence, abdominal pain, weight loss and tremor (see section 4.4). The most common seriousadverse reaction reported with Zavesca treatment in clinical studies was peripheral neuropathy (seesection 4.4).
In 11 clinical trials in different indications 247 patients were treated with Zavesca at dosages of50-200 mg t.i.d. for an average duration of 2.1 years. Of these patients, 132 had type 1 Gaucherdisease, and 40 had Niemann-Pick type C disease. Adverse reactions were generally of mild tomoderate severity and occurred with similar frequency across indications and dosages tested.
Tabulated list of adverse reactionsAdverse reactions from clinical trials and spontaneous reporting, occurring in >1% of patients, arelisted in the table below by system organ class and 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). Within each frequency grouping, adverse reactions are presented in order of decreasingseriousness.
Blood and lymphatic system disordersCommon Thrombocytopenia
Metabolism and nutrition disordersVery common Weight loss, decreased appetite
Psychiatric disordersCommon Depression, insomnia, libido decreased
Nervous system disordersVery common Tremor
Common Peripheral neuropathy, ataxia, amnesia, paraesthesia,hypoaesthesia, headache, dizziness
Gastrointestinal disordersVery common Diarrhoea, flatulence, abdominal pain
Common Nausea, vomiting, abdominal distension/discomfort, constipation,dyspepsia
Musculoskeletal and connective tissue disordersCommon Muscle spasms, muscle weakness
General disorders and administration site reactions
Common Fatigue, asthenia, chills and malaise
InvestigationsCommon Nerve conduction studies abnormal
Description of selected adverse reactionsWeight loss has been reported in 55% of patients. The greatest prevalence was observed between6 and 12 months.
Zavesca has been studied in indications where certain events reported as adverse reactions, such asneurological and neuropsychological symptoms/signs, cognitive dysfunction and thrombocytopeniacould also be due to the underlying conditions.
Reporting of suspected adverse reactionsReporting suspected adverse reactions after authorisation of the medicinal product is important. Itallows continued monitoring of the benefit/risk balance of the medicinal product. Healthcareprofessionals are asked to report any suspected adverse reactions via the national reporting systemlisted in Appendix V.
4.9 Overdose
No acute symptoms of overdose have been identified. Zavesca has been administered at doses of up to3000 mg/day for up to six months in HIV positive patients during clinical trials. Adverse eventsobserved included granulocytopenia, dizziness and paraesthesia. Leukopenia and neutropenia havealso been observed in a similar group of patients receiving 800 mg/day or higher dose.
ManagementIn case of overdose general medical care is recommended.
5. PHARMACOLOGICAL PROPERTIES
5.1 Pharmacodynamic properties
Pharmacotherapeutic group: Other alimentary tract and metabolism products, ATC Code: A16AX06
Type 1 Gaucher disease
Gaucher disease is an inherited metabolic disorder caused by a failure to degrade glucosylceramideresulting in lysosomal storage of this material and widespread pathology. Miglustat is an inhibitor ofglucosylceramide synthase, the enzyme responsible for the first step in the synthesis of mostglycolipids. In vitro, glucosylceramide synthase is inhibited by miglustat with an IC50 of 20-37 µM. Inaddition, inhibitory action on a non-lysosomal glycosylceramidase has been demonstratedexperimentally in vitro. The inhibitory action on glucosylceramide synthase forms the rationale forsubstrate reduction therapy in Gaucher disease.
The pivotal trial of Zavesca was conducted in patients unable or unwilling to receive ERT. Reasonsfor not receiving ERT included the burden of intravenous infusions and difficulties in venous access.
Twenty-eight patients with mild to moderate type 1 Gaucher disease were enrolled in this 12-monthnon-comparative study, and 22 patients completed the study. At 12 months, there was a meanreduction in liver organ volume of 12.1% and a mean reduction in spleen volume of 19.0%. A meanincrease in haemoglobin concentration of 0.26 g/dL and a mean platelet count increase of 8.29 109/Lwere observed. Eighteen patients then continued to receive Zavesca under an optional extendedtreatment protocol. Clinical benefit has been assessed at 24 and 36 months in 13 patients. After 3 yearsof continuous Zavesca treatment, mean reductions in liver and spleen organ volume were 17.5% and29.6%, respectively. There was a mean increase of 22.2 109/L in platelet count, and a mean increaseof 0.95 g/dL in haemoglobin concentration.
A second open, controlled study randomised 36 patients who had received a minimum of 2 years oftreatment with ERT, into three treatment groups: continuation with imiglucerase, imiglucerase incombination with Zavesca, or switch to Zavesca. This study was conducted over a 6-monthrandomised comparison period followed by 18 months extension where all patients received Zavescamonotherapy. In the first 6 months in patients who were switched to Zavesca, liver and spleen organvolumes and haemoglobin levels were unchanged. In some patients there were reductions in plateletcount and increases in chitotriosidase activity indicating that Zavesca monotherapy may not maintainthe same control of disease activity in all patients. 29 patients continued in the extension period. Whencompared to the measurements at 6 months, disease control was unchanged after 18 and 24 months of
Zavesca monotherapy (20 and 6 patients, respectively). No patient showed rapid deterioration of type1 Gaucher disease following the switch to Zavesca monotherapy.
