Omeprex capsules are indicated for:
Adults
• Treatment of duodenal ulcers
• Prevention of relapse of duodenal ulcers
• Treatment of gastric ulcers
• Prevention of relapse of gastric ulcers
• In combination with appropriate antibiotics, Helicobacter pylori (H. pylori)
eradication in peptic ulcer disease
• Treatment of NSAID-associated gastric and duodenal ulcers
• Prevention of NSAID-associated gastric and duodenal ulcers in patients at risk
• Treatment of reflux oesophagitis
• Long-term management of patients with healed reflux oesophagitis
• Treatment of symptomatic gastro-oesophageal reflux disease
• Treatment of Zollinger-Ellison syndrome
Paediatric use
Children over 1 year of age and 10 kg
• Treatment of reflux oesophagitis
• Symptomatic treatment of heartburn and acid regurgitation in gastro-oesophageal
reflux disease
Children and adolescents over 4 years of age
• In combination with antibiotics in treatment of duodenal ulcer caused by H. pylori
 

Posology in adults
Treatment of duodenal ulcers
The recommended dose in patients with an active duodenal ulcer is Omeprex 20 mg
once daily. In most patients healing occurs within two weeks. For those patients who
may not be fully healed after the initial course, healing usually occurs during a
further two weeks treatment period. In patients with poorly responsive duodenal
ulcer Omeprex 40 mg once daily is recommended and healing is usually achieved
within four weeks.
Prevention of relapse of duodenal ulcers
For the prevention of relapse of duodenal ulcer in H. pylori negative patients or
when H. pylori eradication is not possible the recommended dose is Omeprex 20 mg
once daily. In some patients a daily dose of 10 mg may be sufficient. In case of
therapy failure, the dose can be increased to 40 mg.
Treatment of gastric ulcers
The recommended dose is Omeprex 20 mg once daily. In most patients healing
occurs within four weeks. For those patients who may not be fully healed after the
initial course, healing usually occurs during a further four weeks treatment period. In
patients with poorly responsive gastric ulcer Omeprex 40 mg once daily is
recommended and healing is usually achieved within eight weeks.
Prevention of relapse of gastric ulcers
For the prevention of relapse in patients with poorly responsive gastric ulcer the
recommended dose is Omeprex 20 mg once daily. If needed the dose can be
increased to Omeprex 40 mg once daily.
H. pylori eradication in peptic ulcer disease
For the eradication of H. pylori the selection of antibiotics should consider the
individual patient's drug tolerance, and should be undertaken in accordance with
national, regional and local resistance patterns and treatment guidelines.
• Omeprex 20 mg + clarithromycin 500 mg + amoxicillin 1,000 mg, each twice daily
for one week, or
• Omeprex 20 mg + clarithromycin 250 mg (alternatively 500 mg) + metronidazole
400 mg (or 500 mg or tinidazole 500 mg), each twice daily for one week or
• Omeprex 40 mg once daily with amoxicillin 500 mg and metronidazole 400 mg (or
500 mg or tinidazole 500 mg), both three times a day for one week.
In each regimen, if the patient is still H. pylori positive, therapy may be repeated.
Treatment of NSAID-associated gastric and duodenal ulcers
For the treatment of NSAID-associated gastric and duodenal ulcers, the
recommended dose is Omeprex 20 mg once daily. In most patients healing occurs
within four weeks. For those patients who may not be fully healed after the initial
course, healing usually occurs during a further four weeks treatment period.
Prevention of NSAID-associated gastric and duodenal ulcers in patients at risk
For the prevention of NSAID-associated gastric ulcers or duodenal ulcers in patients
at risk (age> 60, previous history of gastric and duodenal ulcers, previous history of
upper GI bleeding) the recommended dose is Omeprex 20 mg once daily.
Treatment of reflux oesophagitis
The recommended dose is Omeprex 20 mg once daily. In most patients healing
occurs within four weeks. For those patients who may not be fully healed after the
initial course, healing usually occurs during a further four weeks treatment period.
In patients with severe oesophagitis Omeprex 40 mg once daily is recommended and
healing is usually achieved within eight weeks.
Long-term management of patients with healed reflux oesophagitis
For the long-term management of patients with healed reflux oesophagitis the
recommended dose is Omeprex 10 mg once daily. If needed, the dose can be
increased to Omeprex 20-40 mg once daily.
Treatment of symptomatic gastro-oesophageal reflux disease
The recommended dose is Omeprex 20 mg daily. Patients may respond adequately
to 10 mg daily, and therefore individual dose adjustment should be considered.
If symptom control has not been achieved after four weeks treatment with Omeprex
20 mg daily, further investigation is recommended.
Treatment of Zollinger-Ellison syndrome
In patients with Zollinger-Ellison syndrome the dose should be individually adjusted
and treatment continued as long as clinically indicated. The recommended initial
dose is Omeprex 60 mg daily. All patients with severe disease and inadequate
response to other therapies have been effectively controlled and more than 90% of
the patients maintained on doses of Omeprex 20-120 mg daily. When dose exceed
Omeprex 80 mg daily, the dose should be divided and given twice daily.
Posology in children
Children over 1 year of age and 10 kg
Treatment of reflux oesophagitis
Symptomatic treatment of heartburn and acid regurgitation in gastro-oesophageal
reflux disease
The posology recommendations are as follows:

