REFLUXID DUO Pantoprazole Sodium / Domperidone 40mg / 30mg Sustained Release Capsule 1's
RXDRUG-DRP-6360-1pc
Discreet Packaging
FDA-registered Products
FDA-licensed Pharmacies
Indications/Uses
It is indicated in the symptomatic management of burning in various acid peptic disorders associated with nausea & vomiting; GERD, reflux esophagitis, non-ulcer dyspepsia, gastroparesis & idiopathic hiccup or any other peptic disease accompanied by nausea &/or vomiting.
Dosage/Direction for Use
1 cap daily before breakfast.
Duodenal ulcer: The recommended oral dose is 40 mg of pantoprazole & 30 mg of domperidone once daily.
Gastric ulcer: The recommended oral dose is 40 mg of pantoprazole & 30 mg of domperidone once daily for 4 to 8 weeks. In the case of a suspected gastric ulcer, malignancy of the gastric ulcer should be excluded, as treatment could conceal the symptoms and may delay diagnosis.
Reflux oesophagitis: The recommended oral dose is 40 mg of pantoprazole & 30 mg of domperidone once daily in the morning for 4 to 8 weeks.
Zollinger-Ellison Syndrome: For the management of Zollinger-Ellison Syndrome patients should start the treatment with a daily dose of 40 mg of pantoprazole & 30 mg of domperidone. Thereafter, the dose can be titrated up or down, as needed using measurements of gastric acid secretion as a guide.
Duodenal ulcer: The recommended oral dose is 40 mg of pantoprazole & 30 mg of domperidone once daily.
Gastric ulcer: The recommended oral dose is 40 mg of pantoprazole & 30 mg of domperidone once daily for 4 to 8 weeks. In the case of a suspected gastric ulcer, malignancy of the gastric ulcer should be excluded, as treatment could conceal the symptoms and may delay diagnosis.
Reflux oesophagitis: The recommended oral dose is 40 mg of pantoprazole & 30 mg of domperidone once daily in the morning for 4 to 8 weeks.
Zollinger-Ellison Syndrome: For the management of Zollinger-Ellison Syndrome patients should start the treatment with a daily dose of 40 mg of pantoprazole & 30 mg of domperidone. Thereafter, the dose can be titrated up or down, as needed using measurements of gastric acid secretion as a guide.
Administration
Should be taken on an empty stomach: Take before breakfast. Swallow whole, do not chew cap.
Contraindications
In patients with known hypersensitivity to pantoprazole or domperidone.
Warnings
Pantoprazole plus Domperidone shall be given with care to patients with renal dysfunction or hepatic dysfunction. Any other gastrointestinal disorders, any allergy and during pregnancy. Avoid prolonged usage of this medication. It may cause dizziness, do not drive a car or operate machinery while taking this medication.
Special Precautions
Not recommended for use in children, pregnancy and lactation. Dopamine-receptor- blocking agents elevate prolactin levels; the elevation persists during chronic administration. In the event that the patient develops galactorrhea and/or gynecomastia, withdrawal of the drug will result in alleviation of these symptoms.
Adverse Reactions
Headache, diarrhea, skin rash, pruritus & dizziness. Galactorrhea in females and gynecomastia in males. Dry mouth, thirst, nervousness, drowsiness, skin rashes and itching.
Drug Interactions
Pantoprazole: Pantoprazole is less likely than Omeprazole to interact with other drugs. The absorption of certain drugs may be affected by stomach acidity, and, as a result, pantoprazole and other PPI's that reduce stomach acid also reduce the absorption and concentration in blood of Ketoconazole and increase the absorption and concentration in blood of Digoxin. This may lead to reduced effectiveness of ketoconazole or increase digoxin toxicity, respectively.
Domperidone: The concomitant administration of anticholinergic drugs may compromise the beneficial effects of domperidone. Since domperidone enhances gastric and small intestinal motility, it may accelerate absorption of drugs from the small bowel while slowing absorption of drugs taken up from the stomach. Care should be exercised when Domperidone is administered in combination with MAO inhibitors. The concomitant administration of domperidone with antacids or H2 receptor blockers does not decrease the absorption of domperidone.
Domperidone: The concomitant administration of anticholinergic drugs may compromise the beneficial effects of domperidone. Since domperidone enhances gastric and small intestinal motility, it may accelerate absorption of drugs from the small bowel while slowing absorption of drugs taken up from the stomach. Care should be exercised when Domperidone is administered in combination with MAO inhibitors. The concomitant administration of domperidone with antacids or H2 receptor blockers does not decrease the absorption of domperidone.
