RAPEED Rabeprazole Sodium 20mg Enteric-Coated Tablet 1's
RXDRUG-DRP-5595-1pc
Discreet Packaging
FDA-registered Products
FDA-licensed Pharmacies
Indications/Uses
EC tab: Rabeprazole Sodium tablets are indicated for the treatment of: Active duodenal ulcer, active benign gastric ulcer, symptomatic erosive or ulcerative gastro-oesophageal reflux disease (GORD).
H. Pylori-positive duodenal ulcers, as part of the eradication programme with appropriate antibiotics.
Maintenance treatment of healed erosive or ulcerative GORD.
Inj: For the treatment of severe (erosive or ulcerative) gastro-oesophageal reflux diseases, active peptic ulcer disease and Zollinger-Ellison syndrome.
H. Pylori-positive duodenal ulcers, as part of the eradication programme with appropriate antibiotics.
Maintenance treatment of healed erosive or ulcerative GORD.
Inj: For the treatment of severe (erosive or ulcerative) gastro-oesophageal reflux diseases, active peptic ulcer disease and Zollinger-Ellison syndrome.
Dosage/Direction for Use
EC tab: Active Duodenal Ulcer and Active Benign Gastric Ulcer: 20 mg to be taken once daily in the morning.
Most patients with active duodenal ulcer heal within four weeks. However 2% of patients may require an additional four weeks of therapy to achieve healing.
Some patients with active duodenal ulcer may respond to one 10 mg tablet to be taken once daily in the morning.
Most patients with active benign gastric ulcer heal within six weeks. However 9% of patients, may require an additional six weeks of therapy to achieve healing.
Erosive or Ulcerative Gastro-Oesophageal Reflux Disease (GORD): 20 mg to be taken once daily for four to eight weeks.
Gastro-Oesophageal Reflux Long-term Management (GORD Maintenance): For longterm management up to 12 months, a maintenance dose of Rabeprazole Sodium 10 mg or 20 mg once daily can be used. Some patients may respond to a maintenance dose of 10 mg/day.
Eradication of H. Pylori: Rabeprazole Sodium is indicated for H. Pylori-positive duodenal ulcers, as part of the eradication programme with appropriate antibiotics.
Rabeprazole Sodium tablets should be taken in the morning, before eating; and although neither the time of day nor food intake was shown to have any effect on rabeprazole sodium activity, this regimen will facilitate treatment compliance.
Patients should be cautioned that the Rabeprazole Sodium tablets should not be chewed or crushed, but should be swallowed whole.
Rabeprazole Sodium tablets should be used within 3 months of first opening the aluminium pouch container.
Renal and hepatic impairment: No dosage adjustment is necessary for patients with renal or hepatic impairment.
Caution is however advised when Rabeprazole Sodium is first initiated in patients with severe hepatic dysfunction, refer Precautions.
Children: Rabeprazole Sodium is not recommended for use in children, as there is no experience of its use in this group.
Inj: Adult: 10-20 mg/day I.V.
Duodenal ulcer: 20 mg/day I.V. for 1 month.
Benign Gastric ulcer: 20 mg/day I.V. for 6 weeks.
Zollinger-Ellison syndrome: Initial dose: 60 mg/day I.V.
Erosive Gastroesophageal reflux disease: 20 mg/day I.V. for 1-2 months.
Gastroesophageal reflux disease long term management: 10-20 mg I.V.
Children: not recommended.
Or as prescribed by the physician.
Most patients with active duodenal ulcer heal within four weeks. However 2% of patients may require an additional four weeks of therapy to achieve healing.
Some patients with active duodenal ulcer may respond to one 10 mg tablet to be taken once daily in the morning.
Most patients with active benign gastric ulcer heal within six weeks. However 9% of patients, may require an additional six weeks of therapy to achieve healing.
Erosive or Ulcerative Gastro-Oesophageal Reflux Disease (GORD): 20 mg to be taken once daily for four to eight weeks.
Gastro-Oesophageal Reflux Long-term Management (GORD Maintenance): For longterm management up to 12 months, a maintenance dose of Rabeprazole Sodium 10 mg or 20 mg once daily can be used. Some patients may respond to a maintenance dose of 10 mg/day.