Special populations
Impaired renal function
Dose adjustment is not needed in patients with impaired renal function (see section
5.2).
Impaired hepatic function
In patients with impaired hepatic function a daily dose of 10–20 mg may be sufficient
(see section 5.2).
Elderly (> 65 years old)
Dose adjustment is not needed in the elderly (see section 5.2).
Method of administration
It is recommended to take Omeprex capsules in the morning, preferably without
food, swallowed whole with half a glass of water. The capsules must not be chewed
or crushed.
For patients with swallowing difficulties and for children who can drink or swallow
semi-solid food
Patients can open the capsule and swallow the contents with half a glass of water or
after mixing the contents in a slightly acidic fluid e.g., fruit juice or applesauce, or in
non-carbonated water. Patients should be advised that the dispersion should be
taken immediately (or within 30 minutes) and always be stirred just before drinking
and rinsed down with half a glass of water.
Alternatively patients can suck the capsule and swallow the pellets with half a glass
of water. The enteric-coated pellets must not be chewed.
 

In the presence of any alarm symptom (e.g. significant unintentional weight loss,
recurrent vomiting, dysphagia, haematemesis or melena) and when gastric ulcer is
suspected or present, malignancy should be excluded, as treatment may alleviate
symptoms and delay diagnosis.
Co-administration of atazanavir with proton pump inhibitors is not recommended
(see section 4.5). If the combination of atazanavir with a proton pump inhibitor is
judged unavoidable, close clinical monitoring (e.g virus load) is recommended in
combination with an increase in the dose of atazanavir to 400 mg with 100 mg of
ritonavir; omeprazole 20 mg should not be exceeded.
Omeprazole, 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.
Omeprazole is a CYP2C19 inhibitor. When starting or ending treatment with
omeprazole, the potential for interactions with drugs metabolised through CYP2C19
should be considered. An interaction is observed between clopidogrel and
omeprazole (see section 4.5). The clinical relevance of this interaction is uncertain.
As a precaution, concomitant use of omeprazole and clopidogrel should be
discouraged.
Severe hypomagnesaemia has been reported in patients treated with proton pump
inhibitors (PPIs) like omeprazole 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
drugs that may cause hypomagnesaemia (e.g. diuretics), healthcare professionals
should consider measuring magnesium levels before starting PPI treatment and
periodically during treatment
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 the elderly or in 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 health care professional
should consider stopping Losec. 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 CgA level may interfere with investigations for neuroendocrine tumours.
To avoid this interference the omeprazole treatment should be temporarily stopped
five days before CgA measurements.
Some children with chronic illnesses may require long-term treatment although it is
not recommended.
Omeprex contains lactose. Patients with rare hereditary problems of galactose
intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should
not take this medicine.
In the presence of ill effects like pain in the joints the patient should seek medical
help promptly and the health care professional.
Treatment with proton pump inhibitors may lead to slightly increased risk of
gastrointestinal infections such as Salmonella and Campylobacter (see section 5.1).
As in all long-term treatments, especially when exceeding a treatment period of 1
year, patients should be kept under regular surveillance.
 

