COMPOSITION : Each capsule contains :-
RABEPRAZOLE 20 mg
LEVOSULPRIDE 75 mg
- Rabeprazole belongs to class of medications called proton pump inhibitors. It blocks the activity of the proton pumps in the stomach wall that produce acid, thereby reducing the amount of acid produced in the stomach.
- Levosulpride belongs to a class of medications called atypical antipsychotic agent. It acts by inhibiting the receptor (D2 and D3) found in the brain and subsequently decreasing the level of chemical compound (dopamine) present in the brain.
Rabeprazole sodium delayed-release capsules are enteric-coated to allow rabeprazole sodium, which is acid-labile, to pass through the stomach relatively intact.
After oral administration of 20 mg rabeprazole, peak plasma concentrations (Cmax) of rabeprazole occur over a range of 2.0 to 5.0 hours (Tmax). The rabeprazole Cmax and AUC are linear over an oral dose range of 10 mg to 40 mg. There is no appreciable accumulation when doses of 10-40 mg are administered every 24 hours; the pharmacokinetics of rabeprazole is not altered by multiple dosing.
Absolute bioavailability for a 20 mg oral capsule of rabeprazole (compared with intravenous administration) is approximately 52%. When rabeprazole sodium capsulesare administered with a high-fat meal, the Tmax is variable; concomitant food intake may delay the absorption up to 4 hours or longer. However, the Cmax and the extent of rabeprazole absorption (AUC) are not significantly altered. Thus, rabeprazole sodium capsules may be taken without regard to timing of meals.
Rabeprazole is 96.3% bound to human plasma proteins.
Rabeprazole is extensively metabolized. A significant portion of rabeprazole is metabolized via systemic non enzymatic reduction to a thioether compound. Rabeprazole is also metabolized to sulphone and desmethyl compounds via cytochrome (CY) P450 in the liver. The thioether and sulphone are the primary metabolites measured in human plasma. These metabolites were not observed to have significant antisecretory activity. In vitro studies have demonstrated that rabeprazole is metabolized in the liver primarily by CYP450 3A (CYP3A) to a sulphone metabolite and CYP450 2C19 (CYP2C19) to desmethyl rabeprazole. The thioether metabolite is formed non-enzymatically by reduction of rabeprazole. CYP2C19 exhibits a known genetic polymorphism due to its deficiency in some sub-populations (e.g. 3-5% of Caucasians and 17-20% of Asians). Rabeprazole metabolism is slow in these sub-populations; therefore, they are referred to as poor metabolizers of the drug.
Following a single 20 mg oral dose of 14C-labelled rabeprazole, approximately 90% of the drug was eliminated in the urine, primarily as thioether carboxylic acid; its glucuronide, and mercapturic acid metabolites. The remainder of the dose was recovered in the faeces. Total recovery of radioactivity was 99.8%. No unchanged rabeprazole was recovered in the urine or faeces.
INDICATION : Erosive or ulcerative gastroesophageal reflux disease, duodenal ulcer
DOSAGE : As directed by the physician .
SIDE EFFECTS :
- Increased risk of infections, Memory loss, Abdominal pain, Constipation, Chills or sore throat, Belching, Flatulence.
- Elevated liver enzymes, Postural hypotension, Neuroleptic malignant syndrome, Muscle rigidity, Drowsiness, Breast enlargement, Sedation, Abnormal and involuntary muscle contractions, Increased level of liver transaminase enzymes, Abnormal menstrual or vaginal bleeding, As well as weight gain