Pantozol 40 mg is indicated for use in adults and adolescents 12 years of age and above for:
− Reflux oesophagitis.
Pantozol 40 mg is indicated in adults for:
− Eradication of Helicobacter pylori (H. pylori) in combination with appropriate antibiotic therapy in
patients with H. pylori associated ulcers.
− Gastric and duodenal ulcer.
− Zollinger-Ellison-Syndrome and other pathological hypersecretory conditions.

Posology
Adults and adolescents 12 years of age and above
Reflux oesophagitis
One tablet of Pantozol 40 mg per day. In individual cases the dose may be doubled (increase to 2 tablets
Pantozol 40 mg daily) especially when there has been no response to other treatment. A 4-week period is
usually required for the treatment of reflux oesophagitis. If this is not sufficient, healing will usually be
achieved within a further 4 weeks.
Adults
Eradication of H. pylori in combination with two appropriate antibiotics
In H. pylori positive patients with gastric and duodenal ulcers, eradication of the germ by a combination
therapy should be achieved. Considerations should be given to official local guidance (e.g. national
recommendations) regarding bacterial resistance and the appropriate use and prescription of antibacterial
agents. Depending upon the resistance pattern, the following combinations can be recommended for the
eradication of H. pylori:
a) twice daily one tablet Pantozol 40 mg
+ twice daily 1000 mg amoxicillin
+ twice daily 500 mg clarithromycin
2
b) twice daily one tablet Pantozol 40 mg
+ twice daily 400 - 500 mg metronidazole (or 500 mg tinidazole)
+ twice daily 250 - 500 mg clarithromycin
c) twice daily one tablet Pantozol 40 mg
+ twice daily 1000 mg amoxicillin
+ twice daily 400 - 500 mg metronidazole (or 500 mg tinidazole)
In combination therapy for eradication of H. pylori infection, the second Pantozol 40 mg tablet should be
taken 1 hour before the evening meal. The combination therapy is implemented for 7 days in general and
can be prolonged for a further 7 days to a total duration of up to two weeks. If, to ensure healing of the
ulcers, further treatment with pantoprazole is indicated, the dose recommendations for duodenal and
gastric ulcers should be considered.
If combination therapy is not an option, e.g. if the patient has tested negative for H. pylori, the following
dose guidelines apply for Pantozol 40 mg monotherapy:
Treatment of gastric ulcer
One tablet of Pantozol 40 mg per day. In individual cases the dose may be doubled (increase to 2 tablets of
Pantozol 40 mg daily) especially when there has been no response to other treatment. A 4-week period is
usually required for the treatment of gastric ulcers. If this is not sufficient, healing will usually be achieved
within a further 4 weeks.
Treatment of duodenal ulcer
One tablet of Pantozol 40 mg per day. In individual cases the dose may be doubled (increase to 2 tablets of
Pantozol 40 mg daily) especially when there has been no response to other treatment. A duodenal ulcer
generally heals within 2 weeks. If a 2-week period of treatment is not sufficient, healing will be achieved
in almost all cases within a further 2 weeks.
Zollinger-Ellison-Syndrome and other pathological hypersecretory conditions
For the long-term management of Zollinger-Ellison-Syndrome and other pathological hypersecretory
conditions patients should start their treatment with a daily dose of 80 mg (2 tablets of Pantozol 40 mg
40 mg). Thereafter, the dose can be titrated up or down as needed using measurements of gastric acid
secretion to guide. With doses above 80 mg daily, the dose should be divided and given twice daily. A
temporary increase of the dose above 160 mg pantoprazole is possible but should not be applied longer
than required for adequate acid control.
Treatment duration in Zollinger-Ellison syndrome and other pathological hypersecretory conditions is not
limited and should be adapted according to clinical needs.
Patients with hepatic impairment
A daily dose of 20 mg pantoprazole (1 tablet of 20 mg pantoprazole) should not be exceeded in patients
with severe liver impairment. Pantozol 40 mg must not be used in combination treatment for eradication
of H. pylori in patients with moderate to severe hepatic dysfunction since currently no data are available
on the efficacy and safety of Pantozol 40 mg in combination treatment of these patients (see section 4.4).
Patients with renal impairment
No dose adjustment is necessary in patients with impaired renal function. Pantozol 40 mg must not be
used in combination treatment for eradication of H. pylori in patients with impaired renal function since
currently no data are available on the efficacy and safety of Pantozol 40 mg in combination treatment for
these patients (see section 5.2).
3
Older people
No dose adjustment is necessary in older people (see section 5.2).
Paediatric population
Pantozol 40 mg is not recommended for use in children below 12 years of age because of limited data on
safety and efficacy in the age group (see section 5.2).
Method of administration
Oral use
The tablets should not be chewed or crushed, and should be swallowed whole 1 hour before a meal with
some water.

