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| Product NDC Code | 73502-288 | ||||
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| Drug Name | Soaanz |
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| Type | Brand | ||||
| Pharm Class | Increased Diuresis at Loop of Henle [PE], Loop Diuretic [EPC] |
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| Active Ingredients |
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| Route | ORAL | ||||
| Dosage Form | TABLET, FILM COATED | ||||
| RxCUI drug identifier | 198371, 2589877, 2589881, 2589883, 2589885, 2589887 |
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| Application Number | NDA213218 | ||||
| Labeler Name | Sarfez Pharmaceuticals Inc | ||||
| Packages |
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| Check if available Online | Get Medication Prices online with Discount |
Overdosage of SOAANZ
Information about signs, symptoms, and laboratory findings of acute ovedosage and the general principles of overdose treatment.10 OVERDOSAGE The signs and symptoms of overdosage can be anticipated to include those of excessive pharmacologic effect: dehydration, hypovolemia, hypotension, hyponatremia, hypokalemia, hypochloremic alkalosis, and hemoconcentration. Treatment of overdosage should consist of fluid and electrolyte replacement. Laboratory determinations of serum levels of torsemide and its metabolites are not widely available. No data are available to suggest physiological maneuvers (e.g., maneuvers to change the pH of the urine) that might accelerate elimination of torsemide and its metabolites. Torsemide is not dialyzable, so hemodialysis will not accelerate elimination.
Adverse reactions
Information about undesirable effects, reasonably associated with use of the drug, that may occur as part of the pharmacological action of the drug or may be unpredictable in its occurrence. Adverse reactions include those that occur with the drug, and if applicable, with drugs in the same pharmacologically active and chemically related class. There is considerable variation in the listing of adverse reactions. They may be categorized by organ system, by severity of reaction, by frequency, by toxicological mechanism, or by a combination of these.6 ADVERSE REACTIONS The following risks are discussed in more detail in other sections: Hypotension and Worsening Renal Function [see Warnings and Precautions (5.1) ] Electrolyte and Metabolic Abnormalities [see Warnings and Precautions (5.2) ] Ototoxicity [see Warnings and Precautions (5.3) ] Discontinuation of therapy due to adverse reactions occurred in 6% of patients treated with SOAANZ ( 6.1 ). To report SUSPECTED ADVERSE REACTIONS, contact Sarfez Pharmaceuticals Inc. at 1-703-627-1934 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch . 6.1 Clinical Trials Experience Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice. In pre-approval studies, SOAANZ has been evaluated for safety in 65 subjects. Discontinuation of therapy due to adverse reactions occurred in 4 out of the 65 of subjects (6%) treated with SOAANZ. 6.2 Postmarketing Experience The following adverse reactions have been identified during the post-approval use of torsemide. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to estimate their frequency reliably or establish a causal relationship to drug exposure. Gastrointestinal System: Pancreatitis, abdominal pain Nervous System: Paresthesia, confusion, visual impairment, loss of appetite Hematologic: Leucopenia, thrombocytopenia, anemia Hepatobiliary: Increase in liver transaminases, gamma-glutamyltransferase Metabolism: Thiamine (vitamin B1) deficiency Skin/hypersensitivity: Stevens-Johnson syndrome, toxic epidermal necrolysis, photosensitivity reaction, pruritus Urogenital: Acute urinary retention
SOAANZ Drug Interactions
