Source:http://www4.wiwiss.fu-berlin.de/dailymed/resource/drugs/2032
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Tekturna (Tablet, Film Coated)
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The usual recommended starting dose of Tekturna (aliskiren) is 150 mg once daily. In patients whose blood pressure is not adequately controlled, the daily dose may be increased to 300 mg. Doses above 300 mg did not give an increased blood pressure response but increased the rate of diarrhea. The antihypertensive effect of a given dose is substantially attained (85%-90%) by 2 weeks. Tekturna may be administered with other antihypertensive agents. Most exposure to date is with diuretics and an angiotensin receptor blocker (valsartan) and the drugs together have a greater effect at their maximum recommended doses than either drug alone. It is not known whether additive effects are present when aliskiren is used with angiotensin-converting enzyme inhibitors or beta blockers. No initial dosage adjustment is required in elderly patients, for patients with mild-to-severe renal impairment, or for patients with mild-to-severe hepatic insufficiency. Care should be exercised when dosing Tekturna in patients with severe renal impairment, as clinical experience with such patients is limited. Patients should establish a routine pattern for taking Tekturna with regard to meals. High fat meals decrease absorption substantially (see Absorption and Distribution).
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Aliskiren, the active component of Tekturna Tablets, is an orally active, nonpeptide, potent renin inhibitor. Aliskiren is present in Tekturna Tablets as its hemifumarate salt. Aliskiren hemifumarate is chemically described as (2S,4S,5S,7S)-N-(2-Carbamoyl-2-methylpropyl)-5-amino-4-hydroxy-2,7-diisopropyl-8-[4-methoxy-3-(3-methoxypropoxy)phenyl]-octanamide hemifumarate and its structural formula is Molecular formula: CHNO���0.5 CHO Aliskiren hemifumarate is a white to slightly yellowish crystalline powder with a molecular weight of 609.8 (free base- 551.8). 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.
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Mechanism of Action: Renin is secreted by the kidney in response to decreases in blood volume and renal perfusion. Renin cleaves angiotensinogen to form the inactive decapeptide angiotensin I (Ang I). Ang I is converted to the active octapeptide angiotensin II (Ang II) by angiotensin-converting enzyme (ACE) and non-ACE pathways. Ang II is a powerful vasoconstrictor and leads to the release of catecholamines from the adrenal medulla and prejunctional nerve endings. It also promotes aldosterone secretion and sodium reabsorption. Together, these effects increase blood pressure. Ang II also inhibits renin release, thus providing a negative feedback to the system. This cycle, from renin through angiotensin to aldosterone and its associated negative feedback loop, is known as the renin-angiotensin-aldosterone system (RAAS). Aliskiren is a direct renin inhibitor, decreasing plasma renin activity (PRA) and inhibiting the conversion of angiotensinogen to Ang I. Whether aliskiren affects other RAAS components, e.g., ACE or non-ACE pathways, is not known. All agents that inhibit the RAAS, including renin inhibitors, suppress the negative feedback loop, leading to a compensatory rise in plasma renin concentration. When this rise occurs during treatment with ACE inhibitors and ARBs, the result is increased levels of PRA. During treatment with 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 in combination with other antihypertensive agents. PRA reductions in clinical trials ranged from approximately 50%-80%, were not dose-related and did not correlate with blood pressure reductions. The clinical implications of the differences in effect on PRA are not known.<br/>Pharmacokinetics: Aliskiren is a poorly absorbed (bioavailability about 2.5%) drug with an approximate accumulation half life of 24 hours. Steady-state blood levels are reached in about 7-8 days.