Nexium Control is indicated for the short-term treatment of reflux symptoms (e.g. heartburn and acid regurgitation) in adults.

Posology The recommended dose is 20 mg esomeprazole (one tablet) per day. It might be necessary to take the tablets for 2-3 consecutive days to achieve improvement of symptoms. The duration of treatment is up to 2 weeks. Once complete relief of symptoms has occurred, treatment should be discontinued. If symptoms worsen or if no symptom relief is obtained within 2 weeks of continuous treatment, the patient should be instructed to consult a doctor. If a dose is forgotten, it should be taken as soon as possible on the same day. A double dose should not be taken to make up for a forgotten dose. For oral administration only. Not recommended for use in children and adolescents under 18 years of age. Special populations Patients with renal impairment Dose adjustment is not required in patients with impaired renal function. Due to limited experience in patients with severe renal insufficiency, such patients should be treated with caution (see section 5.2). Patients with hepatic impairment Dose adjustment is not required in patients with mild to moderate liver impairment. However, patients with severe liver impairment should be advised by a doctor before taking Nexium Control (see sections 4.4 and 5.2). Elderly patients (=65 years old) Dose adjustment is not required in elderly patients. Paediatric population There is no relevant use of Nexium Control in the paediatric population below 18 years of age for the indication of “short-term treatment of reflux symptoms (e.g., heartburn and acid regurgitation)”. Method of administration The tablets should be swallowed whole with half a glass of water. The tablets must not be chewed or crushed. Alternatively, the tablet can be dispersed in half a glass of non-carbonated water. No other liquids should be used as the enteric coating may be dissolved. The water should be stirred until the tablet disintegrates. The liquid with the pellets should be drunk immediately or within 30 minutes. The glass should be rinsed with half a glass of water and the water drunk. The pellets should not be chewed or crushed.

Hypersensitivity to the active substance, substituted benzimidazoles or to any of the excipients listed in section 6.1. Esomeprazole must not be used concomitantly with nelfinavir or rilpivirine (oral formulations) (see section 4.5).

General Patients should be instructed to consult a doctor if: • They have significant unintentional weight loss, recurrent vomiting, dysphagia, haematemesis or melaena and when gastric ulcer is suspected or present, malignancy should be excluded as treatment with esomeprazole may alleviate symptoms and delay diagnosis. • They have had previous gastric ulcer or gastrointestinal surgery. • They have been on continuous symptomatic treatment of indigestion or heartburn for 4 or more weeks. This may be a sign of a more serious condition. • They have jaundice or severe liver disease. • They are aged over 55 years with new or recently changed symptoms. • They have frequent wheezing, particularly with heartburn. Patients with long-term recurrent symptoms of indigestion or heartburn should see their doctor at regular intervals. Patients over 55 years taking any non-prescription indigestion or heartburn remedy on a daily basis should inform their pharmacist or doctor. Patients should not take Nexium Control as a long term preventive medicinal product. Treatment with proton pump inhibitors (PPIs) may lead to a slightly increased risk of gastrointestinal infections such as Salmonella and Campylobacter and in hospitalised patients, also possibly Clostridium difficile (see section 5.1). Patients should consult their doctor before taking this medicinal product if they are due to have an endoscopy or urea breath test. Combination with other medicinal products Co-administration of esomeprazole with atazanavir is not recommended (see section 4.5). If the combination of atazanavir with a PPI is judged unavoidable, close clinical monitoring is recommended in combination with an increase in the dose of atazanavir to 400 mg with 100 mg of ritonavir. Esomeprazole 20 mg should not be exceeded. Esomeprazole is a CYP2C19 inhibitor. When starting or ending treatment with esomeprazole, the potential for

Pregnancy A moderate amount of data on pregnant women (between 300-1,000 pregnancy outcomes) indicate no malformative or feto/ neonatal toxicity of esomeprazole. Animal studies do not indicate direct or indirect harmful effects with respect to reproductive toxicity (see section 5.3). As a precautionary measure, it is preferable to avoid the use of Nexium Control during pregnancy. Breast-feeding Limited information indicates that maternal doses of esomeprazole produce low levels in breast milk. There is insufficient information on the effects of esomeprazole in newborns/infants. Esomeprazole should not be used during breast-feeding. Fertility Animal studies with the racemic mixture omeprazole, given by oral administration do not indicate effects with respect to fertility.

