WARNINGS: Fetal/Neonatal Morbidity and Mortality.DESCRIPTION Aliskiren, the activeponent of Tekturna(R) Tablets, is an orally active, nonpeptide, potent renin inhibitor.Is present in Tekturna Tablets as its hemifumarate salt.Hemifumarate is chemically described as (2S,4S,5S,7S)-N-(2-Carbamoyl-2-methylpropyl)-5-amino-4-hydroxy-2,7-diisopropyl-8octanamide hemifumarate and its structural formula is Molecular formula: C30H53N3O6 0.Aliskiren hemifumarate is a white to slightly yellowish crystalline powder with a molecular weight of 609.551.It is soluble in phosphate buffer, n-Octanol, and highly soluble in water.Tekturna is available for oral administration as film-coated tablets containing 150 mg, and 300 mg of aliskiren base and the following inactive ingredients: colloidal silicon dioxide, crospovidone, hypromellose, iron oxide colorants, magnesium stearate, microcrystalline cellulose, polyethylene glycol, povidone, talc, and titanium dioxide.CLINICAL PHARMACOLOGY MECHANISM OF ACTION Renin is secreted by the kidney in response to decreases in blood volume and renal perfusion.Cleaves angiotensinogen to form the inactive decapeptide angiotensin I (Ang I).I is converted to the active octapeptide angiotensin II (Ang II) by angiotensin-converting enzyme (ACE) and non-ACE pathways.II is a powerful vasoconstrictor and leads to the release of catecholamines from the adrenal medulla and prejunctional nerve endings.Also promotes aldosterone secretion and sodium reabsorption.These effects increase blood pressure.II also inhibits renin release, thus providing a negative feedback to the system.Cycle, from renin through angiotensin to aldosterone and its associated negative feedback loop, is known as the renin-angiotensin-aldosterone system (RAAS).Is a direct renin inhibitor, decreasing plasma renin activity (PRA) and inhibiting the conversion of angiotensinogen to Ang I.Aliskiren affects other RAASponents, e.ACE or non-ACE pathways, is not known.All agents that inhibit the RAAS, including renin inhibitors, suppress the negative feedback loop, leading to apensatory rise in plasma renin concentration.This rise occurs during treatment with ACE inhibitors and ARBs, the result is increased levels of PRA.Aliskiren, however, the effect of increased renin levels is blocked, so that PRA, Ang I and Ang II are all reduced, whether aliskiren is used as monotherapy or inbination with other antihypertensive agents.Reductions in clinical trials ranged from approximately 50%-80%, were not dose-related and did not correlate with blood pressure reductions.Clinical implications of the differences in effect on PRA are not known.PHARMACOKINETICS Aliskiren is a poorly absorbed (bioavailability about 2.With an approximate accumulation half life of 24 hours.Blood levels are reached in about 7-8 days.ABSORPTION AND DISTRIBUTION Following oral administration, peak plasma concentrations of aliskiren are reached within 1 to 3 hours.Taken with a high fat meal, mean AUC and Cmax of aliskiren are decreased by 71% and 85%, respectively.The clinical trials of aliskiren, it was administered without requiring a fixed relation of administration to meals.METABOLISM AND ELIMINATION About one-fourth of the absorbed dose appears in the urine as parent drug.Read more Recent studies of vytorin, avandia prompt debate about fda approval process for new medications
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