Information about and practical guidance on preventing clinically significant drug/drug and drug/food interactions that may occur in people taking the drug.7 DRUG INTERACTIONS Non-steroidal anti-inflammatory drugs (NSAIDs): Reduced diuretic, natriuretic, and antihypertensive effects; risk of renal impairment. ( 7.1 ) CYP2C9: Concomitant use with CYP2C9 inhibitors can decrease torsemide clearance. Torsemide may affect the efficacy and safety of sensitive CYP2C9 substrates or of substrates with a narrow therapeutic range, such as warfarin or phenytoin. ( 7.2 ) Cholestyramine: Decreased exposure of SOAANZ. ( 7.3 ) Organic anion drugs: may decrease diuretic activity of SOAANZ. ( 7.4 ) Lithium: Risk of lithium toxicity. ( 7.5 ) Renin-angiotensin inhibitors: Increased risk of hypotension and renal impairment. ( 7.7 ) Radiocontrast agents: Increased risk of renal toxicity. ( 7.8 ) Corticosteroids and ACTH: Increased risk of hypokalemia. ( 7.9 ) 7.1 Nonsteroidal Anti-inflammatory Drugs Because torsemide and salicylates compete for secretion by renal tubules, patients receiving high doses of salicylates may experience salicylate toxicity when SOAANZ is concomitantly administered. Concomitant use of nonsteroidal anti-inflammatory drugs (NSAIDs) and torsemide has been associated with the development of acute renal failure. The diuretic effects of torsemide can be reduced by NSAIDs. Partial inhibition of the natriuretic effect of torsemide by concomitant administration of indomethacin has been demonstrated for torsemide under conditions of dietary sodium restriction (50 mEq/day) but not in the presence of normal sodium intake (150 mEq/day). 7.2 Cytochrome P450 2C9 Inhibitors and Inducers Torsemide is a substrate of CYP2C9. Concomitant use of CYP2C9 inhibitors (e.g., amiodarone, fluconazole, miconazole, oxandrolone) can decrease torsemide clearance and increase torsemide plasma concentrations. Concomitant use of CYP2C9 inducers (e.g., rifampin) increase torsemide clearance and decrease plasma torsemide concentrations. Monitor diuretic effect and blood pressure when used in combination with CYP2C9 inhibitor or inducer. Adjust SOAANZ dose, if necessary. Because of its inhibition of CYP2C9 metabolism, torsemide may affect the efficacy and safety of sensitive CYP2C9 substrates, such as celecoxib, or of substrates with a narrow therapeutic range, such as warfarin or phenytoin. Monitor patients and adjust dosages if necessary. 7.3 Cholestyramine Concomitant use of torsemide and cholestyramine has not been studied in humans but, in a study in animals, coadministration of cholestyramine decreased the absorption of orally administered torsemide. If SOAANZ and cholestyramine should be coadministered, administer SOAANZ at least one hour before or 4 to 6 h after cholestyramine administration. 7.4 Organic Anion Drugs Coadministration of organic anion drugs (e.g., probenecid) that undergo significant renal tubular secretion have the potential to reduce secretion of torsemide into the proximal tubule which thereby decreases the diuretic activity of SOAANZ. Monitor diuretic effect and blood pressure during coadministration. 7.5 Lithium Like other diuretics, torsemide reduces the renal clearance of lithium, inducing a high risk of lithium toxicity. Monitor lithium levels periodically when SOAANZ is coadministered. 7.6 Ototoxic Drugs Loop diuretics increase the ototoxic potential of other ototoxic drugs, including aminoglycoside antibiotics and ethacrynic acid. This effect has been reported with concomitant use of torsemide and gentamycin. Avoid concomitant use of SOAANZ and aminoglycoside antibiotics, if possible. 7.7 Renin-angiotensin Inhibitors Coadministration of SOAANZ with ACE inhibitors or angiotensin receptor blockers can increase the risk of hypotension and renal impairment. 7.8 Radiocontrast Agents SOAANZ can increase the risk of renal toxicity related to administration of radiocontrast agents. 7.9 Corticosteroids and ACTH Concomitant use with SOAANZ may increase risk of hypokalemia.