Hepatic impairment
In patients with severe liver impairment, the liver enzymes should be monitored regularly during treatment
with pantoprazole, particularly on long-term use. In the case of a rise of the liver enzymes, the treatment
should be discontinued (see section 4.2).
Combination therapy
In the case of combination therapy, the summaries of product characteristics of the respective medicinal
products should be observed.
Gastric malignancy
Symptomatic response to pantoprazole may mask the symptoms of gastric malignancy and may delay
diagnosis. In the presence of any alarm symptom (e. g. significant unintentional weight loss, recurrent
vomiting, dysphagia, haematemesis, anaemia or melaena) and when gastric ulcer is suspected or present,
malignancy should be excluded.
Further investigation is to be considered if symptoms persist despite adequate treatment.
Co-administration with HIV protease inhibitors
Co-administration of pantoprazole is not recommended with HIV protease inhibitors for which absorption
is dependent on acidic intragastric pH such as atazanavir, due to significant reduction in their
bioavailability (see section 4.5).
Influence on vitamin B12 absorption
In patients with Zollinger-Ellison syndrome and other pathological hypersecretory conditions requiring
long-term treatment, pantoprazole, as all acid-blocking medicines, may reduce the absorption of
vitamin B12 (cyanocobalamin) due to hypo- or achlorhydria. This should be considered in patients with
reduced body stores or risk factors for reduced vitamin B12 absorption on long-term therapy or if
respective clinical symptoms are observed.
Long term treatment
In long-term treatment, especially when exceeding a treatment period of 1 year, patients should be kept
under regular surveillance.
4
Gastrointestinal infections caused by bacteria
Treatment with Pantozol 40 mg may lead to a slightly increased risk of gastrointestinal infections caused
by bacteria such as Salmonella and Campylobacter or C. difficile.
Hypomagnesaemia
Severe hypomagnesaemia has been reported in patients treated with PPIs like pantoprazole for at least
three months, and in most cases for a year. Serious manifestations of hypomagnesaemia such as fatigue,
tetany, delirium, convulsions, dizziness and ventricular arrhythmia can occur but they may begin
insidiously and be overlooked. In most affected patients, hypomagnesaemia improved after magnesium
replacement and discontinuation of the PPI.
For patients expected to be on prolonged treatment or who take PPIs with digoxin or medicinal products
that may cause hypomagnesaemia (e.g. diuretics), health care professionals should consider measuring
magnesium levels before starting PPI treatment and periodically during treatment.
Bone fractures
Proton pump inhibitors, especially if used in high doses and over long durations (>1 year), may modestly
increase the risk of hip, wrist and spine fracture, predominantly in older people or in the presence of other
recognised risk factors. Observational studies suggest that proton pump inhibitors may increase the overall
risk of fracture by 10–40%. Some of this increase may be due to other risk factors. Patients at risk of
osteoporosis should receive care according to current clinical guidelines and they should have an adequate
intake of vitamin D and calcium.
Subacute cutaneous lupus erythematosus (SCLE)
Proton pump inhibitors are associated with very infrequent cases of SCLE. If lesions occur, especially in
sun exposed areas of the skin, and if accompanied by arthralgia, the patient should seek medical help
promptly and the healthcare professional should consider stopping Pantozol 40 mg. SCLE after previous
treatment with a proton pump inhibitor may increase the risk of SCLE with other proton pump inhibitors.
Interference with Laboratory Tests
Increased Chromogranin A (CgA) level may interfere with investigations for neuroendocrine tumours. To
avoid this interference, Pantozol 40 mg treatment should be stopped for at least 5 days before CgA
measurements (see section 5.1). If CgA and gastrin levels have not returned to reference range after initial
measurement, measurements should be repeated 14 days after cessation of proton pump inhibitor
treatment.