Esomeprazole has minor influence on the ability to drive or use machines. Adverse reactions such as dizziness and visual disturbances are uncommon (see section 4.8). If affected, patients should not drive or use machines.

Summary of the safety profile Headache, abdominal pain, diarrhoea and nausea are among those adverse reactions that have been most commonly reported in clinical studies (and also from post-marketing use). In addition, the safety profile is similar for different formulations, treatment indications, age groups and patient populations. No dose-related adverse reactions have been identified. Tabulated list of adverse reactions The following adverse reactions have been identified or suspected in the clinical studies programme for esomeprazole and post-marketing. The reactions are classified according to MedDRA frequency 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). Common Uncommon Rare Very rare Not known Blood and lymphatic system disorders leukopenia, thrombocytope -nia agranulocytosi s, pancytopenia Immune system disorders hypersensitivit y reactions e.g. fever, angioedema and anaphylactic reaction/shock Common Uncommon Rare Very rare Not known Metabolism and nutrition disorders peripheral oedema hyponatraemia hypomagne -saemia; severe hypomagne -saemia can correlate with hypocalcae- mia; hypomagne -saemia may also result in hypokalae m-ia Psychiatric disorders insomnia agitation, confusion, depression aggression, hallucinations Nervous system disorders headache dizziness, paraesthesi a, somnolence taste disturbance Eye disorders blurred vision Ear and labyrinth disorders vertigo Respiratory, thoracic and mediastinal disorders bronchospasm Gastrointestinal disorders abdominal pain, constipa- tion, diarrhoea, flatulence, nausea/ vomiting, fundic gland polyps (benign) dry mouth stomatitis, gastrointestina l candidiasis microscopi c colitis Common Uncommon Rare Very rare Not known Hepatobiliary disorders increased liver enzymes hepatitis with or without jaundice hepatic failure, hepatic encephalopath y in patients with pre- existing liver disease Skin and subcutaneous tissue disorders dermatitis, pruritus, rash urticaria alopecia, photosensitivit y erythema multiforme, Stevens- Johnson syndrome, toxic epidermal necrolysis (TEN), Drug reaction with eosinophilia and systemic symptoms (DRESS) Subacute cutaneous lupus erythematos us (see section 4.4). Musculoskeleta l and connective tissue disorders arthralgia, myalgia muscular weakness Renal and urinary disorders Interstitial nephritis Reproductive system and breast disorders gynaecomastia General disorders and administration site disorders malaise, increased sweating 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 via the Yellow Card Scheme at www.mhra.gov.uk/yellowcard or search for MHRA Yellow Card in the Google Play or Apple App Store.

There is very limited experience to date with deliberate . The symptoms described in connection with 280 mg esomeprazole were gastrointestinal symptoms and weakness. Single doses of 80 mg esomeprazole were uneventful. No specific antidote is known. Esomeprazole is extensively plasma protein bound and is therefore not readily dialysable. Treatment should be symptomatic and general supportive measures should be utilised.