Clinical pharmacology
Information about the clinical pharmacology and actions of the drug in humans.12 CLINICAL PHARMACOLOGY 12.1 Mechanism of Action Micropuncture studies in animals have shown that torsemide acts from within the lumen of the thick ascending portion of the loop of Henle, where it inhibits the Na+/K+/2Cl--carrier system. Clinical pharmacology studies have confirmed this site of action in humans, and effects in other segments of the nephron have not been demonstrated. Diuretic activity thus correlates better with the rate of drug excretion in the urine than with the concentration in the blood. Torsemide increases the urinary excretion of sodium, chloride, and water, but it does not significantly alter glomerular filtration rate, renal plasma flow, or acid-base balance. 12.2 Pharmacodynamics With oral dosing of SOAANZ, the onset of diuresis occurs within 1 hour and the peak effect occurs during the first four hours and diuresis lasts about 6 to 8 hours.The mean increase in potassium excretion over 23 hours following a single oral dose of SOAANZ 20 mg in healthy adults was 12.7 mEq. Edema Torsemide has been studied in controlled trials in patients with New York Heart Association Class II to Class IV heart failure. Patients who received 10 mg to 20 mg of daily torsemide in these studies achieved significantly greater reductions in weight and edema than did patients who received placebo. When torsemide is first administered, daily urinary sodium excretion increases for at least a week. With chronic administration, however, daily sodium loss comes into balance with dietary sodium intake. If the administration of torsemide is suddenly stopped, blood pressure returns to pretreatment levels over several days, without overshoot. Torsemide has been administered together with β-adrenergic blocking agents, ACE inhibitors, and calcium-channel blockers. Adverse drug interactions have not been observed, and special dosage adjustment has not been necessary. 12.3 Pharmacokinetics Absorption Torsemide reaches peak plasma concentration (C max ) within 2.5 hours after oral administration of SOAANZ. C max and area under the serum concentration-time curve (AUC) of torsemide after oral administration are proportional to dose over the range of 2.5 mg to 200 mg. Effect of Food Administration of SOAANZ with a high fat, high calorie meal in healthy adults delays the time to C max by about 45 minutes, increases C max by 100% and increases area under the plasma concentration over time curve (AUC) by 48%. No clinically significant change in overall diuretic activity was observed. Distribution The volume of distribution of torsemide is 12 to 15 liters in normal adults or in patients with mild to moderate renal failure or congestive heart failure. In patients with hepatic cirrhosis, the volume of distribution is approximately doubled. Torsemide is extensively bound to plasma protein (>99%). Metabolism Torsemide is metabolized by the hepatic cytochrome CYP2C9 and, to a minor extent, CYP2C8 and CYP2C18. Three main metabolites have been identified in humans. Metabolite M1 is formed by methylhydroxylation of torsemide, metabolite M3 is formed by ring hydroxylation of torsemide, and metabolite M5 is formed by oxidation of M1. The major metabolite in humans is the carboxylic acid derivative M5, which is biologically inactive. Metabolites M1 and M3 possess some pharmacological activity; however, their systemic exposures are much lower when compared to torsemide. Elimination In normal subjects the elimination half-life of torsemide is approximately 3.5 hours. Torsemide is cleared from the circulation by both hepatic metabolism (approximately 80% of total clearance) and excretion into the urine (approximately 20% of total clearance in patients with normal renal function). Because torsemide is extensively bound to plasma protein (>99%), very little enters tubular urine via glomerular filtration. Most renal clearance of torsemide occurs via active secretion of the drug by the proximal tubules into tubular urine. After a single oral dose, the amounts recovered in urine were: torsemide 21%, metabolite M1 12%, metabolite M3 2%, and metabolite M5 34%. Renal Impairment In patients with renal failure, renal clearance of torsemide is markedly decreased but total plasma clearance is not significantly altered. A smaller fraction of the administered dose is delivered to the intraluminal site of action, and the natriuretic action of any given dose of diuretic is reduced. Hepatic Impairment In patients with hepatic cirrhosis, the volume of distribution, plasma half-life, and renal clearance are all increased, but total clearance is unchanged. Geriatric Patients The renal clearance of torsemide is lower in elderly subjects as compared to younger adults, which is related to the decline in renal function that commonly occurs with aging. However, total plasma clearance and elimination half-life remain unchanged. Heart Failure In patients with decompensated congestive heart failure, hepatic and renal clearance are both reduced, probably because of hepatic congestion and decreased renal plasma flow, respectively. The total clearance of torsemide is approximately 50% of that seen in healthy volunteers, and the plasma half-life and AUC are correspondingly increased. Because of reduced renal clearance, a smaller fraction of any given dose is delivered to the intraluminal site of action, so at any given dose there is less natriuresis in patients with heart failure than in normal subjects. Drug Interactions Digoxin : Coadministration of digoxin is reported to increase the AUC for torsemide by 50%, but dose adjustment of SOAANZ is not necessary. Torsemide does not affect the pharmacokinetics of digoxin. Spironolactone : In healthy subjects, coadministration of torsemide was associated with significant reduction in the renal clearance of spironolactone, with corresponding increases in the AUC. However, the pharmacokinetic profile and diuretic activity of torsemide are not altered by spironolactone. Torsemide does not affect the protein binding of glyburide or warfarin. Cimetidine : The pharmacokinetic profile and diuretic activity of torsemide are not altered by cimetidine.