Storage
Store at temperatures not exceeding 30°C and protect from light and moisture.
Shelf-Life: 24 Months.
Shelf-Life: 24 Months.
Action
Pharmacology: Mechanism of Action: Pantoprazole, a benzimidazole sulfoxide derived prodrug, is an irreversible proton-pump inhibitor. Pantoprazole, being a weak base, is highly ionized at low pH and readily accumulated in the highly acidic canalicular lumen of the stimulated parietal cell in the stomach. In this acidic environment, it is protonated and rapidly converted to a cationic cyclic sulfonamide. The sulfonamide binds covalently to cysteine residues on the luminal (acidic) surface of H+/K+-ATPase to form a mixed disulfide; thus causing irreversible inhibition of the gastric proton pump. This inhibition of the gastric proton pump or H+/K+-ATPase (which represents the final step in the secretory process), suppresses gastric acid secretion.
Domperidone, a benzimidazole derivative (structurally related to the butyrophenones), acts by selectively antagonizing the peripheral dopaminergic, receptors in the gastrointestinal wall, thereby enhancing gastrointestinal peristalsis and motility and increasing lower esophageal sphincter (LES) tone.
Rationale of Combination: The mode of action of both pantoprazole and domperidone are different and complimentary to each other. Upper gastrointestinal disorders are frequently associated with a combination of hyperacidity and dysmotility. As a result, acidic chyme may either stagnate in stomach and duodenum or may be evacuated by reverse peristalsis (vomiting or nausea). Reflux of acid contents of stomach cause erosions of lower part of esophagus which may further aggravate nausea and vomiting. Since both hyperacidity and dysmotility are present at the same time in disorders like gastroesophageal reflux disease (GERD) and nonulcer dyspepsia (NUD), a combination of drugs which will take care of both would be ideal. Pantoprazole is a potent gastric acid inhibitor that blocks the final stage of acid secretion. Hence, whatever may be the stimulus, hyperacidity will be controlled by pantoprazole. In contrast, domperidone increases gastrointestinal motility, thereby facilitating the movement of acid contents further down in the intestine preventing reflux esophagitis and thereby controlling nausea and vomiting. Hence, the pharmacology of pantoprazole and domperidone corroborates their use in combined form for the treatment of GERD, NUD and related disorders. Domperidone is usually administered at a dose of 10-20 mg, 2-3 times daily before meals. In order to enhance patient compliance, without compromising on its efficacy, domperidone SR is developed. Domperidone SR (30 mg) is for once-daily administration since its plasma t½ is otherwise 12-16 hrs.
Pharmacokinetics: Pantoprazole is rapidly absorbed after oral administration, with peak plasma concentrations (Cmax) of 1.1-3.1 (mean 2.1) mg/L occurring within 2-4 (mean 2.7) hrs (tmax) after ingestion of an enteric-coated 40 mg tablet. The volume of distribution is low (mean 0.16 L/kg at steady state) due to high degree of plasma protein-binding (-98%). Plasma pantoprazole concentrations decline monophasically after oral administration, with a mean plasma terminal t½ (ty,P) of 0.9-1.9 hrs. However, since inhibition of acid secretion is noncompetitive or irreversible, there is no correlation between plasma levels and the duration of action of pantoprazole. Concomitant intake of food has no influence on the bioavailability of pantoprazole and any possible retardant effect of food on the rate of drug absorption is not of clinical relevance, considering the prolonged antisecretory action of pantoprazole. The enteric coating does not influence the bioavailability of pantoprazole. Pantoprazole undergoes extensive hepatic metabolism via cytochrome P-450 oxidase followed by sulfate conjugation. Elimination of pantoprazole is predominantly renal, with -80% of an oral dose being excreted as urinary metabolite; the remainder is excreted in the feces and originates primary from biliary secretion.
Domperidone is rapidly and almost completely (93%) absorbed after oral administration. Peak plasma concentrations occur within 30 min after oral administration. The peak plasma concentration value after a 20-mg oral dose is in the range of 15-19 ng/mL. The mean elimination t½ ranges from 12-16 hrs for an oral dose. Oral bioavailability of domperidone is 13-17% because of extensive presystemic metabolism in gut wall and liver. Administration of domperidone 90 min after a meal increases bioavailability whereas cimetidine or alkali pretreatment reduces bioavailability. Domperidone is strongly bound to plasma proteins (90-93%). Domperidone undergoes extensive biotransformation with <1%excreted unchanged in urine.
