Each film-coated tablet contains Valsartan 160 mg.
Valsartan blocks the vasoconstrictor and aldosterone-secreting effects of Angiotensin II by selectively blocking the binding of Aldosterone II to the AT1 receptor in many tissues, such as vascular smooth muscle and the adrenal gland. Its action is therefore independent of the pathways for angiotensin II synthesis.
Pharmacology: Pharmacokinetics: Absorption: Valsartan peak plasma concentration is reached 2 to 4 hours after dosing. Absolute bioavailability for Valsartan is about 25%. Food decreases the exposure (as measured by AUC) to Valsartan by about 40% and peak plasma concentration (Cmax) by about 50%. AUC and Cmax values of Valsartan increases approximately linearly with increasing dose over the clinical dosing range. Valsartan does not accumulate appreciably in plasma following repeated administration.
Metabolism and Elimination: Valsartan, when administered as an oral solution, is primarily recovered in feces (about 83% of dose) and urine (about 13% of dose). The recovery is mainly as unchanged drug, with only about 20% of dose recovered as metabolites. The enzymes responsible for Valsartan metabolism have not been identified but do not seem to be CYP450 isoenzymes.
Distribution: Valsartan is highly bound to serum proteins (95%), mainly serum albumin.
Special Population: Pediatric: The pharmacokinetics of Valsartan has not been investigated in patients <18 years of age.
Geriatric: Exposure (measured by AUC) to Valsartan is higher by 70% and the half-life is longer by 35% in the elderly than in younger populations. No dosage adjustment is necessary.
Gender: Pharmacokinetics of Valsartan does not differ significantly between males and females.
Heart Failure: The average time to peak concentration and elimination half-life of Valsartan in heart failure patients are similar to that observed in healthy volunteers. AUC and Cmax values of Valsartan increase linearly and are almost proportional with increasing dose over the clinical dosing range (40 to 160 mg twice a day). The average accumulation factor is about 1.7. The apparent clearance of Valsartan following oral administration is approximately 4.5 L/h. Age does not affect clearance in heart failure patients.
Used in the management of hypertension, to reduce cardiovascular mortality in patients with left ventricular dysfunction after myocardial infarction, and in the management of heart failure.
Hypertension: The recommended dose of Valsartan tablet is 80 mg once daily. The antihypertensive effect is substantially present within 2 weeks, and maximal effects are attained within 4 weeks. In some patients whose blood pressure is not adequately controlled, the dose can be increased to 160 mg and to a maximum of 320 mg.
Heart Failure: The recommended starting dose of Valsartan is 40 mg twice daily. Up titration to 80 mg and 160 mg twice daily should be done at intervals of at least two weeks to the highest dose, as tolerated by the patient. Consideration should be given to reduce the dose of concomitant diuretics. Evaluation of patients with heart failure should always include assessment of renal function.
Myocardial infarction: Initial dose is 20 mg twice daily. Valsartan therapy should be titrated to 40, 80 and 160 mg twice daily over the next few weeks. The starting dose is provided by the 40 mg divisible tablet.
Valsartan is contraindicated in patients who are hypersensitive to any component of the product.
Renal Insufficiency: There is no apparent correlation between renal function (measured by creatinine clearance) and exposure (measured by AUC) to Valsartan in patients with different degrees of renal impairment.
Hepatic Insufficiency: In patients with mild to moderate hepatic impairment without cholestasis, no dosage adjustment is required. However, Valsartan should be used with caution.
Concomitant Therapy in Patients with Heart Failure: In patients with heart failure, concomitant use of Valsartan, an ACE inhibitor, and a beta-blocker is not recommended. In the Valsartan Heart Failure Trial, this triple combination was associated with an unfavorable heart failure.
Due to the mechanism of action of angiotensin II receptor antagonists, a risk for the fetus cannot be excluded. In utero exposure to ACE inhibitors given to pregnant women during the 2nd and 3rd trimesters has been reported to cause injury and death to the developing fetus. As for any drug that also acts directly on the renin-angiotensin-aldosterone system, Valsartan should not be used during pregnancy. If pregnancy is detected during therapy, Valsartan should be discontinued as soon as possible.
Because no information is available regarding the use of Valsartan during breast-feeding, Valsartan is not recommended and alternative treatments with better established safety profile during breast-feeding are preferable, especially while nursing a newborn or preterm infant.
Adverse experiences have generally been mild and transient in nature and have only infrequently required discontinuation of therapy. The overall incidence of adverse experiences with Valsartan was comparable to placebo. Some adverse drug reactions such as dizziness, coughing, diarrhea, nausea, etc. may be observed.
No clinically significant pharmacokinetic interactions were observed when Valsartan was co-administered with amlodipine, atenolol, cimetidine, digoxin, furosemide, glyburide, hydrochlorothiazide or indomethacin.
Store at temperatures not exceeding 30°C. Protect from light.
C09CA03 - valsartan ; Belongs to the class of angiotensin II receptor blockers (ARBs). Used in the treatment of cardiovascular disease.
Valatan FC tab 160 mg
30's
Sign Out