Mechanism of action
Information about the established mechanism(s) of the drugÕs action in humans at various levels (for example receptor, membrane, tissue, organ, whole body). If the mechanism of action is not known, this field contains a statement about the lack of information.12.1 Mechanism of Action Micropuncture studies in animals have shown that torsemide acts from within the lumen of the thick ascending portion of the loop of Henle, where it inhibits the Na+/K+/2Cl--carrier system. Clinical pharmacology studies have confirmed this site of action in humans, and effects in other segments of the nephron have not been demonstrated. Diuretic activity thus correlates better with the rate of drug excretion in the urine than with the concentration in the blood. Torsemide increases the urinary excretion of sodium, chloride, and water, but it does not significantly alter glomerular filtration rate, renal plasma flow, or acid-base balance.
Pharmacodynamics
Information about any biochemical or physiologic pharmacologic effects of the drug or active metabolites related to the drugÕs clinical effect in preventing, diagnosing, mitigating, curing, or treating disease, or those related to adverse effects or toxicity.12.2 Pharmacodynamics With oral dosing of SOAANZ, the onset of diuresis occurs within 1 hour and the peak effect occurs during the first four hours and diuresis lasts about 6 to 8 hours.The mean increase in potassium excretion over 23 hours following a single oral dose of SOAANZ 20 mg in healthy adults was 12.7 mEq. Edema Torsemide has been studied in controlled trials in patients with New York Heart Association Class II to Class IV heart failure. Patients who received 10 mg to 20 mg of daily torsemide in these studies achieved significantly greater reductions in weight and edema than did patients who received placebo. When torsemide is first administered, daily urinary sodium excretion increases for at least a week. With chronic administration, however, daily sodium loss comes into balance with dietary sodium intake. If the administration of torsemide is suddenly stopped, blood pressure returns to pretreatment levels over several days, without overshoot. Torsemide has been administered together with β-adrenergic blocking agents, ACE inhibitors, and calcium-channel blockers. Adverse drug interactions have not been observed, and special dosage adjustment has not been necessary.
Pharmacokinetics
Information about the clinically significant pharmacokinetics of a drug or active metabolites, for instance pertinent absorption, distribution, metabolism, and excretion parameters.12.3 Pharmacokinetics Absorption Torsemide reaches peak plasma concentration (C max ) within 2.5 hours after oral administration of SOAANZ. C max and area under the serum concentration-time curve (AUC) of torsemide after oral administration are proportional to dose over the range of 2.5 mg to 200 mg. Effect of Food Administration of SOAANZ with a high fat, high calorie meal in healthy adults delays the time to C max by about 45 minutes, increases C max by 100% and increases area under the plasma concentration over time curve (AUC) by 48%. No clinically significant change in overall diuretic activity was observed. Distribution The volume of distribution of torsemide is 12 to 15 liters in normal adults or in patients with mild to moderate renal failure or congestive heart failure. In patients with hepatic cirrhosis, the volume of distribution is approximately doubled. Torsemide is extensively bound to plasma protein (>99%). Metabolism Torsemide is metabolized by the hepatic cytochrome CYP2C9 and, to a minor extent, CYP2C8 and CYP2C18. Three main metabolites have been identified in humans. Metabolite M1 is formed by methylhydroxylation of torsemide, metabolite M3 is formed by ring hydroxylation of torsemide, and metabolite M5 is formed by oxidation of M1. The major metabolite in humans is the carboxylic acid derivative M5, which is biologically inactive. Metabolites M1 and M3 possess some pharmacological activity; however, their systemic exposures are much lower when compared to torsemide. Elimination In normal subjects the elimination half-life of torsemide is approximately 3.5 hours. Torsemide is cleared from the circulation by both hepatic metabolism (approximately 80% of total clearance) and excretion into the urine (approximately 20% of total clearance in patients with normal renal function). Because torsemide is extensively