<br/>Absorption and Distribution: Following oral administration, peak plasma concentrations of aliskiren are reached within 1 to 3 hours. When taken with a high fat meal, mean AUC and Cof aliskiren are decreased by 71% and 85%, respectively. In the clinical trials of aliskiren, it was administered without requiring a fixed relation of administration to meals.<br/>Metabolism and Elimination: About one-fourth of the absorbed dose appears in the urine as parent drug. How much of the absorbed dose is metabolized is unknown. Based on the in vitro studies, the major enzyme responsible for aliskiren metabolism appears to be CYP 3A4.<br/>Special Populations: Pediatric The pharmacokinetics of aliskiren have not been investigated in patients<18 years of age. Geriatric The pharmacokinetics of aliskiren were studied in the elderly (���65 years). Exposure (measured by AUC) is increased in elderly patients. Adjustment of the starting dose is not required in these patients (see DOSAGE AND ADMINISTRATION). Race The pharmacokinetic differences between Blacks, Caucasians and the Japanese are minimal. Renal Insufficiency The pharmacokinetics of aliskiren were evaluated in patients with varying degrees of renal insufficiency. Rate and extent of exposure (AUC and C) of aliskiren in subjects with renal impairment did not show a consistent correlation with the severity of renal impairment. Adjustment of the starting dose is not required in these patients (see DOSAGE AND ADMINISTRATION). Hepatic Insufficiency The pharmacokinetics of aliskiren were not significantly affected in patients with mild-to- severe liver disease. Consequently, adjustment of the starting dose is not required in these patients (see DOSAGE AND ADMINISTRATION). Cardiac Electrophysiology Aliskiren's effects on ECG intervals were studied in a randomized, double-blind, placebo and active-controlled (moxifloxacin), 7-day repeat dosing study with Holter-monitoring and 12-lead ECGs throughout the interdosing interval. No effect of aliskiren on QT interval was seen.<br/>Drug Interactions:<br/>Effects of Other Drugs on Aliskiren: Based on in-vitro studies, aliskiren is metabolized by CYP 3A4. Co-administration of lovastatin, atenolol, warfarin, furosemide, digoxin, celecoxib, hydrochlorothiazide, ramipril, valsartan, metformin and amlodipine did not result in clinically significant increases in aliskiren exposure. Co-administration of irbesartan reduced aliskiren Cup to 50% after multiple dosing. P-glycoprotein Effects Pgp (MDR1/Mdr1a/1b) was found to be the major efflux system involved in absorption and disposition of aliskiren in preclinical studies. The potential for drug interactions at the Pgp site will likely depend on the degree of inhibition of this transporter. Co-administration of aliskiren with Pgp substrates or weak to moderate inhibitors such as atenolol, digoxin, and amlodipine did not result in clinically relevant interactions. Co-administration of atorvastatin, a potent Pgp inhibitor, resulted in about a 50% increase in aliskiren Cand AUC after multiple dosing. Ketoconazole Co-administration of 200 mg twice-daily ketoconazole, a potent Pgp inhibitor, with aliskiren resulted in an approximate 80% increase in plasma levels of aliskiren. A 400 mg once-daily dose was not studied but would be expected to increase aliskiren blood levels further. Cyclosporine Co-administration of 200 mg and 600 mg cyclosporine, a highly potent Pgp inhibitor, with 75 mg aliskiren resulted in an approximately 2.5 fold increase in Cand 5 fold increase in AUC of aliskiren. Concomitant use of aliskiren with cyclosporine is not recommended.<br/>Effects of Aliskiren on Other Drugs: Aliskiren does not inhibit the CYP450 isoenzymes (CYP1A2, 2C8, 2C9, 2C19, 2D6, 2E1, and CYP 3A) or induce CYP 3A4. Co-administration of aliskiren did not significantly affect the pharmacokinetics of lovastatin, digoxin, valsartan, amlodipine, metformin, celecoxib, atenolol, atorvastatin, ramipril or hydrochlorothiazide. Warfarin The effects of aliskiren on warfarin pharmacokinetics have not been evaluated in a well-controlled clinical trial. Furosemide When aliskiren was co-administered with furosemide, the AUC and Cof furosemide were reduced by about 30% and 50%, respectively.