Medicinal products with pH-Dependent Absorption Pharmacokinetics
Because of profound and long lasting inhibition of gastric acid secretion, pantoprazole may interfere with
the absorption of other medicinal products where gastric pH is an important determinant of oral
availability, e.g. some azole antifungals such as ketoconazole, itraconazole, posaconazole and other
medicine such as erlotinib.
HIV protease inhibtiors
Co-administration of pantoprazole is not recommended with HIV protease inhibitors for which absorption
is dependent on acidic intragastric pH such as atazanavir due to significant reduction in their
bioavailability (see section 4.4).
If the combination of HIV protease inhibitors with a proton pump inhibitor is judged unavoidable, close
clinical monitoring (e.g virus load) is recommended. . A pantoprazole dose of 20 mg per day should not be
exceeded. Dosage of the HIV protease inhibitors may need to be adjusted.
5
Coumarin anticoagulants (phenprocoumon or warfarin)
Co-administration of pantoprazole with warfarin or phenprocoumon did not affect the pharmacokinetics of
warfarin, phenprocoumon or INR. However, there have been reports of increased INR and prothrombin
time in patients receiving PPIs and warfarin or phenprocoumon concomitantly. Increases in INR and
prothrombin time may lead to abnormal bleeding, and even death. Patients treated with pantoprazole and
warfarin or phenprocoumon may need to be monitored for increase in INR and prothrombin time..
Methotrexate
Concomitant use of high dose methotrexate (e.g. 300 mg) and proton-pump inhibitors has been reported to
increase methotrexate levels in some patients. Therefore in settings where high-dose methotrexate is used,
for example cancer and psoriasis, a temporary withdrawal of pantoprazole may need to be considered.
Other interactions studies
Pantoprazole is extensively metabolized in the liver via the cytochrome P450 enzyme system. The main
metabolic pathway is demethylation by CYP2C19 and other metabolic pathways include oxidation by
CYP3A4.
Interaction studies with medicinal products also metabolized with these pathways, like carbamazepine,
diazepam, glibenclamide, nifedipine, and an oral contraceptive containing levonorgestrel and ethinyl
oestradiol, did not reveal clinically significant interactions.
An interaction of pantoprazole with other medicinal products or compounds, which are metabolized using
the same enzyme system, cannot be excluded.
Results from a range of interaction studies demonstrate that pantoprazole does not affect the metabolism
of active substances metabolised by CYP1A2 (such as caffeine, theophylline), CYP2C9 (such as
piroxicam, diclofenac, naproxen), CYP2D6 (such as metoprolol), CYP2E1 (such as ethanol), or does not
interfere with p-glycoprotein related absorption of digoxin.
There were no interactions with concomitantly administered antacids.
Interaction studies have also been performed by concomitantly administering pantoprazole with the
respective antibiotics (clarithromycin, metronidazole, amoxicillin). No clinically relevant interactions
were found.
Medicinal products that inhibit or induce CYP2C19:
Inhibitors of CYP2C19 such as fluvoxamine could increase the systemic exposure of pantoprazole. A dose
reduction may be considered for patients treated long-term with high doses of pantoprazole, or those with
hepatic impairment.
Enzyme inducers affecting CYP2C19 and CYP3A4 such as rifampicin and St John´s wort (Hypericum
perforatum) may reduce the plasma concentrations of PPIs that are metabolized through these enzyme
systems.

Pregnancy
A moderate amount of data on pregnant women (between 300-1000 pregnancy outcomes) indicate no
malformative or feto/ neonatal toxicity of Pantozol 40 mg.
Animal studies have shown reproductive toxicity (see section 5.3).
As a precautionary measure, it is preferable to avoid the use of Pantozol 40 mg during pregnancy.
6
Breast-feeding
Animal studies have shown excretion of pantoprazole in breast milk. There is insufficient information on
the excretion of pantoprazole in human milk but excretion into human milk has been reported. A risk to
the newborns/infants cannot be excluded. Therefore, a decision on whether to discontinue breast-feeding
or to discontinue/abstain from Pantozol 40 mg therapy taking into account the benefit of breast-feeding
for the child, and the benefit of Pantozol 40 mg therapy for the woman.
Fertility
There was no evidence of impaired fertility following the administration of pantoprazole in animal studies
(see section 5.3).

Pantoprazole has no or negligible influence on the ability to drive and use machines.
Adverse drug reactions, such as dizziness and visual disturbances may occur (see section 4.8). If affected,
patients should not drive or operate machines.