bound to plasma protein (>99%), very little enters tubular urine via glomerular filtration. Most renal clearance of torsemide occurs via active secretion of the drug by the proximal tubules into tubular urine. After a single oral dose, the amounts recovered in urine were: torsemide 21%, metabolite M1 12%, metabolite M3 2%, and metabolite M5 34%. Renal Impairment In patients with renal failure, renal clearance of torsemide is markedly decreased but total plasma clearance is not significantly altered. A smaller fraction of the administered dose is delivered to the intraluminal site of action, and the natriuretic action of any given dose of diuretic is reduced. Hepatic Impairment In patients with hepatic cirrhosis, the volume of distribution, plasma half-life, and renal clearance are all increased, but total clearance is unchanged. Geriatric Patients The renal clearance of torsemide is lower in elderly subjects as compared to younger adults, which is related to the decline in renal function that commonly occurs with aging. However, total plasma clearance and elimination half-life remain unchanged. Heart Failure In patients with decompensated congestive heart failure, hepatic and renal clearance are both reduced, probably because of hepatic congestion and decreased renal plasma flow, respectively. The total clearance of torsemide is approximately 50% of that seen in healthy volunteers, and the plasma half-life and AUC are correspondingly increased. Because of reduced renal clearance, a smaller fraction of any given dose is delivered to the intraluminal site of action, so at any given dose there is less natriuresis in patients with heart failure than in normal subjects. Drug Interactions Digoxin : Coadministration of digoxin is reported to increase the AUC for torsemide by 50%, but dose adjustment of SOAANZ is not necessary. Torsemide does not affect the pharmacokinetics of digoxin. Spironolactone : In healthy subjects, coadministration of torsemide was associated with significant reduction in the renal clearance of spironolactone, with corresponding increases in the AUC. However, the pharmacokinetic profile and diuretic activity of torsemide are not altered by spironolactone. Torsemide does not affect the protein binding of glyburide or warfarin. Cimetidine : The pharmacokinetic profile and diuretic activity of torsemide are not altered by cimetidine.
Contraindications
Information about situations in which the drug product is contraindicated or should not be used because the risk of use clearly outweighs any possible benefit, including the type and nature of reactions that have been reported.4 CONTRAINDICATIONS SOAANZ is contraindicated in patients with known hypersensitivity to SOAANZ. SOAANZ is contraindicated in patients who are anuric. SOAANZ is contraindicated in patients with hepatic coma. Hypersensitivity to SOAANZ, anuria, and hepatic coma. ( 4 )
Description
General information about the drug product, including the proprietary and established name of the drug, the type of dosage form and route of administration to which the label applies, qualitative and quantitative ingredient information, the pharmacologic or therapeutic class of the drug, and the chemical name and structural formula of the drug.11 DESCRIPTION SOAANZ contains torsemide, a diuretic of the pyridine-sulfonylurea class. Its chemical name is 1-isopropyl-3-[(4-m-toluidino-3-pyridyl) sulfonyl] urea and its structural formula is: Its empirical formula is C 16 H 20 N 4 O 3 S, its pKa is 6.42, and its molecular weight is 348.42. Torsemide is a white to off-white crystalline powder. The tablets for oral administration also contain colloidal silicon dioxide, hypromellose, iron oxide yellow, iron oxide red, lactose, magnesium stearate, microcrystalline cellulose, talc, polyethylene glycol and titanium dioxide. Chemical Structure
Dosage and administration
Information about the drug product’s dosage and administration recommendations, including starting dose, dose range, titration regimens, and any other clinically sigificant information that affects dosing recommendations.2 DOSAGE AND ADMINISTRATION The recommended initial dose is 20 mg oral SOAANZ once daily. If the diuretic response is inadequate, titrate upward by approximately doubling until the desired diuretic response is obtained. Doses higher than 200 mg have not been adequately studied. The recommended initial dose is 20 mg orally once daily. Titrate dose by approximately doubling until desired diuretic response is obtained. Doses above 200 mg have not been studied.( 2 )