Eradication of H. Pylori: Rabeprazole Sodium is indicated for H. Pylori-positive duodenal ulcers, as part of the eradication programme with appropriate antibiotics.
Rabeprazole Sodium tablets should be taken in the morning, before eating; and although neither the time of day nor food intake was shown to have any effect on rabeprazole sodium activity, this regimen will facilitate treatment compliance.
Patients should be cautioned that the Rabeprazole Sodium tablets should not be chewed or crushed, but should be swallowed whole.
Rabeprazole Sodium tablets should be used within 3 months of first opening the aluminium pouch container.
Renal and hepatic impairment: No dosage adjustment is necessary for patients with renal or hepatic impairment.
Caution is however advised when Rabeprazole Sodium is first initiated in patients with severe hepatic dysfunction, refer Precautions.
Children: Rabeprazole Sodium is not recommended for use in children, as there is no experience of its use in this group.
Inj: Adult: 10-20 mg/day I.V.
Duodenal ulcer: 20 mg/day I.V. for 1 month.
Benign Gastric ulcer: 20 mg/day I.V. for 6 weeks.
Zollinger-Ellison syndrome: Initial dose: 60 mg/day I.V.
Erosive Gastroesophageal reflux disease: 20 mg/day I.V. for 1-2 months.
Gastroesophageal reflux disease long term management: 10-20 mg I.V.
Children: not recommended.
Or as prescribed by the physician.
Overdosage
Experience to date with deliberate or accidental overdose is limited. The maximum established exposure has not exceeded 60 mg twice daily, or 160 mg once daily. Effects are generally minimal, representative of the known adverse event profile and reversible without further medical intervention. No specific antidote is known. Rabeprazole sodium is extensively protein bound and is, therefore, not dialysable. As in any case of overdose, treatment should be symptomatic and general supportive measures should be utilised.
Administration
May be taken with or without food: EC tab: Best taken in the morning before meals. Swallow whole, do not chew/crush.
Contraindications
Rabeprazole is contraindicated in patients with known hypersensitivity to rabeprazole, substituted benzimidazoles or to any component of the formulation.
Special Precautions
EC tab: Symptomatic response to therapy with rabeprazole sodium does not preclude the presence of gastric or oesophageal malignancy, therefore the possibility of malignancy should be excluded prior to commencing treatment with Rabeprazole 20 mg Delayed-release Tablets.
Patients on long-term treatment (particularly those treated for more than a year) should be kept under regular surveillance.
A risk of cross-hypersensitivity reactions with other proton pump inhibitor or substituted benzimidazoles cannot be excluded.
Patients should be cautioned that Rabeprazole 20 mg Delayed-release Tablets should not be chewed or crushed, but should be swallowed whole.
Paediatric population: Rabeprazole 20 mg Delayed-release Tablets is not recommended for use in children due to a lack of data on safety and efficacy.
There have been post marketing reports of blood dyscrasias (thrombocytopenia and neutropenia). In the majority of cases where an alternative aetiology cannot be identified, the events were uncomplicated and resolved on discontinuation of rabeprazole.
Hepatic enzyme abnormalities have been seen in clinical trials and have also been reported since market authorisation. In the majority of cases where an alternative aetiology cannot be identified, the events were uncomplicated and resolved on discontinuation of rabeprazole.
No evidence of significant drug related safety problems was seen in a study of patients with mild to moderate hepatic impairment versus normal age and sex matched controls. However because there are no clinical data on the use of rabeprazole in the treatment of patients with severe hepatic dysfunction the prescriber is advised to exercise caution when treatment with Rabeprazole 20mg Delayed-release Tablets is first initiated in such patients.
Co-administration of atazanavir with rabeprazole is not recommended.
Treatment with proton pump inhibitors, including rabeprazole, may possibly increase the risk of gastrointestinal infections such as Salmonella, Campylobacter and Clostridium difficile.
Hypomagnesaemia: Severe hypomagnesaemia has been reported in patients treated with PPIs like rabeprazole 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), health care 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.
Use in children: The safety and effectiveness of Rabeprazole in pediatric patients have not been established.
Inj: Special precautions are to be exercised specifically in the event of Hepatic Impairment, monitor gastric malignancy.