Pharmacotherapeutic group: Drugs for acid related disorders, proton pump inhibitors, ATC code: A02BC05. Esomeprazole is the S-isomer of omeprazole and reduces gastric acid secretion through a specific targeted mechanism of action. It is a specific inhibitor of the acid pump in the parietal cell. Both the R- and S-isomer of omeprazole have similar pharmacodynamic activity. Mechanism of action Esomeprazole is a weak base and is concentrated and converted to the active form in the highly acidic environment of the secretory canaliculi of the parietal cell, where it inhibits the enzyme H+K+-ATPase (the acid pump) and inhibits both basal and stimulated acid secretion. Pharmacodynamic effects After oral dosing with esomeprazole 20 mg and 40 mg the onset of effect occurs within one hour. After repeated administration with 20 mg esomeprazole once daily for five days, mean peak acid output after pentagastrin stimulation is decreased 90% when measured 6-7 hours after dosing on day five. After five days of oral dosing with 20 mg and 40 mg of esomeprazole, intragastric pH above 4 was maintained for a mean time of 13 hours and 17 hours, respectively over 24 hours in symptomatic gastroesophageal reflux disease (GERD) patients. The proportion of patients maintaining an intragastric pH above 4 for at least 8, 12 and 16 hours respectively were for esomeprazole 20 mg 76%, 54% and 24%. Corresponding proportions for esomeprazole 40 mg were 97%, 92% and 56%. Using AUC as a surrogate parameter for plasma concentration, a relationship between inhibition of acid secretion and exposure has been shown. 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. An increased number of ECL cells possibly related to the increased serum gastrin levels, have been observed in some patients during long-term treatment with esomeprazole. Decreased gastric acidity due to any means including PPIs, increases gastric counts of bacteria normally present in the gastrointestinal tract. Treatment with PPIs may lead to slightly increased risk of gastrointestinal infections such as Salmonella and Campylobacter and in hospitalised patients, also possibly Clostridium difficile. Clinical efficacy Esomeprazole 20 mg has been demonstrated to effectively treat frequent heartburn in subjects receiving one dose per 24 hours over 2 weeks. In two multicenter, randomized, double-blind, placebo-controlled pivotal studies 234 subjects with a recent history of frequent heartburn were treated with 20 mg esomeprazole for 4 weeks. Symptoms associated with acid reflux (such as heartburn and acid regurgitation) were evaluated retrospectively over a 24 hour period. In both studies esomeprazole 20 mg was significantly better compared to placebo for the primary endpoint, complete resolution of heartburn, defined as no heartburn episodes during the last 7 days prior to the final visit (33.9% - 41.6% vs. placebo 11.9 – 13.7%, (p<0.001). The secondary endpoint of complete resolution of heartburn, defined as no heartburn on the patient’s diary card for 7 consecutive days, was statistically significant at both week 1 (10.0% - 15.2% vs placebo 0.9% - 2.4%, p = 0.014, p<0.001) and week 2 (25.2% - 35.7% vs placebo 3.4% - 9.0%, p<0.001). Other secondary endpoints were supportive of the primary endpoint, including relief of heartburn at week 1 and week 2, percentage of 24 hour days without heartburn at week 1 and week 2, mean heartburn severity at week 1 and week 2, and time to initial and sustained resolution of heartburn over a 24 hour period and during the night compared to placebo. Approximately 78% of the subjects on 20 mg esomeprazole reported first resolution of heartburn within the first week of treatment compared to 52 – 58% for placebo. Time to sustained resolution of heartburn, defined as when 7 consecutive days of no heartburn was first recorded, was significantly shorter in the esomeprazole 20 mg group (39.7% - 48.7% by day 14 vs placebo 11.0% - 20.2%). The median time to first resolution of night-time heartburn was 1 day, statistically significant compared to placebo in one study (p=0.048) and approaching significance in the other (p=0.069). About 80% of nights were heartburn free during all time periods and 90% of nights were heartburn free by week 2 of each clinical study, compared to 72.4 – 78.3% for placebo. The investigators’ assessments of heartburn resolution were consistent with the subjects’ assessments, showing statistically significant differences between esomeprazole (34.7% - 41.8%) compared to placebo (8.0% - 11.4%). The investigators also found esomeprazole to be significantly more effective than placebo in resolving acid regurgitation (58.5% - 63.6% vs placebo 28.3% - 37.4%) during the week 2 evaluation. Following Overall Treatment Evaluation (OTE) of patients at week 2, 78.0-80.7% of patients on esomeprazole 20 mg, compared to 72.4 – 78.3% for placebo, reported their condition as improved. The majority of these rated the importance of this change to be Important to Extremely Important in performing their activities of daily living (79 - 86% at week 2).