Approximately 5 % of patients can be expected to experience adverse drug reactions (ADRs). The most
commonly reported ADRs are diarrhoea and headache, both occurring in approximately 1 % of patients.
The table below lists adverse reactions reported with pantoprazole, ranked under 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).
For all adverse reactions reported from post-marketing experience, it is not possible to apply any Adverse
Reaction frequency and therefore they are mentioned with a “not known” frequency.
Within each frequency grouping, adverse reactions are presented in order of decreasing seriousness.
Table 1. Adverse reactions with pantoprazole in clinical trials and post-marketing experience
Frequency
System
Organ Class
Common Uncommon Rare Very rare Not known
Blood and
lymphatic system
disorders
Agranulocytosis Thrombocytopenia;
Leukopenia;
Pancytopenia
Immune system
disorders
Hypersensitivity
(including
anaphylactic
reactions and
anaphylactic
shock)
Metabolism and
nutrition
disorders
Hyperlipidaemias
and lipid
increases
(triglycerides,
cholesterol);
Weight changes
Hyponatraemia;
Hypomagnesaemia
(see section 4.4);
Hypocalcaemia (1);
Hypokalaemia
Psychiatric Sleep disorders Depression (and Disorientation (and Hallucination;
Frequency
System
Organ Class
Common Uncommon Rare Very rare Not known
disorders all aggravations) all aggravations) Confusion
(especially in predisposed
patients,
as well as the
aggravation of
these symptoms in
case of preexistence)
Nervous system
disorders
Headache;
Dizziness
Taste disorders Parasthesia
Eye disorders Disturbances in
vision / blurred
vision
Gastrointestinal
disorders
Fundic
gland
polyps
(benign)
Diarrhoea;
Nausea /
vomiting;
Abdominal
distension and
bloating;
Constipation;
Dry mouth;
Abdominal
pain and
discomfort
Microscopic
colitis
Hepatobiliary
disorders
Liver enzymes
increased
(transaminases,
γ-GT)
Bilirubin
increased
Hepatocellular
injury; Jaundice;
Hepatocellular
failure
Skin and subcutaneous
tissue
disorders
Rash /
exanthema /
eruption;
Pruritus
Urticaria;
Angioedema
Stevens-Johnson
syndrome; Lyell
syndrome;
Erythema
multiforme;
Photosensitivity;
Subacute
cutaneous lupus
erythematosus (see
section 4.4)
Musculoskeletal
and connective
tissue disorders
Fracture of the
hip, wrist or
spine (see
section 4.4)
Arthralgia;
Myalgia
Muscle spasm (2)
Renal and
urinary disorders
Interstitial
nephritis (with
possible
progression to
renal failure)
Reproductive
system and
breast
Gynaecomastia
Frequency
System
Organ Class
Common Uncommon Rare Very rare Not known
disorders
General disorders
and
administration
site conditions
Asthenia,
fatigue and
malaise
Body
temperature
increased;
Oedema
peripheral
1. Hypocalcemia in association with hypomagnesemia
2. Muscle spasm as a consequence of electrolyte disturbance
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 medical product. Healthcare professionals are
asked to report any suspected adverse reactions via Bundesinstitut für Arzneimittel und Medizinprodukte
Abt. Pharmakovigilanz
Kurt-Georg-Kiesinger-Allee 3
53175 Bonn
Website: www.bfarm.de.

There are no known symptoms of overdose in man.
Systemic exposure with up to 240 mg administered intravenously over 2 minutes, were well tolerated.
As pantoprazole is extensively protein bound, it is not readily dialysable.
In the case of an overdose with clinical signs of intoxication, apart from symptomatic and supportive
treatment, no specific therapeutic recommendations can be made.