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Tekturna (aliskiren) is supplied as a light-pink, biconvex unscored round tablet containing 150 mg of aliskiren, and as a light-red biconvex ovaloid tablet containing 300 mg of aliskiren. Tablets are imprinted with NVR on one side and IL, IU, on the other side of the 150, and 300 mg tablets, respectively. All strengths are packaged in bottles and unit-dose blister packages (10 strips of 10 tablets) as described below in Table 4.<br/>Storage: Store at 25��C (77��F); excursions permitted to 15-30��C (59-86��F) [see USP Controlled Room Temperature]. Protect from moisture. Dispense in tight container (USP). REV: DECEMBER 2007 T2007-111 Distributed by: Novartis Pharmaceuticals Corporation East Hanover, New Jersey 07936 ��Novartis
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USE IN PREGNANCY: When used in pregnancy drugs that act directly on the renin-angiotensin system can cause injury and even death to the developing fetus. When pregnancy is detected, Tekturna should be discontinued as soon as possible. See WARNINGS: Fetal/Neonatal Morbidity and Mortality.
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dailymed-ingredient:colloidal_silicon_dioxide,
dailymed-ingredient:crospovidone,
dailymed-ingredient:hypromellose,
dailymed-ingredient:iron_oxide_colorants,
dailymed-ingredient:magnesium_stearate,
dailymed-ingredient:microcrystalline_cellulose,
dailymed-ingredient:polyethylene_glycol,
dailymed-ingredient:povidone,
dailymed-ingredient:talc,
dailymed-ingredient:titanium_dioxide
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General:<br/>Impaired Renal Function: Patients with greater than moderate renal dysfunction (creatinine 1.7 mg/dL for women and 2.0 mg/dL for men and/or estimated GFR<30 mL/min), a history of dialysis, nephrotic syndrome, or renovascular hypertension were excluded from clinical trials of Tekturna (aliskiren) in hypertension. Caution should be exercised in these patients because of the paucity of safety information with Tekturna in these patients and the potential for other drugs acting on the renin-angiotensin system to increase serum creatinine and blood urea nitrogen.<br/>Hyperkalemia: Increases in serum potassium>5.5 meq/L were infrequent with Tekturna alone (0.9% compared to 0.6% with placebo). However, when used in combination with an ACE inhibitor in a diabetic population, increases in serum potassium were more frequent (5.5%). Routine monitoring of electrolytes and renal function is indicated in this population. Concomitant use of Tekturna with potassium-sparing diuretics, potassium supplements, salt substitutes containing potassium, or other drugs that increase potassium levels may lead to increases in serum potassium. If concomitant use is considered necessary, caution should be exercised.<br/>Renal Artery Stenosis: No data are available on the use of Tekturnain patients with unilateral or bilateral renal artery stenosis or stenosis of the artery to a solitary kidney.<br/>Information for Patients:<br/>Pregnancy: Female patients of childbearing age should be told about the consequences of exposure to drugs that act on the renin-angiotensin system. Discuss other treatment options with female patients planning to become pregnant. Patients should be asked to report pregnancies to their physicians as soon as possible.<br/>Angioedema: Angioedema, including laryngeal edema, may occur at any time during treatment with Tekturna. Patients should be so advised and told to report immediately any signs or symptoms suggesting angioedema (swelling of face, extremities, eyes, lips, tongue, difficulty in swallowing or breathing) and to take no more drug until they have consulted with the prescribing physician.<br/>Drug Interactions: Patients should report any medications they take with aliskiren.<br/>Furosemide: When aliskiren was given with furosemide, the blood concentrations of furosemide were reduced significantly. Patients receiving furosemide could find its effect diminished after starting aliskiren.<br/>Cyclosporine: When aliskiren was given with cyclosporine, the blood concentrations of aliskiren were significantly increased. Concomitant use of aliskiren with cyclosporine is not recommended.