Patients on long-term treatment (particularly those treated for more than a year) should be kept under regular surveillance.
A risk of cross-hypersensitivity reactions with other proton pump inhibitor or substituted benzimidazoles cannot be excluded.
Patients should be cautioned that Rabeprazole 20 mg Delayed-release Tablets should not be chewed or crushed, but should be swallowed whole.
Paediatric population: Rabeprazole 20 mg Delayed-release Tablets is not recommended for use in children due to a lack of data on safety and efficacy.
There have been post marketing reports of blood dyscrasias (thrombocytopenia and neutropenia). In the majority of cases where an alternative aetiology cannot be identified, the events were uncomplicated and resolved on discontinuation of rabeprazole.
Hepatic enzyme abnormalities have been seen in clinical trials and have also been reported since market authorisation. In the majority of cases where an alternative aetiology cannot be identified, the events were uncomplicated and resolved on discontinuation of rabeprazole.
No evidence of significant drug related safety problems was seen in a study of patients with mild to moderate hepatic impairment versus normal age and sex matched controls. However because there are no clinical data on the use of rabeprazole in the treatment of patients with severe hepatic dysfunction the prescriber is advised to exercise caution when treatment with Rabeprazole 20mg Delayed-release Tablets is first initiated in such patients.
Co-administration of atazanavir with rabeprazole is not recommended.
Treatment with proton pump inhibitors, including rabeprazole, may possibly increase the risk of gastrointestinal infections such as Salmonella, Campylobacter and Clostridium difficile.
Hypomagnesaemia: Severe hypomagnesaemia has been reported in patients treated with PPIs like rabeprazole 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), health care 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.
Use in children: The safety and effectiveness of Rabeprazole in pediatric patients have not been established.
Inj: Special precautions are to be exercised specifically in the event of Hepatic Impairment, monitor gastric malignancy.
Use In Pregnancy & Lactation
Pregnancy: There are no data on the safety of rabeprazole in human pregnancy. Reproduction studies performed in rats and rabbits have revealed no evidence of impaired fertility or harm to the foetus due to rabeprazole sodium, although low foeto-placental transfer occurs in rats.
Rabeprazole 20 mg Delayed-release Tablets is contraindicated during pregnancy.
Breastfeeding: It is not known whether rabeprazole sodium is excreted in human breast milk. No studies in lactating women have been performed. Rabeprazole sodium is however excreted in rat mammary secretions. Therefore Rabeprazole 20 mg Delayed-release Tablets must not be used during breast feeding.
Rabeprazole 20 mg Delayed-release Tablets is contraindicated during pregnancy.
Breastfeeding: It is not known whether rabeprazole sodium is excreted in human breast milk. No studies in lactating women have been performed. Rabeprazole sodium is however excreted in rat mammary secretions. Therefore Rabeprazole 20 mg Delayed-release Tablets must not be used during breast feeding.
Adverse Reactions
EC tab: The most common adverse events were headache, diarrhoea and nausea. Other adverse events were rhinitis, abdominal pain, asthenia, flatulence, pharyngitis, vomiting, non-specific pain/back pain, dizziness, flu syndrome, infection, cough, constipation and insomnia. Further less frequent adverse events were rash, myalgia, chest pain, dry mouth, dyspepsia, nervousness, somnolence, bronchitis, sinusitis, chills, eruction, leg cramps, urinary tract infection, arthralgia and fever.
In isolated cases, anorexia, gastritis, weight gain, depression, pruritus, vision or taste disturbances, stomatitis, sweating and leucocytosis have been observed.
Increased hepatic enzymes have been observed in 2% of patients.
There have been reports of thrombocytopenia, neutropenia and leukopenia.
Inj: Most common adverse effects observed with rabeprazole are Diarrhea, Nausea, Headache, Vomiting, Abdominal pain, Dizziness, Flatulence, Constipation, Dyspepsia, Flu like syndrome, Insomnia, Back pain, Cough, Rhinitis, Pharyngitis and Rash.
In isolated cases, anorexia, gastritis, weight gain, depression, pruritus, vision or taste disturbances, stomatitis, sweating and leucocytosis have been observed.
Increased hepatic enzymes have been observed in 2% of patients.
There have been reports of thrombocytopenia, neutropenia and leukopenia.