Absorption Esomeprazole is acid labile and is administered orally as enteric-coated granules. In vivo conversion to the R-isomer is negligible. Absorption of esomeprazole is rapid, with peak plasma levels occurring approximately 1-2 hours after dose. The absolute bioavailability is 64% after a single dose of 40 mg and increases to 89% after repeated once-daily administration. For 20 mg esomeprazole the corresponding values are 50% and 68% respectively. Food intake both delays and decreases the absorption of esomeprazole although this has no significant influence on the effect of esomeprazole on intragastric acidity. Distribution The apparent volume of distribution at steady state in healthy subjects is approximately 0.22 l/kg body weight. Esomeprazole is 97% plasma protein bound. Biotransformation Esomeprazole is completely metabolised by the cytochrome P450 system (CYP). The major part of the metabolism of esomeprazole is dependent on the polymorphic CYP2C19, responsible for the formation of the hydroxy- and desmethyl metabolites of esomeprazole. The remaining part is dependent on another specific isoform, CYP3A4, responsible for the formation of esomeprazole sulphone, the main metabolite in plasma. Elimination The parameters below reflect mainly the pharmacokinetics in individuals with a functional CYP2C19 enzyme, extensive metabolisers. Total plasma clearance is about 17 l/h after a single dose and about 9 l/h after repeated administration. The plasma elimination half-life is about 1.3 hours after repeated once-daily dosing. Esomeprazole is completely eliminated from plasma between doses with no tendency for accumulation during once-daily administration. The major metabolites of esomeprazole have no effect on gastric acid secretion. Almost 80% of an oral dose of esomeprazole is excreted as metabolites in the urine, the remainder in the faeces. Less than 1% of the parent compound is found in urine. Linearity/non-linearity The pharmacokinetics of esomeprazole has been studied in doses up to 40 mg b.i.d. The area under the plasma concentration-time curve increases with repeated administration of esomeprazole. This increase is dose-dependent and results in a more than dose proportional increase in AUC 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 esomeprazole and/or its sulphone metabolite. Special patient populations Poor metabolisers Approximately 2.9±1.5% of the population lack a functional CYP2C19 enzyme and are called poor metabolisers. In these individuals the metabolism of esomeprazole is probably mainly catalysed by CYP3A4. After repeated once-daily administration of 40 mg esomeprazole, the mean area under the plasma concentration-time curve was approximately 100% higher in poor metabolisers than in subjects having a functional CYP2C19 enzyme (extensive metabolisers). Mean peak plasma concentrations were 60% higher. These findings have no implications for the posology of esomeprazole. Gender Following a single dose of 40 mg esomeprazole the mean are under the plasma concentration-time curve is approximately 30% higher in females than in males. No gender difference is seen after repeated once-daily administration. These findings have no implications for the posology of esomeprazole. Hepatic impairment The metabolism of esomeprazole in patients with mild to moderate liver dysfunction may be impaired. The metabolic rate is decreased in patients with severe liver dysfunction resulting in a doubling of the area under the plasma concentration-time curve of esomeprazole. Therefore, a maximum of 20 mg should not be exceeded in patients with severe dysfunction. Esomeprazole or its major metabolites do not show any tendency to accumulate with once-daily dosing. Renal impairment No studies have been performed in patients with decreased renal function. Since the kidney is responsible for the excretion of the metabolites of esomeprazole but not for the elimination of the parent compound, the metabolism of esomeprazole is not expected to be changed in patients with impaired renal function. Elderly patients (=65 years old) The metabolism of esomeprazole is not significantly changed in elderly patients (71-80 years of age).

Non-clinical data reveal no particular hazard for humans based on conventional studies of safety pharmacology, repeated dose toxicity, genotoxicity, and toxicity to reproduction and development. Adverse reactions not observed in clinical studies, but seen in animals at exposure levels similar to clinical exposure levels and with possible relevance to clinical use were as follows: Carcinogenicity studies in the rat with the racemic mixture have shown gastric ECL-cell hyperplasia and carcinoids. These gastric effects in the rat are the result of sustained, pronounced hypergastrinaemia secondary to reduced production of gastric acid and are observed after long-term treatment in the rat with inhibitors of gastric acid secretion.

Glycerol monostearate 40-55 Hydroxypropylcellulose Hypromellose 2910 (6 mPa·s) Reddish-brown iron oxide (E172) Yellow iron oxide (E172) Magnesium stearate Methacrylic acid ethylacrylate copolymer (1:1) dispersion 30 per cent Cellulose microcrystalline Synthetic Paraffin Macrogol 6000 Polysorbate 80 Crospovidone (Type A) Sodium stearyl fumarate Sugar spheres (sucrose and maize starch) Talc Titanium dioxide (E171) Triethyl citrate

Not Applicable

3 Years

Do not store above 30°C Store in the original package in order to protect from moisture. Keep out of reach and sight of children.

Aluminium blister. Pack size of 28 gastro-resistant tablets.

No special requirements

Feb. 5, 2026

spc-doc_PLGB 44673-0225.pdf

Bulk SPC upload Feb2026