Effects of omeprazole on the pharmacokinetics of other active substances
Active substances with pH dependent absorption
The decreased intragastric acidity during treatment with omeprazole might increase
or decrease the absorption of active substances with a gastric pH dependent
absorption.
Nelfinavir, atazanavir
The plasma levels of nelfinavir and atazanavir are decreased in case of coadministration with omeprazole.
Concomitant administration of omeprazole with nelfinavir is contraindicated (see
section 4.3). Co-administration of omeprazole (40 mg once daily) reduced mean
nelvinavir exposure by ca. 40% and the mean exposure of the pharmacologically
active metabolite M8 was reduced by ca. 75 –90%. The interaction may also involve
CYP2C19 inhibition.
Concomitant administration of omeprazole with atazanavir is not recommended (see
section 4.4). Concomitant administration of omeprazole (40 mg once daily) and
atazanavir 300 mg/ritonavir 100 mg to healthy volunteers resulted in a 75% decrease
of the atazanavir exposure. Increasing the atazanavir dose to 400 mg did not
compensate for the impact of omeprazole on atazanavir exposure. The co-
administration of omeprazole (20 mg once daily) with atazanavir 400 mg/ritonavir
100 mg to healthy volunteers resulted in a decrease of approximately 30% in the
atazanavir exposure as compared to atazanavir 300 mg/ritonavir 100 mg once daily.
Digoxin
Concomitant treatment with omeprazole (20 mg daily) and digoxin in healthy
subjects increased the bioavailability of digoxin by 10%. Digoxin toxicity has been
rarely reported. However caution should be exercised when omeprazole is given at
high doses in elderly patients. Therapeutic drug monitoring of digoxin should be then
be reinforced.
Clopidogrel
In a crossover clinical study, clopidogrel (300 mg loading dose followed by 75
mg/day) alone and with omeprazole (80 mg at the same time as clopidogrel) were
administered for 5 days. The exposure to the active metabolite of clopidogrel was
decreased by 46% (Day 1) and 42% (Day 5) when clopidogrel and omeprazole were
administered together. Mean inhibition of platelet aggregation (IPA) was diminished
by 47% (24 hours) and 30% (Day 5) when clopidogrel and omeprazole were
administered together. In another study it was shown that administering clopidogrel
and omeprazole at different times did not prevent their interaction that is likely to
be driven by the inhibitory effect of omeprazole on CYP2C19. Inconsistent data on
the clinical implications of this PK/PD interaction in terms of major cardiovascular
events have been reported from observational and clinical studies.
Other active substances
The absorption of posaconazole, erlotinib, ketoconazol and itraconazol is
significantly reduced and thus clinical efficacy may be impaired. For posaconazol and
erlotinib concomitant use should be avoided.
Active substances metabolised by CYP2C19
Omeprazole is a moderate inhibitor of CYP2C19, the major omeprazole metabolising
enzyme. Thus, the metabolism of concomitant active substances also metabolised by
CYP2C19, may be decreased and the systemic exposure to these substances
increased. Examples of such drugs are R-warfarin and other vitamin K antagonists,
cilostazol, diazepam and phenytoin.
Cilostazol
Omeprazole, given in doses of 40 mg to healthy subjects in a cross-over study,
increased Cmax and AUC for cilostazol by 18% and 26% respectively, and one of its
active metabolites by 29% and 69% respectively.
Phenytoin
Monitoring phenytoin plasma concentration is recommended during the first two
weeks after initiating omeprazole treatment and, if a phenytoin dose adjustment is
made, monitoring and a further dose adjustment should occur upon ending
omeprazole treatment.
Unknown mechanism
Saquinavir
Concomitant administration of omeprazole with saquinavir/ritonavir resulted in
increased plasma levels up to approximately 70% for saquinavir associated with good
tolerability in HIV-infected patients.
Tacrolimus
Concomitant administration of omeprazole has been reported to increase the serum
levels of tacrolimus. A reinforced monitoring of tacrolimus concentrations as well as
renal function (creatinine clearance) should be performed, and dosage of tacrolimus
adjusted if needed.
Effects of other active substances on the pharmacokinetics of omeprazole
Inhibitors CYP2C19 and/or CYP3A4
Since omeprazole is metabolised by CYP2C19 and CYP3A4, active substances known
to inhibit CYP2C19 or CYP3A4 (such as clarithromycin and voriconazole) may lead to
increased omeprazole serum levels by decreasing omeprazole's rate of metabolism.
Concomitant voriconazole treatment resulted in more than doubling of the
omeprazole exposure. As high doses of omeprazole have been well-tolerated
adjustment of the omeprazole dose is not generally required. However, dose
adjustment should be considered in patients with severe hepatic impairment and if
long-term treatment is indicated.
Inducers of CYP2C19 and/or CYP3A4
Active substances known to induce CYP2C19 or CYP3A4 or both (such as rifampicin
and St John's wort) may lead to decreased omeprazole serum levels by increasing
omeprazole's rate of metabolism.
 