<br/>Carcinogenesis/Mutagenesis/Impairment of Fertility: Carcinogenic potential was assessed in a 2-year rat study and a 6-month transgenic (rasH2) mouse study with aliskiren hemifumarate at oral doses of up to 1500 mg aliskiren/kg/day. Although there were no statistically significant increases in tumor incidence associated with exposure to aliskiren, mucosal epithelial hyperplasia (with or without erosion/ulceration) was observed in the lower gastrointestinal tract at doses of 750 or more mg/kg/day in both species, with a colonic adenoma identified in one rat and a cecal adenocarcinoma identified in another, rare tumorsin the strain of rat studied. On a systemic exposure (AUC) basis, 1500 mg/kg/day in the rat is about 4 times, and is in the mouse about 1.5 times, the maximum recommended human dose (300 mg aliskiren/day). Mucosal hyperplasia in the cecum or colon of rats was also observed at oral doses of 250 mg/kg/day (the lowest tested dose) as well as at higher doses in 4- and 13-week studies. Aliskiren hemifumarate was devoid of genotoxic potential in the Ames reverse mutation assay with S. typhimurium and E. coli, the in vitro Chinese hamster ovary cell chromosomal aberration assay, the in vitro Chinese hamster V79 cell gene mutation test and the in vivo mouse bone marrow micronucleus assay. Fertility of male and female rats was unaffected at doses of up to 250 mg aliskiren/kg/day (8 times the maximum recommended human dose of 300 mg Tekturna/60 kg on a mg/mbasis.<br/>Pregnancy: Pregnancy Categories C (first trimester) and D (second and third trimesters) (see WARNINGS, Fetal/Neonatal Morbidity and Mortality).<br/>Nursing Mothers: It is not known whether aliskiren is excreted in human milk. Aliskiren was secreted in the milk of lactating rats. Because of the potential for adverse effects on the nursing infant, a decision should be made whether to discontinue nursing or discontinue the drug, taking into account the importance of the drug to the mother.<br/>Pediatric Use: Safety and effectiveness of aliskiren in pediatric patients have not been established.<br/>Geriatric Use: Of the total number of patients receiving aliskiren in clinical studies, 1,275 (19%) were 65 years or older and 231 (3.4%) were 75 years or older. Blood pressure responses and adverse effects were generally similar to those in younger patients.
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Limited data are available related to overdosage in humans. The most likely manifestation of overdosage would be hypotension. If symptomatic hypotension should occur, supportive treatment should be initiated.
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aliskiren fumarate
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Tekturna (Tablet, Film Coated)
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Tekturna(aliskiren) has been evaluated for safety in more than 6,460 patients, including over 1,740 treated for longer than 6 months, and more than 1,250 for longer than 1 year. In placebo-controlled clinical trials, discontinuation of therapy due to a clinical adverse event, including uncontrolled hypertension occurred in 2.2% of patients treated with Tekturna, vs. 3.5% of patients given placebo. Two cases of angioedema with respiratory symptoms were reported with aliskiren use in the clinical studies. Two other cases of periorbital edema without respiratory symptoms were reported as possible angioedema and resulted in discontinuation. The rate of these angioedema cases in the completed studies was 0.06%. In addition, 26 other cases of edema involving the face, hands, or whole body were reported with aliskiren use, including 4 leading to discontinuation. In the placebo controlled studies, however, the incidence of edema involving the face, hands or whole body was 0.4% with aliskiren compared with 0.5% with placebo. In a long term active control study with aliskiren and HCTZ arms, the incidence of edema involving the face, hand or whole body was 0.4% in both treatment arms. Aliskiren produces dose-related gastrointestinal (GI) adverse effects. Diarrhea was reported by 2.3% of patients at 300 mg, compared to 1.2% in placebo patients. In women and the elderly (age���65) increases in diarrhea rates were evident starting at a dose of 150 mg daily, with rates for these subgroups at 150 mg comparable to those seen at 300 