A total daily dose of 300 mg Zavesca administered in three divided doses was used in the above twostudies. An additional monotherapy study was performed in 18 patients at a total daily dose of 150 mg,and results indicate reduced efficacy compared to a total daily dose of 300 mg.
An open-label, non-comparative, 2-year study enrolled 42 patients with type 1 Gaucher disease, whohad received a minimum of 3 years of ERT and who fulfilled criteria of stable disease for at least 2years. The patients were switched to monotherapy with miglustat 100 mg t.i.d. Liver volume (primaryefficacy variable) was unchanged from baseline to the end of treatment. Six patients had miglustattreatment prematurely discontinued for potential disease worsening, as defined in the study. Thirteenpatients discontinued treatment due to an adverse event. Small mean reductions in haemoglobin [-0.95 g/dL (95% CI: -1.38, -0.53)] and platelet count [-44.1 × 109/L (95% CI: -57.6, -30.7)] wereobserved between baseline and end of study. Twenty-one patients completed 24 months of miglustattreatment. Of these, 18 patients at baseline were within established therapeutic goals for liver andspleen volume, haemoglobin levels, and platelet counts, and 16 patients remained within all thesetherapeutic goals at Month 24.
Bone manifestations of type 1 Gaucher disease were evaluated in 3 open-label clinical studies inpatients treated with miglustat 100 mg t.i.d. for up to 2 years (n = 72). In a pooled analysis ofuncontrolled data, bone mineral density Z-scores at the lumbar spine and femoral neck increased bymore than 0.1 units from baseline in 27 (57%) and 28 (65%) of the patients with longitudinal bonedensity measurements. There were no events of bone crisis, avascular necrosis or fracture during thetreatment period.
Niemann-Pick type C disease
Niemann-Pick type C disease is a very rare, invariably progressive and eventually fatalneurodegenerative disorder characterised by impaired intracellular lipid trafficking. The neurologicalmanifestations are considered secondary to the abnormal accumulation of glycosphingolipids inneuronal and glial cells.
Data to support safety and efficacy of Zavesca in Niemann-Pick type C disease come from aprospective open-label clinical trial and a retrospective survey. The clinical trial included 29 adult andjuvenile patients in a 12-month controlled period, followed by extension therapy for an average totalduration of 3.9 years and up to 5.6 years. In addition 12 paediatric patients were enrolled in anuncontrolled substudy for an overall average duration of 3.1 years and up to 4.4 years. Among the 41patients enrolled in the trial 14 patients were treated with Zavesca for more than 3 years. The surveyincluded a case series of 66 patients treated with Zavesca outside of the clinical trial for a meanduration of 1.5 years. Both data sets included paediatric, adolescent and adult patients with an agerange of 1 year to 43 years. The usual dose of Zavesca in adult patients was 200 mg t.i.d., and wasadjusted according to body surface area in paediatric patients.
Overall the data show that treatment with Zavesca can reduce the progression of clinically relevantneurological symptoms in patients with Niemann-Pick type C disease.
The benefit of treatment with Zavesca for neurological manifestations in patients with Niemann-Picktype C disease should be evaluated on a regular basis, e.g. every 6 months; continuation of therapyshould be re-appraised after at least 1 year of treatment with Zavesca, (see section 4.4).
5.2 Pharmacokinetic properties
Pharmacokinetic parameters of miglustat were assessed in healthy subjects, in a small number ofpatients with type 1 Gaucher disease, Fabry disease, HIV-infected patients, and in adults, adolescentsand children with Niemann-Pick type C disease or type 3 Gaucher disease.
The kinetics of miglustat appear to be dose linear and time independent. In healthy subjects miglustatis rapidly absorbed. Maximum plasma concentrations are reached about 2 hours after dose. Absolutebioavailability has not been determined. Concomitant administration of food decreases the rate ofabsorption (Cmax was decreased by 36% and tmax delayed 2 hours), but has no statistically significanteffect on the extent of absorption of miglustat (AUC decreased by 14%).
The apparent volume of distribution of miglustat is 83 L. Miglustat does not bind to plasma proteins.
Miglustat is mainly eliminated by renal excretion, with urinary recovery of unchanged drugaccounting for 70-80% of the dose. Apparent oral clearance (CL/F) is 230 ± 39 mL/min. The averagehalf-life is 6-7 hours.
Following administration of a single dose of 100 mg 14C-miglustat to healthy volunteers, 83% of theradioactivity was recovered in urine and 12% in faeces. Several metabolites were identified in urineand faeces. The most abundant metabolite in urine was miglustat glucuronide accounting for 5% of thedose. The terminal half-life of radioactivity in plasma was 150 h suggesting the presence of one ormore metabolites with very long half-life. The metabolite accounting for this has not been identified,but may accumulate and reach concentrations exceeding those of miglustat at steady state.