Dosage forms and strengths
Information about all available dosage forms and strengths for the drug product to which the labeling applies. This field may contain descriptions of product appearance.3 DOSAGE FORMS AND STRENGTHS Tablets: 20 mg, 40 mg and 60 mg ( 3 ) Tablets: 20 mg, yellow, round, film-coated tablet debossed with "T20" on one side 40 mg, orange, round, film-coated tablet debossed with "T40" on one side 60 mg, pink, round, film-coated tablet debossed with "T60" on one side
Indications and usage
A statement of each of the drug products indications for use, such as for the treatment, prevention, mitigation, cure, or diagnosis of a disease or condition, or of a manifestation of a recognized disease or condition, or for the relief of symptoms associated with a recognized disease or condition. This field may also describe any relevant limitations of use.1 INDICATIONS AND USAGE SOAANZ is indicated in adults for the treatment of edema associated with heart failure or renal disease. SOAANZ is a loop diuretic indicated in adults for the treatment of edema associated with heart failure or renal disease. ( 1 )
Spl product data elements
Usually a list of ingredients in a drug product.SOAANZ Torsemide Torsemide Torsemide Silicon Dioxide Ferric Oxide Yellow Ferric Oxide Red Lactose, unspecified form Magnesium Stearate Microcrystalline Cellulose 101 Talc POLYETHYLENE GLYCOL, UNSPECIFIED Titanium Dioxide Biconvex T20 SOAANZ Torsemide Torsemide Torsemide Silicon Dioxide Ferric Oxide Yellow Ferric Oxide Red Lactose, unspecified form Magnesium Stearate Microcrystalline Cellulose 101 Talc POLYETHYLENE GLYCOL, UNSPECIFIED Titanium Dioxide Biconvex T60 SOAANZ Torsemide Torsemide Torsemide Silicon Dioxide Ferric Oxide Yellow Ferric Oxide Red Lactose, unspecified form Magnesium Stearate Microcrystalline Cellulose 101 Talc POLYETHYLENE GLYCOL, UNSPECIFIED Titanium Dioxide Biconvex T40 SOAANZ Torsemide Torsemide Torsemide Silicon Dioxide Ferric Oxide Yellow Ferric Oxide Red Lactose, unspecified form Magnesium Stearate Microcrystalline Cellulose 101 Talc POLYETHYLENE GLYCOL, UNSPECIFIED Titanium Dioxide Biconvex T20 SOAANZ Torsemide Torsemide Torsemide Silicon Dioxide Ferric Oxide Yellow Ferric Oxide Red Lactose, unspecified form Magnesium Stearate Microcrystalline Cellulose 101 Talc POLYETHYLENE GLYCOL, UNSPECIFIED Titanium Dioxide Biconvex T40 SOAANZ Torsemide Torsemide Torsemide Silicon Dioxide Ferric Oxide Yellow Ferric Oxide Red Lactose, unspecified form Magnesium Stearate Microcrystalline Cellulose 101 Talc POLYETHYLENE GLYCOL, UNSPECIFIED Titanium Dioxide Biconvex T60
Carcinogenesis and mutagenesis and impairment of fertility
Information about carcinogenic, mutagenic, or fertility impairment potential revealed by studies in animals. Information from human data about such potential is part of the warnings field.13.1 Carcinogenesis, Mutagenesis, Impairment of Fertility No overall increase in tumor incidence was found when torsemide was given to rats and mice throughout their lives at doses up to 9 mg/kg/day (rats) and 32 mg/kg/day (mice). On a body-weight basis, these doses are 27 to 96 times a human dose of 20 mg; on a body-surface-area basis, they are 5 to 8 times this dose. In the rat study, the high-dose female group demonstrated renal tubular injury, interstitial inflammation, and a statistically significant increase in renal adenomas and carcinomas. The tumor incidence in this group was, however, not much higher than the incidence sometimes seen in historical controls. Similar signs of chronic non-neoplastic renal injury have been reported in high-dose animal studies of other diuretics such as furosemide and hydrochlorothiazide. No mutagenic activity was detected in any of a variety of in vivo and in vitro tests of torsemide and its major human metabolite. The tests included the Ames test in bacteria (with and without metabolic activation), tests for chromosome aberrations and sister-chromatid exchanges in human lymphocytes, tests for various nuclear anomalies in cells found in hamster and murine bone marrow, tests for unscheduled DNA synthesis in mice and rats, and others. In doses up to 25 mg/kg/day (75 times a human dose of 20 mg on a body-weight basis; 13 times this dose on a body-surface-area basis), torsemide had no adverse effect on the reproductive performance of male or female rats.