mg for men or younger patients (all rates about 2.0%-2.3%). Other GI symptoms included abdominal pain, dyspepsia, and gastroesophageal reflux, although increased rates for abdominal pain and dyspepsia were distinguished from placebo only at 600 mg daily. Diarrhea and other GI symptoms were typically mild and rarely led to discontinuation. Aliskiren was associated with a slight increase in cough in the placebo-controlled studies (1.1% for any aliskiren use vs. 0.6% for placebo). In active-controlled trials with ACE inhibitor (ramipril, lisinopril) arms, the rates of cough for the aliskiren arms were about one-third to one-half the rates in the ACE inhibitor arms. Other adverse effects with increased rates for aliskiren compared to placebo included rash (1% vs. 0.3%), elevated uric acid (0.4% vs. 0.1%), gout (0.2% vs. 0.1%), and renal stones (0.2% vs. 0%). Single episodes of tonic-clonic seizures with loss of consciousness were reported in two patients treated with aliskiren in the clinical trials. One of these patients did have predisposing causes for seizures and had a negative electroencephalogram (EEG) and cerebral imaging following the seizures (for the other patient EEG and imaging results were not reported). Aliskiren was discontinued and there was no rechallenge. The following adverse events occurred in placebo-controlled clinical trials at an incidence of more than 1% of patients treated with aliskiren, but also occurred at about the same or greater incidence in patients receiving placebo: headache, nasopharyngitis, dizziness, fatigue, upper respiratory tract infection, back pain, and cough.<br/>Clinical Laboratory Findings: In controlled clinical trials, clinically relevant changes in standard laboratory parameters were rarely associated with the administration of Tekturna. In multiple-dose studies in hypertensive patients Tekturna had no clinically important effects on total cholesterol, HDL, fasting triglycerides, fasting glucose, or uric acid.<br/>Blood Urea Nitrogen, Creatinine: Minor increases in blood urea nitrogen (BUN) or serum creatinine were observed in less than 7% of patients with essential hypertension treated with Tekturna alone vs. 6% on placebo.<br/>Hemoglobin and Hematocrit: Small decreases in hemoglobin and hematocrit (mean decreases of approximately 0.08 g/dL and 0.16 volume percent, respectively, for all aliskiren monotherapy) were observed. The decreases were dose-related and were 0.24 g/dL and 0.79 volume percent for 600 mg daily. This effect is also seen with other agents acting on the renin angiotensin system, such as angiotensin inhibitors and angiotensin receptor blockers, and may be mediated by reduction of angiotensin II which stimulates erythropoietin production via the AT1 receptor. These decreases led to slight increases in rates of anemia with aliskiren compared to placebo were observed (0.1% for any aliskiren use, 0.3% for aliskiren 600 mg daily, vs. 0% for placebo). No patients discontinued therapy due to anemia.<br/>Serum Potassium: Increases in serum potassium>5.5 meq/L were infrequent in patients with essential hypertension treated with Tekturna alone (0.9% compared to 0.6% with placebo). However, when used in combination with an angiotensin-converting enzyme inhibitor (ACEI) in a diabetic population increases in serum potassium were more frequent (5.5%) and routine monitoring of electrolytes and renal function is indicated in this population.<br/>Serum Uric Acid: Aliskiren monotherapy produced small median increases in serum uric acid levels (about 6��mol/L) while HCTZ produced larger increases (about 30��mol/L). The combination of aliskiren with HCTZ appears to be additive (about a 40��mol/L increase). The increases in uric acid appear to lead to slight increases in uric acid-related AEs: elevated uric acid (0.4% vs. 0.1%), gout (0.2% vs. 0.1%), and renal stones (0.2% vs. 0%).<br/>Creatine Kinase: Increases in creatine kinase of>300% were recorded in about 1% of aliskiren monotherapy patients vs. 0.5% of placebo patients. Five cases of creatine kinase rises, three leading to discontinuation and one diagnosed as subclinical rhabdomyolysis and another as myositis, were reported as adverse events with aliskiren use in the clinical trials. No cases were associated with renal dysfunction.