The pharmacokinetics of miglustat is similar in adult type 1 Gaucher disease patients and
Niemann-Pick type C disease patients when compared to healthy subjects.
Paediatric populationPharmacokinetic data were obtained in paediatric patients with type 3 Gaucher disease aged 3 to15 years, and patients with Niemann-Pick type C disease aged 5-16 years. Dosing in children at200 mg t.i.d. adjusted for body surface area resulted in Cmax and AUC values which wereapproximately two-fold those attained after 100 mg t.i.d. in type 1 Gaucher disease patients, consistentwith the dose-linear pharmacokinetics of miglustat. At steady state, the concentration of miglustat incerebrospinal fluid of six type 3 Gaucher disease patients was 31.4-67.2% of that in plasma.
Limited data in patients with Fabry disease and impaired renal function showed that CL/F decreaseswith decreasing renal function. While the numbers of subjects with mild and moderate renalimpairment were very small, the data suggest an approximate decrease in CL/F of 40% and 60%respectively, in mild and moderate renal impairment (see section 4.2). Data in severe renal impairmentare limited to two patients with creatinine clearance in the range 18 - 29 mL/min and cannot beextrapolated below this range. These data suggest a decrease in CL/F by at least 70% in patients withsevere renal impairment.
Over the range of data available, no significant relationships or trends were noted between miglustatpharmacokinetic parameters and demographic variables (age, BMI, gender or race).
There are no pharmacokinetic data available in patients with liver impairment or in the elderly(> 70 years).
5.3 Preclinical safety data
The main effects common to all species were weight loss and diarrhoea, and, at higher doses, damageto the gastrointestinal mucosa (erosions and ulceration). Further effects seen in animals at doses thatresult in exposure levels similar to or moderately higher than the clinical exposure level were: changesin lymphoid organs in all species tested, transaminase changes, vacuolation of thyroid and pancreas,cataracts, nephropathy and myocardial changes in rats. These findings were considered to besecondary to debilitation.
Administration of miglustat to male and female Sprague-Dawley rats by oral gavage for 2 years atdose levels of 30, 60 and 180 mg/kg/day resulted in an increased incidence of testicular interstitial cell(Leydig cell) hyperplasia and adenomas in male rats at all dose levels. The systemic exposure at thelowest dose was below or comparable to that observed in humans (based on AUC0-) at therecommended human dose. A No Observed Effect Level (NOEL) was not established and the effectwas not dose dependent. There was no drug-related increase in tumour incidence in male or femalerats in any other organ. Mechanistic studies revealed a rat specific mechanism which is considered tobe of low relevance for humans.
Administration of miglustat to male and female CD1 mice by oral gavage at dose levels of 210, 420and 840/500 mg/kg/day (dose reduction after half a year) for 2 years resulted in an increased incidenceof inflammatory and hyperplastic lesions in the large intestine in both sexes. Based on mg/kg/day andcorrected for differences in faecal excretion, the doses corresponded to 8, 16 and 33/19 times thehighest recommended human dose (200 mg t.i.d.). Carcinomas in the large intestine occurredoccasionally at all doses with a statistically significant increase in the high dose group. A relevance ofthese findings to humans cannot be excluded. There was no drug-related increase in tumour incidencein any other organ.
Miglustat did not show any potential for mutagenic or clastogenic effects in the standard battery ofgenotoxicity tests.
Repeated-dose toxicity studies in rats showed seminiferous tubule degeneration and atrophy. Otherstudies revealed changes in sperm parameters (sperm concentration, motility and morphology)consistent with an observed reduction in fertility. These effects occurred at dose levels adjusted forbody surface area similar to those in patients, but showed reversibility. Miglustat decreasedembryo/foetal survival in rats and rabbits. Prolonged parturition was reported, post-implantation losseswere increased, and an increased incidence of vascular anomalies occurred in rabbits. These effectsmay be partly related to maternal toxicity.
Changes in lactation were observed in female rats in a 1-year study. The mechanism for this effect isunknown.
6. PHARMACEUTICAL PARTICULARS
6.1 List of excipients
Sodium starch glycollate,
Povidone (K30),
Magnesium stearate.
Capsule shellGelatin,
Titanium dioxide (E171).
Printing inkBlack iron oxide (E172),
Shellac.
6.2 Incompatibilities
Not applicable.
6.3 Shelf life
5 years.
6.4 Special precautions for storage
Do not store above 30°C.
6.5 Nature and contents of container
ACLAR/ALU blister strips supplied as a box of 4 blister strips, each blister strip containing21 capsules providing a total of 84 capsules.
6.6 Special precautions for disposal and other handling
No special requirements for disposal.
10. DATE OF REVISION OF THE TEXT
Detailed information on this medicinal product is available on the website of the European Medicines
Agency http://www.ema.europa.eu.