Inj: Most common adverse effects observed with rabeprazole are Diarrhea, Nausea, Headache, Vomiting, Abdominal pain, Dizziness, Flatulence, Constipation, Dyspepsia, Flu like syndrome, Insomnia, Back pain, Cough, Rhinitis, Pharyngitis and Rash.
Drug Interactions
EC tab: Rabeprazole sodium produces a profound and long lasting inhibition of gastric acid secretion. An interaction with compounds whose absorption is pH dependent may occur. Co-administration of rabeprazole sodium with ketoconazole or itraconazole may result in a significant decrease in antifungal plasma levels. Therefore individual patients may need to be monitored to determine if a dosage adjustment is necessary when ketoconazole or itraconazole are taken concomitantly with Rabeprazole.
In clinical trials, antacids were used concomitantly with the administration of Rabeprazole and, in a specific drug-drug interaction study, no interaction with liquid antacids was observed.
Co-administration of atazanavir 300 mg/ritonavir 100 mg with omeprazole (40 mg once daily) or atazanavir 400 mg with lansoprazole (60 mg once daily) to healthy volunteers resulted in a substantial reduction in atazanavir exposure. The absorption of atazanavir is pH dependent. Although not studied, similar results are expected with other proton pump inhibitors. Therefore PPIs, including rabeprazole, should not be co-administered with atazanavir.
Methotrexate: Case reports, published population pharmacokinetic studies, and retrospective analyses suggest that concomitant administration of PPIs and methotrexate (primarily at high dose; see methotrexate prescribing a information) may elevate and prolong serum levels of methotrexate and/or its metabolite hydroxymethotrexate. However, no formal drug interaction studies of methotrexate with PPIs have been conducted.
Inj: Patients receiving proton pump inhibitors, including rabeprazole and warfarin concomitantly may lead to abnormal bleeding and even death because of increases in INR and prothrombin time. Co-administration of rabeprazole sodium results in a 33% decrease in ketoconazole levels. Rabeprazole-Digoxin co-administration results in increased trough digoxin levels in normal subjects.
In clinical trials, antacids were used concomitantly with the administration of Rabeprazole and, in a specific drug-drug interaction study, no interaction with liquid antacids was observed.
Co-administration of atazanavir 300 mg/ritonavir 100 mg with omeprazole (40 mg once daily) or atazanavir 400 mg with lansoprazole (60 mg once daily) to healthy volunteers resulted in a substantial reduction in atazanavir exposure. The absorption of atazanavir is pH dependent. Although not studied, similar results are expected with other proton pump inhibitors. Therefore PPIs, including rabeprazole, should not be co-administered with atazanavir.
Methotrexate: Case reports, published population pharmacokinetic studies, and retrospective analyses suggest that concomitant administration of PPIs and methotrexate (primarily at high dose; see methotrexate prescribing a information) may elevate and prolong serum levels of methotrexate and/or its metabolite hydroxymethotrexate. However, no formal drug interaction studies of methotrexate with PPIs have been conducted.
Inj: Patients receiving proton pump inhibitors, including rabeprazole and warfarin concomitantly may lead to abnormal bleeding and even death because of increases in INR and prothrombin time. Co-administration of rabeprazole sodium results in a 33% decrease in ketoconazole levels. Rabeprazole-Digoxin co-administration results in increased trough digoxin levels in normal subjects.
Caution For Usage
Inj: Direction for Reconstitution: Dissolve the contents in 5 mL of Water for Injection USP. The reconstituted solution is stable up to 4 hrs at 25°C. Discard the unused portion.
Not to be used if reconstituted solution contains visible solid particles.
Not to be used if reconstituted solution contains visible solid particles.
Storage
EC tab: Store at temperatures not exceeding 30°C. Store in a dry place and protect from light.
Action
Pharmacology: Inj: Rabeprazole sodium is a proton pump inhibitor. It is a prodrug. After administration it diffuses in to the parietal cell of the stomach and accumulates in the secretory canaliculi. In the acidic medium Rabeprazole is converted to sulfenamide. This sulfenamide covalently interacts with sulfhydryl (SH) group in the proton pump (H+ K+ATPase) and inhibits the exchange of extracellular K+ for intracellular H+ion. Rabeprazole produces fastest acid suppression and helps in mucin synthesis.