Pharmacotherapeutic group: Proton pump inhibitors, ATC code: A02BC02
Mechanism of action
Pantoprazole is a substituted benzimidazole which inhibits the secretion of hydrochloric acid in the
stomach by specific blockade of the proton pumps of the parietal cells.
Pantoprazole is converted to its active form in the acidic environment in the parietal cells where it inhibits
the H+, K+-ATPase enzyme, i.e. the final stage in the production of hydrochloric acid in the stomach. The
inhibition is dose-dependent and affects both basal and stimulated acid secretion. In most patients,
freedom from symptoms is achieved within 2 weeks. As with other proton pump inhibitors and
H2 receptor inhibitors, treatment with pantoprazole reduces acidity in the stomach and thereby increases
gastrin in proportion to the reduction in acidity. The increase in gastrin is reversible. Since pantoprazole
binds to the enzyme distal to the cell receptor level, it can inhibit hydrochloric acid secretion
independently of stimulation by other substances (acetylcholine, histamine, gastrin). The effect is the same
whether the product is given orally or intravenously.
Pharmacodynamic effects
The fasting gastrin values increase under pantoprazole. On short-term use, in most cases they do not
exceed the upper limit of normal. During long-term treatment, gastrin levels double in most cases. An
excessive increase, however, occurs only in isolated cases. As a result, a mild to moderate increase in the
number of specific endocrine (ECL) cells in the stomach is observed in a minority of cases during longterm
treatment (simple to adenomatoid hyperplasia). However, according to the studies conducted so far,
the formation of carcinoid precursors (atypical hyperplasia) or gastric carcinoids as were found in animal
experiments (see section 5.3) have not been observed in humans.
An influence of a long term treatment with pantoprazole exceeding one year cannot be completely ruled
out on endocrine parameters of the thyroid according to results in animal studies.
During treatment with antisecretory medicinal products, serum gastrin increases in response to the
decreased acid secretion. Also CgA increases due to decreased gastric acidity. The increased CgA level
may interfere with investigations for neuroendocrine tumours.
Available published evidence suggests that proton pump inhibitors should be discontinued between 5 days
and 2 weeks prior to CgA measurements. This is to allow CgA levels that might be spuriously elevated
following PPI treatment to return to reference range.

Absorption
Pantoprazole is rapidly absorbed and the maximal plasma concentration is achieved even after one single
40 mg oral dose. On average at about 2.5 h p.a. the maximum serum concentrations of about 2 - 3 μg/ml
are achieved, and these values remain constant after multiple administration.
Pharmacokinetics does not vary after single or repeated administration. In the dose range of 10 to 80 mg,
the plasma kinetics of pantoprazole are linear after both oral and intravenous administration.
The absolute bioavailability from the tablet was found to be about 77 %. Concomitant intake of food had
no influence on AUC, maximum serum concentration and thus bioavailability. Only the variability of the
lag-time will be increased by concomitant food intake.
Distribution
Pantoprazole's serum protein binding is about 98 %. Volume of distribution is about 0.15 l/kg.
Biotransformation
The substance is almost exclusively metabolized in the liver. The main metabolic pathway is
demethylation by CYP2C19 with subsequent sulphate conjugation, other metabolic pathway includes
oxidation by CYP3A4.
Elimination
Terminal half-life is about 1 hour and clearance is about 0.1 l/h/kg. There were a few cases of subjects
with delayed elimination. Because of the specific binding of pantoprazole to the proton pumps of the
parietal cell the elimination half-life does not correlate with the much longer duration of action (inhibition
of acid secretion).
Renal elimination represents the major route of excretion (about 80 %) for the metabolites of
pantoprazole, the rest is excreted with the faeces. The main metabolite in both the serum and urine is
desmethylpantoprazole which is conjugated with sulphate. The half-life of the main metabolite (about
1.5 hours) is not much longer than that of pantoprazole.
Special populations
Poor metabolisers
Approximately 3 % of the European population lack a functional CYP2C19 enzyme and are called poor
metabolisers. In these individuals the metabolism of pantoprazole is probably mainly catalysed by
CYP3A4. After a single-dose administration of 40 mg pantoprazole, the mean area under the plasma
concentration-time curve was approximately 6 times higher in poor metabolisers than in subjects having a
functional CYP2C19 enzyme (extensive metabolisers). Mean peak plasma concentrations were increased
by about 60 %. These findings have no implications for the posology of pantoprazole.
Renal impairment
No dose reduction is recommended when pantoprazole is administered to patients with impaired renal
function (including dialysis patients). As with healthy subjects, pantoprazole's half-life is short. Only very
small amounts of pantoprazole are dialyzed. Although the main metabolite has a moderately delayed halflife
(2 - 3 h), excretion is still rapid and thus accumulation does not occur.
Hepatic impairment
Although for patients with liver cirrhosis (classes A and B according to Child) the half-life values
increased to between 7 and 9 h and the AUC values increased by a factor of 5 - 7, the maximum serum
concentration only increased slightly by a factor of 1.5 compared with healthy subjects.
Older people
A slight increase in AUC and Cmax in elderly volunteers compared with younger counterparts is also not
clinically relevant.
Paediatric population
Following administration of single oral doses of 20 or 40 mg pantoprazole to children aged 5 - 16 years
AUC and Cmax were in the range of corresponding values in adults.
Following administration of single i.v. doses of 0.8 or 1.6 mg/kg pantoprazole to children aged
2 - 16 years there was no significant association between pantoprazole clearance and age or weight. AUC
and volume of distribution were in accordance with data from adults.