Pregnancy
Results from three prospective epidemiological studies (more than 1000 exposed
outcomes) indicate no adverse effects of omeprazole on pregnancy or on the health
of the foetus/newborn child. Omeprazole can be used during pregnancy.
Breastfeeding
Omeprazole is excreted in breast milk but is not likely to influence the child when
therapeutic doses are used.
Fertility
Animal studies with the racemic mixture omeprazole, given by oral administration do
not indicate effects with respect to fertility
 

Omeprex is not likely to affect the ability to drive or 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 machinery.
 

Summary of the safety profile
The most common side effects (1-10% of patients) are headache, abdominal pain,
constipation, diarrhoea, flatulence and nausea/vomiting.
Tabulated list of adverse reactions
The following adverse drug reactions have been identified or suspected in the clinical
trials programme for omeprazole and post-marketing. None was found to be doserelated. Adverse reactions listed below are classified according to frequency and
System Organ Class (SOC). Frequency categories are defined 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 < 1/1,000), Very rare (<
1/10,000), Not known (cannot be estimated from the available data).

Paediatric population
The safety of omeprazole has been assessed in a total of 310 children aged 0 to 16
years with acid-related disease. There are limited long term safety data from 46
children who received maintenance therapy of omeprazole during a clinical study for
severe erosive oesophagitis for up to 749 days. The adverse event profile was
generally the same as for adults in short- as well as in long-term treatment. There
are no long term data regarding the effects of omeprazole treatment on puberty and
growth.

There is limited information available on the effects of overdoses of omeprazole in
humans. In the literature, doses of up to 560 mg have been described, and
occasional reports have been received when single oral doses have reached up to
2,400 mg omeprazole (120 times the usual recommended clinical dose). Nausea,
vomiting, dizziness, abdominal pain, diarrhoea and headache have been reported.
Also apathy, depression and confusion have been described in single cases.
The symptoms described have been transient, and no serious outcome has been
reported. The rate of elimination was unchanged (first order kinetics) with increased
doses. Treatment, if needed, is symptomatic.
 