EC tab: Pharmacodynamics: Mechanism of Action: Rabeprazole sodium belongs to the class of antisecretory compounds, the substituted benzimidazoles, that do not exhibit anticholinergic or H2 histamine antagonist properties, but suppress gastric acid secretion by the specific inhibition of the H+/K+-ATPase enzyme at the secretory surface of the gastric parietal cell. This enzyme system is regarded as the acid (proton) pump, and therefore rabeprazole sodium is classified as a gastric proton-pump inhibitor blocking the final step of acid production. This effect is dose-related and leads to inhibition of both basal and stimulated acid secretion irrespective of the stimulus. Animal studies indicate that after administration, rabeprazole sodium rapidly disappears from both the plasma and gastric mucosa.
Anti-secretory Activity: After oral administration of a 20 mg dose of rabeprazole sodium the onset of the anti-secretory effect occurs within one hour with the maximum effect occurring within two to four hours. Inhibition of basal and food stimulated acid secretion 23 hours after the first dose of rabeprazole sodium are 69% and 82% respectively and the duration of inhibition lasts up to 48 hours. This duration of pharmacodynamic action is much longer than the pharmacokinetic half life (approximately one hour) would predict. This effect is probably due to the prolonged binding to the parietal H+/K+-ATPase enzyme. The inhibitory effect of rabeprazole sodium on acid secretion increases slightly with repeated once-daily dosing, achieving steady state inhibition after three days. When the drug is discontinued, secretory activity normalises over 2 to 3 days.
Serum Gastrin Effects: In clinical studies patients were treated once daily with 10 or 20 mg rabeprazole sodium, for up to 24 months duration. Serum gastrin levels increased during the first 2 to 8 weeks reflecting the inhibitory effects on acid secretion. Gastrin values returned to pre-treatment levels, usually within 1 to 2 weeks after discontinuation of therapy.
Pharmacokinetics: Rabeprazole sodium is acid-labile, and is therefore administered orally as an enteric-coated (gastro-resistant) tablet formulation. Absorption of rabeprazole sodium therefore begins only after the tablet leaves the stomach. Absorption is rapid, with peak plasma levels of rabeprazole sodium occurring approximately 3.5 hours after a 20 mg dose. Peak plasma concentrations (Cmax) of rabeprazole sodium and AUC are linear over the dose range of 10 mg to 40 mg. Absolute bioavailability of an oral 20 mg dose (compared to intravenous administration) is about 52% due in large part to pre-systemic metabolism. Additionally the bioavailability does not appear to increase with repeat administration. In healthy subjects the plasma half-life is approximately one hour (range 0.7 to 1.5 hours), and the total body clearance is estimated to be 283 + 98 mL/min. In patients with chronic hepatic disease, the AUC doubled compared to healthy volunteers, reflecting a decreased first-pass effect, and the plasma half-life increased 2-3 fold.
Rabeprazole sodium is approximately 97% bound to human plasma proteins.
The main plasma metabolites are thioether (M1) and carboxylic acid (M6). Minor metabolites observed at lower levies include sulphone (M2), desmethyl-thioether (M4) and mercapturic acid conjugate (M5). Only the desmethyl metabolite (M3) has a small amount of antisecretory activity, but it is not present in plasma.
Excretion is mainly urinary (90%), with no unchanged drug excreted in the urine. The rest of the metabolites are excreted via the faeces. Total recovery was 99.8% implying a low biliary excretion of the metabolites of rabeprazole sodium.
In patients with stable, end-stage, renal failure requiring maintenance haemodialysis (creatinine clearance <5 mL/min/1.73 m²), the disposition of rabeprazole sodium was very similar to that in healthy volunteers. Elimination of rabeprazole sodium was somewhat decreased in the elderly. Following 7 days of daily dosing with 20 mg of rabeprazole sodium, the AUC approximately doubled, the Cmax increased by 60% as compared to young healthy volunteers. However there was no evidence of rabeprazole sodium accumulation.
