DR RAM 2.5
DR RAM 2.5
Pack: Strip of 10 tablets
Composition: Ramipril Tablets 2.5 mg
COMPOSITION: Each tablet contains :-
Ramipril 2.5 mg
Ramipril belongs to a class of drugs called ACE inhibitors (angiotensin converting enzyme inhibitors), Ramipril inhibits the chemical ACE (angiotensin converting enzyme). As a result, there is relaxation of blood vessels leading to a fall in blood pressure which makes it easier for the heart to pump blood.
Following oral administration of Ramipril, peak plasma concentrations (Cmax) of Ramipril are reached within 1 hour. The extent of absorption is at least 50% to 60%, and is not significantly influenced by the presence of food in the gastrointestinal tract, although the rate of absorption is reduced.
In a trial in which subjects received Ramipril capsules or the contents of identical capsules dissolved in water, dissolved in apple juice, or suspended in applesauce, serum Ramiprilat levels were essentially unrelated to the use or non-use of the concomitant liquid or food.
Cleavage of the ester group (primarily in the liver) converts Ramipril to its active diacid metabolite, Ramiprilat. Peak plasma concentrations of Ramiprilat are reached 2 to 4 hours after drug intake. The serum protein binding of Ramipril is about 73% and that of Ramiprilat about 56%; in vitro, these percentages are independent of concentration over the range of 0.01 mcg/mL to 10 mcg/mL.
Ramipril is almost completely metabolized to Ramiprilat, which has about 6 times the ACE inhibitory activity of Ramipril, and to the diketopiperazine ester, the diketopiperazine acid, and the glucuronides of Ramipril and Ramiprilat, all of which are inactive.
Plasma concentrations of Ramipril and Ramiprilat increase with increased dose, but are not strictly dose-proportional. The 24-hour AUC for Ramiprilat, however, is dose-proportional over the 2 .5 mg to 20 mg dose range. The absolute bioavailabilities of Ramipril and Ramiprilat were 28% and 44%, respectively, when 5 mg of oral Ramipril was compared with the same dose of Ramipril given intravenously.
After once-daily dosing, steady-state plasma concentrations of Ramiprilat are reached by the fourth dose. Steady-state concentrations of Ramiprilat are somewhat higher than those seen after the first dose of Ramipril, especially at low doses (2.5 mg), but the difference is clinically insignificant.
Plasma concentrations of Ramiprilat decline in a triphasic manner (initial rapid decline, apparent elimination phase, terminal elimination phase). The initial rapid decline, which represents distribution of the drug into a large peripheral compartment and subsequent binding to both plasma and tissue ACE, has a half-life of 2 to 4 hours. Because of its potent binding to ACE and slow dissociation from the enzyme, Ramiprilat shows two elimination phases. The apparent elimination phase corresponds to the clearance of free Ramiprilat and has a half-life of 9 to 18 hours. The terminal elimination phase has a prolonged half-life (>50 hours) and probably represents the binding/dissociation kinetics of the Ramiprilat/ACE complex. It does not contribute to the accumulation of the drug. After multiple daily doses of Ramipril 5 mg to 10 mg, the half-life of Ramiprilat concentrations within the therapeutic range was 13 to 17 hours.
In patients with creatinine clearance <40 mL/min/1.73 m2, peak levels of Ramiprilat are approximately doubled, and trough levels may be as much as quintupled. In multiple-dose regimens, the total exposure to Ramiprilat (AUC) in these patients is 3 to 4 times as large as it is in patients with normal renal function who receive similar doses.
In patients with impaired liver function, the metabolism of Ramipril to Ramiprilat appears to be slowed, possibly because of diminished activity of hepatic esterases, and plasma Ramipril levels in these patients are increased about 3-fold. Peak concentrations of Ramiprilat in these patients, however, are not different from those seen in subjects with normal hepatic function, and the effect of a given dose on plasma ACE activity does not vary with hepatic function.
After oral administration of Ramipril, about 60% of the parent drug and its metabolites are eliminated in the urine, and about 40% is found in the feces. Drug recovered in the feces may represent both biliary excretion of metabolites and/or unabsorbed drug, however the proportion of a dose eliminated by the bile has not been determined. Less than 2% of the administered dose is recovered in urine as unchanged Ramipril.
The urinary excretion of Ramipril, Ramiprilat, and their metabolites is reduced in patients with impaired renal function. Compared to normal subjects, patients with creatinine clearance <40 mL/min/1.73 m2had higher peak and trough Ramiprilat levels and slightly longer times to peak concentrations.
INDICATION : Post myocardial infarction.
DOSAGE: As directed by the Physician
SIDE EFFECTS : Cough or shortness of breath, Drowsiness, Swelling of hands and feet, Cns depression, Fainting, Dizziness or lightheadedness, Rapid weight gain, Diarrhea and nausea, Excessive tiredness.
|S. No.||COMPETITIOR||COMPANY||MRP / Tab|
|5||Cardiopril||Dr. Reddy ‘s||48.41/10|