Non-clinical data reveal no special hazard to humans based on conventional studies of safety
pharmacology, repeated dose toxicity and genotoxicity.
In the two-year carcinogenicity studies in rats neuroendocrine neoplasms were found. In addition,
squamous cell papillomas were found in the forestomach of rats. The mechanism leading to the formation
of gastric carcinoids by substituted benzimidazoles has been carefully investigated and allows the
conclusion that it is a secondary reaction to the massively elevated serum gastrin levels occurring in the rat
during chronic high-dose treatment. In the two-year rodent studies an increased number of liver tumors
was observed in rats and in female mice and was interpreted as being due to pantoprazole's high metabolic
rate in the liver.
A slight increase of neoplastic changes of the thyroid was observed in the group of rats receiving the
highest dose (200 mg/kg). The occurrence of these neoplasms is associated with the pantoprazole-induced
changes in the breakdown of thyroxine in the rat liver. As the therapeutic dose in man is low, no harmful
effects on the thyroid glands are expected.
In a peri-postnatal rat reproduction study designed to assess bone development, signs of offspring toxicity
(mortality, lower mean body weight, lower mean body weight gain and changes in bone parameters) were
observed at exposures (Cmax) approximately 2x the human clinical exposure. Changes in bone parameters
were considered secondary to overall growth suppression and not direct effects on bone development. By
the end of the recovery phase, bone parameters were similar across groups and body weights were also
trending toward reversibility after a drug-free recovery period. A previous peri-postnatal study in rats at
slightly lower doses found no adverse effects at 3 mg/kg compared with a low dose of 5 mg/kg in this
study.
Investigations revealed no evidence of impaired fertility or teratogenic effects.
Penetration of the placenta was investigated in the rat and was found to increase with advanced gestation.
As a result, concentration of pantoprazole in the foetus is increased shortly before birth.

Core:
Sodium carbonate, anhydrous
Mannitol (E421)
Crospovidone
Povidone K90
Calcium stearate
Coating:
Hypromellose
Povidone K25
Titanium dioxide (E171)
Yellow iron oxide (E172)
Propylene glycol
Methacrylic acid-ethyl acrylate copolymer (1:1)
Polysorbate 80
Sodium laurilsulfate
Triethyl citrate
Printing ink:
Shellac
Red iron oxide (E172)
Black iron oxide (E172)
Yellow iron oxide (E172)
Ammonia solution, concentrated

Not applicable.

This medicinal product does not require any special storage conditions.

HDPE bottles with LDPE screw cap closure.
7 gastro-resistant tablets
10 gastro-resistant tablets
14 gastro-resistant tablets
15 gastro-resistant tablets
24 gastro-resistant tablets
28 gastro-resistant tablets
30 gastro-resistant tablets
48 gastro-resistant tablets
49gastro-resistant tablets
56 gastro-resistant tablets
60 gastro-resistant tablets
84 gastro-resistant tablets
90 gastro-resistant tablets
98 gastro-resistant tablets
98 (2x49) gastro-resistant tablets
100 gastro-resistant tablets
Hospital pack with 50 gastro-resistant tablets
90 gastro-resistant tablets
100 gastro-resistant tablets
140 gastro-resistant tablets
140 (10x14) gastro-resistant tablets
150 (10x15) gastro-resistant tablets
700 (5x140) gastro-resistant tablets
Blister (ALU/ALU blister) without cardboard reinforcement.
Blister (ALU/ALU blister) with cardboard reinforcement (blister wallet).
7 gastro-resistant tablets
10 gastro-resistant tablets
14 gastro-resistant tablets
15 gastro-resistant tablets
28 gastro-resistant tablets
30 gastro-resistant tablets
49gastro-resistant tablets
56 gastro-resistant tablets
60 gastro-resistant tablets
84 gastro-resistant tablets
90 gastro-resistant tablets
98 gastro-resistant tablets
98 (2x49) gastro-resistant tablets
100 gastro-resistant tablets
112 gastro-resistant tablets
168 gastro-resistant tablets
Hospital pack with 50 gastro-resistant tablets
90 gastro-resistant tablets
100 gastro-resistant tablets
140 gastro-resistant tablets
140 (10x14) gastro-resistant tablets
150 (10x15) gastro-resistant tablets
700 (5x140) gastro-resistant tablets
Not all pack sizes may be marketed.

No special requirements.
Any unused medicinal product or waste material should be disposed of in accordance with local
requirements.