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| dailymed-instance:warning |
Fetal/Neonatal Morbidity and Mortality: Drugs that act directly on the renin-angiotensin system can cause fetal and neonatal morbidity and death when administered to pregnant women. Several dozen cases have been reported in the world literature in patients who were taking angiotensin-converting enzyme inhibitors. When pregnancy is detected, Tekturna (aliskiren) should be discontinued as soon as possible. The use of drugs that act directly on the renin-angiotensin system during the second and third trimesters of pregnancy has been associated with fetal and neonatal injury, including hypotension, neonatal skull hypoplasia, anuria, reversible or irreversible renal failure, and death. Oligohydramnios has also been reported, presumably resulting from decreased fetal renal function; oligohydramnios in this setting has been associated with fetal limb contractures, craniofacial deformation, and hypoplastic lung development. Prematurity, intrauterine growth retardation, and patent ductus arteriosus have also been reported, although it is not clear whether these occurrences were due to exposure to the drug. In addition, first trimester use of ACE inhibitors, a specific class of drugs acting on the renin-angiotensin system, has been associated with a potential risk of birth defects in retrospective data. Healthcare professionals that prescribe drugs acting directly on the renin-angiotensin system should counsel women of childbearing potential about the potential risks of these agents during pregnancy. Rarely (probably less often than once in every thousand pregnancies), no alternative to a drug acting on the renin-angiotensin system will be found. In these rare cases, the mothers should be apprised of the potential hazards to their fetuses, and serial ultrasound examinations should be performed to assess the intra-amniotic environment. If oligohydramnios is observed, Tekturna should be discontinued unless it is considered life-saving for the mother. Contraction stress testing (CST), a nonstress test (NST), or biophysical profiling (BPP) may be appropriate, depending upon the week of pregnancy. Patients and physicians should be aware, however, that oligohydramnios may not appear until after the fetus has sustained irreversible injury. Infants with histories of in-utero exposure to a renin inhibitor should be closely observed for hypotension, oliguria, and hyperkalemia. If oliguria occurs, attention should be directed toward support of blood pressure and renal perfusion. Exchange transfusion or dialysis may be required as means of reversing hypotension and/or substituting for disordered renal function. There is no clinical experience with the use of Tekturna in pregnant women. Reproductive toxicity studies of aliskiren hemifumarate did not reveal any evidence of teratogenicity at oral doses up to 600 mg aliskiren/kg/day (20 times the maximum recommended human dose (MRHD) of 300 mg/day on a mg/mbasis) in pregnant rats or up to 100 mg aliskiren/kg/day (seven times the MRHD on a mg/mbasis) in pregnant rabbits. Fetal birth weight was adversely affected in rabbits at 50 mg/kg/day (3.2 times the MRHD on a mg/mbasis). Aliskiren was present in placenta, amniotic fluid and fetuses of pregnant rabbits.<br/>Head and Neck Angioedema: Angioedema of the face, extremities, lips, tongue, glottis and/or larynx has been reported in patients treated with aliskiren. This may occur at any time during treatment. ACE inhibitors have been associated with a higher rate of angioedema in Black than in non-Black patients, but whether angioedema rates are higher in Blacks with aliskiren is not known. Tekturna should be promptly discontinued and appropriate therapy and monitoring provided until complete and sustained resolution of signs and symptoms has occurred. Experience with ACE inhibitors indicates that evenin those instances where only swelling of the tongue is seen initially, without respiratory distress, patients may require prolonged observation since treatment with antihistamines and corticosteroids may not be sufficient to prevent respiratory involvement. Very rarely, fatalities have been reported in patients with angioedema associated with laryngeal edema or tongue edema with ACE inhibitors. Patients with involvement of the tongue, glottis or larynx are more likely to experience airway obstruction, especially those with a history of airway surgery. Where there is involvement of the tongue, glottis or larynx, appropriate therapy, e.g., subcutaneous epinephrine solution 1:1000 (0.3 mL to 0.5 mL) and measures necessary to ensure a patent airway should be promptly provided (see ADVERSE REACTIONS).<br/>Hypotension: An excessive fall in blood pressure was rarely seen (0.1%) in patients with uncomplicated hypertension treated with Tekturna alone. Hypotension was also infrequent during combination therapy with other antihypertensive agents (<1%). In patients with an activated renin-angiotensin system, such as volume- or salt-depleted patients (e.g., those receiving high doses of diuretics), symptomatic hypotension could occur after initiation of treatment with Tekturna. This condition should be corrected prior to administration of Tekturna, or the treatment should start under close medical supervision. If an excessive fall in blood pressure occurs, the patient should be placed in the supine position and, if necessary, given an intravenous infusion of normal saline (see DOSAGE AND ADMINISTRATION). A transient hypotensive response is not a contraindication to further treatment, which usually can be continued without difficulty once the blood pressure has stabilized.
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Tekturna (aliskiren) is indicated for the treatment of hypertension. It may be used alone or in combination with other antihypertensive agents. Use with maximal doses of ACE inhibitors has not been adequately studied.
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Tekturna
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