EC tab: Pharmacodynamics: Mechanism of Action: Rabeprazole sodium belongs to the class of antisecretory compounds, the substituted benzimidazoles, that do not exhibit anticholinergic or H2 histamine antagonist properties, but suppress gastric acid secretion by the specific inhibition of the H+/K+-ATPase enzyme at the secretory surface of the gastric parietal cell. This enzyme system is regarded as the acid (proton) pump, and therefore rabeprazole sodium is classified as a gastric proton-pump inhibitor blocking the final step of acid production. This effect is dose-related and leads to inhibition of both basal and stimulated acid secretion irrespective of the stimulus. Animal studies indicate that after administration, rabeprazole sodium rapidly disappears from both the plasma and gastric mucosa.
Anti-secretory Activity: After oral administration of a 20 mg dose of rabeprazole sodium the onset of the anti-secretory effect occurs within one hour with the maximum effect occurring within two to four hours. Inhibition of basal and food stimulated acid secretion 23 hours after the first dose of rabeprazole sodium are 69% and 82% respectively and the duration of inhibition lasts up to 48 hours. This duration of pharmacodynamic action is much longer than the pharmacokinetic half life (approximately one hour) would predict. This effect is probably due to the prolonged binding to the parietal H+/K+-ATPase enzyme. The inhibitory effect of rabeprazole sodium on acid secretion increases slightly with repeated once-daily dosing, achieving steady state inhibition after three days. When the drug is discontinued, secretory activity normalises over 2 to 3 days.
Serum Gastrin Effects: In clinical studies patients were treated once daily with 10 or 20 mg rabeprazole sodium, for up to 24 months duration. Serum gastrin levels increased during the first 2 to 8 weeks reflecting the inhibitory effects on acid secretion. Gastrin values returned to pre-treatment levels, usually within 1 to 2 weeks after discontinuation of therapy.
Pharmacokinetics: Rabeprazole sodium is acid-labile, and is therefore administered orally as an enteric-coated (gastro-resistant) tablet formulation. Absorption of rabeprazole sodium therefore begins only after the tablet leaves the stomach. Absorption is rapid, with peak plasma levels of rabeprazole sodium occurring approximately 3.5 hours after a 20 mg dose. Peak plasma concentrations (Cmax) of rabeprazole sodium and AUC are linear over the dose range of 10 mg to 40 mg. Absolute bioavailability of an oral 20 mg dose (compared to intravenous administration) is about 52% due in large part to pre-systemic metabolism. Additionally the bioavailability does not appear to increase with repeat administration. In healthy subjects the plasma half-life is approximately one hour (range 0.7 to 1.5 hours), and the total body clearance is estimated to be 283 + 98 mL/min. In patients with chronic hepatic disease, the AUC doubled compared to healthy volunteers, reflecting a decreased first-pass effect, and the plasma half-life increased 2-3 fold.
Rabeprazole sodium is approximately 97% bound to human plasma proteins.
The main plasma metabolites are thioether (M1) and carboxylic acid (M6). Minor metabolites observed at lower levies include sulphone (M2), desmethyl-thioether (M4) and mercapturic acid conjugate (M5). Only the desmethyl metabolite (M3) has a small amount of antisecretory activity, but it is not present in plasma.
Excretion is mainly urinary (90%), with no unchanged drug excreted in the urine. The rest of the metabolites are excreted via the faeces. Total recovery was 99.8% implying a low biliary excretion of the metabolites of rabeprazole sodium.
In patients with stable, end-stage, renal failure requiring maintenance haemodialysis (creatinine clearance <5 mL/min/1.73 m²), the disposition of rabeprazole sodium was very similar to that in healthy volunteers. Elimination of rabeprazole sodium was somewhat decreased in the elderly. Following 7 days of daily dosing with 20 mg of rabeprazole sodium, the AUC approximately doubled, the Cmax increased by 60% as compared to young healthy volunteers. However there was no evidence of rabeprazole sodium accumulation.
MedsGo Class
Antacids, Antireflux Agents & Antiulcerants
Features
Brand
Rapeed
Full Details
Dosage Strength
20 mg
Drug Ingredients
- Rabeprazole
Drug Packaging
Enteric-Coated Tablet 1's
Generic Name
Rabeprazole Sodium
Dosage Form
Enteric-Coated Tablet
Registration Number
DRP-5595
Drug Classification
Prescription Drug (RX)
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