Pharmacotherapeutic group: Proton pump inhibitors, ATC code: A02BC01
Mechanism of action
Omeprazole, a racemic mixture of two enantiomers reduces gastric acid secretion
through a highly targeted mechanism of action. It is a specific inhibitor of the acid
pump in the parietal cell. It is rapidly acting and provides control through reversible
inhibition of gastric acid secretion with once daily dosing.
Omeprazole is a weak base and is concentrated and converted to the active form in
the highly acidic environment of the intracellular canaliculi within the parietal cell,
where it inhibits the enzyme H+ K+-ATPase - the acid pump. This effect on the final
step of the gastric acid formation process is dose-dependent and provides for highly
effective inhibition of both basal acid secretion and stimulated acid secretion,
irrespective of stimulus.
Pharmacodynamic effects
All pharmacodynamic effects observed can be explained by the effect of omeprazole
on acid secretion.
Effect on gastric acid secretion
Oral dosing with omeprazole once daily provides for rapid and effective inhibition of
daytime and night-time gastric acid secretion with maximum effect being achieved
within 4 days of treatment. With omeprazole 20 mg, a mean decrease of at least
80% in 24-hour intragastric acidity is then maintained in duodenal ulcer patients,
with the mean decrease in peak acid output after pentagastrin stimulation being
about 70% 24 hours after dosing.
Oral dosing with omeprazole 20 mg maintains an intragastric pH of 3 for a mean
time of 17 hours of the 24-hour period in duodenal ulcer patients.
As a consequence of reduced acid secretion and intragastric acidity, omeprazole
dose-dependently reduces/normalizes acid exposure of the oesophagus in patients
with gastro-oesophageal reflux disease.
The inhibition of acid secretion is related to the area under the plasma
concentration-time curve (AUC) of omeprazole and not to the actual plasma
concentration at a given time.
No tachyphylaxis has been observed during treatment with omeprazole.
Effect on H. pylori
H. pylori is associated with peptic ulcer disease, including duodenal and gastric ulcer
disease. H. pylori is a major factor in the development of gastritis. H. pylori together
with gastric acid are major factors in the development of peptic ulcer disease. H.
pylori is a major factor in the development of atrophic gastritis which is associated
with an increased risk of developing gastric cancer.
Eradication of H. pylori with omeprazole and antimicrobials is associated with, high
rates of healing and long-term remission of peptic ulcers.
Dual therapies have been tested and found to be less effective than triple therapies.
They could, however, be considered in cases where known hypersensitivity
precludes use of any triple combination.
Other effects related to acid inhibition
During long-term treatment gastric glandular cysts have been reported in a
somewhat increased frequency. These changes are a physiological consequence of
pronounced inhibition of acid secretion, are benign and appear to be reversible.
Decreased gastric acidity due to any means including proton pump inhibitors,
increases gastric counts of bacteria normally present in the gastrointestinal tract.
Treatment with acid-reducing drugs may lead to slightly increased risk of
gastrointestinal infections such as Salmonella and Campylobacter.
Chromogranin A (CgA) also increases due to decreased gastric acidity. This CgA
modifying effect cannot be demonstrated five days after stopping treatment with
PPIs. .
Paediatric use
In a non-controlled study in children (1 to 16 years of age) with severe reflux
oesophagitis, omeprazole at doses of 0.7 to 1.4 mg/kg improved oesophagitis level in
90% of the cases and significantly reduced reflux symptoms. In a single-blind study,
children aged 0–24 months with clinically diagnosed gastro-oesophageal reflux
disease were treated with 0.5, 1.0 or 1.5 mg omeprazole/kg. The frequency of
vomiting/regurgitation episodes decreased by 50% after 8 weeks of treatment
irrespective of the dose.
Eradication of H. pylori in children
A randomised, double blind clinical study (Héliot study) concluded that omeprazole
in combination with two antibiotics (amoxicillin and clarithromycin), was safe and
effective in the treatment of H. pylori infection in children age 4 years old and above
with gastritis: H. pylori eradication rate: 74.2% (23/31 patients) with omeprazole +
amoxicillin + clarithromycin versus 9.4% (3/32 patients) with amoxicillin +
clarithromycin. However, there was no evidence of any clinical benefit with respect
to dyspeptic symptoms. This study does not support any information for children
aged less than 4 years.
 