Domperidone, a benzimidazole derivative (structurally related to the butyrophenones), acts by selectively antagonizing the peripheral dopaminergic, receptors in the gastrointestinal wall, thereby enhancing gastrointestinal peristalsis and motility and increasing lower esophageal sphincter (LES) tone.
Rationale of Combination: The mode of action of both pantoprazole and domperidone are different and complimentary to each other. Upper gastrointestinal disorders are frequently associated with a combination of hyperacidity and dysmotility. As a result, acidic chyme may either stagnate in stomach and duodenum or may be evacuated by reverse peristalsis (vomiting or nausea). Reflux of acid contents of stomach cause erosions of lower part of esophagus which may further aggravate nausea and vomiting. Since both hyperacidity and dysmotility are present at the same time in disorders like gastroesophageal reflux disease (GERD) and nonulcer dyspepsia (NUD), a combination of drugs which will take care of both would be ideal. Pantoprazole is a potent gastric acid inhibitor that blocks the final stage of acid secretion. Hence, whatever may be the stimulus, hyperacidity will be controlled by pantoprazole. In contrast, domperidone increases gastrointestinal motility, thereby facilitating the movement of acid contents further down in the intestine preventing reflux esophagitis and thereby controlling nausea and vomiting. Hence, the pharmacology of pantoprazole and domperidone corroborates their use in combined form for the treatment of GERD, NUD and related disorders. Domperidone is usually administered at a dose of 10-20 mg, 2-3 times daily before meals. In order to enhance patient compliance, without compromising on its efficacy, domperidone SR is developed. Domperidone SR (30 mg) is for once-daily administration since its plasma t½ is otherwise 12-16 hrs.
Pharmacokinetics: Pantoprazole is rapidly absorbed after oral administration, with peak plasma concentrations (Cmax) of 1.1-3.1 (mean 2.1) mg/L occurring within 2-4 (mean 2.7) hrs (tmax) after ingestion of an enteric-coated 40 mg tablet. The volume of distribution is low (mean 0.16 L/kg at steady state) due to high degree of plasma protein-binding (-98%). Plasma pantoprazole concentrations decline monophasically after oral administration, with a mean plasma terminal t½ (ty,P) of 0.9-1.9 hrs. However, since inhibition of acid secretion is noncompetitive or irreversible, there is no correlation between plasma levels and the duration of action of pantoprazole. Concomitant intake of food has no influence on the bioavailability of pantoprazole and any possible retardant effect of food on the rate of drug absorption is not of clinical relevance, considering the prolonged antisecretory action of pantoprazole. The enteric coating does not influence the bioavailability of pantoprazole. Pantoprazole undergoes extensive hepatic metabolism via cytochrome P-450 oxidase followed by sulfate conjugation. Elimination of pantoprazole is predominantly renal, with -80% of an oral dose being excreted as urinary metabolite; the remainder is excreted in the feces and originates primary from biliary secretion.
Domperidone is rapidly and almost completely (93%) absorbed after oral administration. Peak plasma concentrations occur within 30 min after oral administration. The peak plasma concentration value after a 20-mg oral dose is in the range of 15-19 ng/mL. The mean elimination t½ ranges from 12-16 hrs for an oral dose. Oral bioavailability of domperidone is 13-17% because of extensive presystemic metabolism in gut wall and liver. Administration of domperidone 90 min after a meal increases bioavailability whereas cimetidine or alkali pretreatment reduces bioavailability. Domperidone is strongly bound to plasma proteins (90-93%). Domperidone undergoes extensive biotransformation with <1%excreted unchanged in urine.
MedsGo Class
Antacids, Antireflux Agents & Antiulcerants
Features
Brand
Refluxid Duo
Full Details
Dosage Strength
40 mg / 30 mg
Drug Ingredients
- Domperidone
- Pantoprazole
Drug Packaging
Sustained Release Capsule 1's
Generic Name
Pantoprazole Sodium / Domperidone
Dosage Form
Sustained Release Capsule
Registration Number
DRP-6360
Drug Classification
Prescription Drug (RX)
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