Absorption
Omeprazole and omeprazole magnesium are acid labile and are therefore
administered orally as enteric-coated granules in capsules or tablets. Absorption of
omeprazole is rapid, with peak plasma levels occurring approximately 1-2 hours after
dose. Absorption of omeprazole takes place in the small intestine and is usually
completed within 3-6 hours. Concomitant intake of food has no influence on the
bioavailability. The systemic availability (bioavailability) from a single oral dose of
omeprazole is approximately 40%. After repeated once-daily administration, the
bioavailability increases to about 60%.
Distribution
The apparent volume of distribution in healthy subjects is approximately 0.3 l/kg
body weight. Omeprazole is 97% plasma protein bound.
Metabolism
Omeprazole is completely metabolised by the cytochrome P450 system (CYP). The
major part of its metabolism is dependent on the polymorphically expressed
CYP2C19, responsible for the formation of hydroxyomeprazole, the major metabolite
in plasma. The remaining part is dependent on another specific isoform, CYP3A4,
responsible for the formation of omeprazole sulphone. As a consequence of high
affinity of omeprazole to CYP2C19, there is a potential for competitive inhibition and
metabolic drug-drug interactions with other substrates for CYP2C19. However, due
to low affinity to CYP3A4, omeprazole has no potential to inhibit the metabolism of
other CYP3A4 substrates. In addition, omeprazole lacks an inhibitory effect on the
main CYP enzymes.
Approximately 3% of the Caucasian population and 15-20% of Asian populations lack
a functional CYP2C19 enzyme and are called poor metabolisers. In such individuals
the metabolism of omeprazole is probably mainly catalysed by CYP3A4. After
repeated once-daily administration of 20 mg omeprazole, the mean AUC was 5 to 10
times higher in poor metabolisers than in subjects having a functional CYP2C19
enzyme (extensive metabolisers). Mean peak plasma concentrations were also
higher, by 3 to 5 times. These findings have no implications for the posology of
omeprazole.
Elemenation
The plasma elimination half-life of omeprazole is usually shorter than one hour both
after single and repeated oral once-daily dosing. Omeprazole is completely
eliminated from plasma between doses with no tendency for accumulation during
once-daily administration. Almost 80% of an oral dose of omeprazole is excreted as
metabolites in the urine, the remainder in the faeces, primarily originating from bile
secretion.
Linearity/non-linearity
The AUC of omeprazole increases with repeated administration. This increase is
dose-dependent and results in a non-linear dose-AUC relationship after repeated
administration. This time- and dose-dependency is due to a decrease of first pass
metabolism and systemic clearance probably caused by an inhibition of the CYP2C19
enzyme by omeprazole and/or its metabolites (e.g. the sulphone).
No metabolite has been found to have any effect on gastric acid secretion.
Special populations
Impaired hepatic function
The metabolism of omeprazole in patients with liver dysfunction is impaired,
resulting in an increased AUC. Omeprazole has not shown any tendency to
accumulate with once daily dosing.
Impaired renal function
The pharmacokinetics of omeprazole, including systemic bioavailability and
elimination rate, are unchanged in patients with reduced renal function.
Elderly
The metabolism rate of omeprazole is somewhat reduced in elderly subjects (75-79
years of age).
Paediatric patients
During treatment with the recommended doses to children from the age of 1 year,
similar plasma concentrations were obtained as compared to adults. In children
younger than 6 months, clearance of omeprazole is low due to low capacity to
metabolise omeprazole.
 

Gastric ECL-cell hyperplasia and carcinoids, have been observed in life-long studies in
rats treated with omeprazole. These changes are the result of sustained
hypergastrinaemia secondary to acid inhibition. Similar findings have been made
after treatment with H2-receptor antagonists, proton pump inhibitors and after
partial fundectomy. Thus, these changes are not from a direct effect of any individual
active substance.
 

Manitol, Lactose, Sucrose, Hydroxypropyl methyl Cellulose, Methacrylic acid
copolymer, Polyethylene glycol 6000, Empty Gelatin Capsule.
 

Not applicable.
 

Store below 25°C.
 

Forming Aluminum / Aluminum blister.
Packs of 14 or 28 Capsule
 

No special requirements.