Nonclinical toxicology
Information about toxicology in non-human subjects.13 NONCLINICAL TOXICOLOGY 13.1 Carcinogenesis, Mutagenesis, Impairment of Fertility No overall increase in tumor incidence was found when torsemide was given to rats and mice throughout their lives at doses up to 9 mg/kg/day (rats) and 32 mg/kg/day (mice). On a body-weight basis, these doses are 27 to 96 times a human dose of 20 mg; on a body-surface-area basis, they are 5 to 8 times this dose. In the rat study, the high-dose female group demonstrated renal tubular injury, interstitial inflammation, and a statistically significant increase in renal adenomas and carcinomas. The tumor incidence in this group was, however, not much higher than the incidence sometimes seen in historical controls. Similar signs of chronic non-neoplastic renal injury have been reported in high-dose animal studies of other diuretics such as furosemide and hydrochlorothiazide. No mutagenic activity was detected in any of a variety of in vivo and in vitro tests of torsemide and its major human metabolite. The tests included the Ames test in bacteria (with and without metabolic activation), tests for chromosome aberrations and sister-chromatid exchanges in human lymphocytes, tests for various nuclear anomalies in cells found in hamster and murine bone marrow, tests for unscheduled DNA synthesis in mice and rats, and others. In doses up to 25 mg/kg/day (75 times a human dose of 20 mg on a body-weight basis; 13 times this dose on a body-surface-area basis), torsemide had no adverse effect on the reproductive performance of male or female rats.
Package label principal display panel
The content of the principal display panel of the product package, usually including the product’s name, dosage forms, and other key information about the drug product.PRINCIPAL DISPLAY PANEL - 20 mg Tablet Bottle Label - 786-07 NDC 73502-786-07 SOAANZ ® (torsemide) Tablets 20 mg 30 Tablets Rx only SARFEZ ® PRINCIPAL DISPLAY PANEL - 20 mg Tablet Bottle Label - 786-07
PRINCIPAL DISPLAY PANEL - 20 mg Tablet Bottle Label - 786-08 NDC 73502-786-08 SOAANZ ® (torsemide) Tablets 20 mg 90 Tablets Rx only SARFEZ ® PRINCIPAL DISPLAY PANEL - 20 mg Tablet Bottle Label - 786-08
PRINCIPAL DISPLAY PANEL - 60 mg Tablet Bottle Label - 687-13 NDC 73502-687-13 SOAANZ ® (torsemide) Tablets 60 mg 30 Tablets Rx only SARFEZ ® PRINCIPAL DISPLAY PANEL - 60 mg Tablet Bottle Label - 687-13
PRINCIPAL DISPLAY PANEL - 60 mg Tablet Bottle Label - 687-14 NDC 73502-687-14 SOAANZ ® (torsemide) Tablets 60 mg 90 Tablets Rx only SARFEZ ® PRINCIPAL DISPLAY PANEL - 60 mg Tablet Bottle Label - 687-14
PRINCIPAL DISPLAY PANEL - 40 mg Tablet Bottle Label - 586-10 NDC 73502-586-10 SOAANZ ® (torsemide) Tablets 40 mg 30 Tablets Rx only SARFEZ ® PRINCIPAL DISPLAY PANEL - 40 mg Tablet Bottle Label - 586-10
PRINCIPAL DISPLAY PANEL - 40 mg Tablet Bottle Label - 586-11 NDC 73502-586-11 SOAANZ ® (torsemide) Tablets 40 mg 90 Tablets Rx only SARFEZ ® PRINCIPAL DISPLAY PANEL - 40 mg Tablet Bottle Label - 586-11
PRINCIPAL DISPLAY PANEL - 20 mg Tablet Blister Pack Label NDC 73502-286-09 SOAANZ ® (torsemide) Tablets 20 mg Manufactured for: Sarfez Pharmaceuticals Inc. KR/DRUGS/KTK/25/460/2001 LOT: EXP: PRINCIPAL DISPLAY PANEL - 20 mg Tablet Blister Pack Label
PRINCIPAL DISPLAY PANEL - 20 mg Tablet Blister Pack Carton NDC 73502-286-15 SOAANZ ® (torsemide) Tablets 20 mg per tablet 30 Tablets (5 blister cards x 6 tablets each) Rx only SARFEZ ® PRINCIPAL DISPLAY PANEL - 20 mg Tablet Blister Pack Carton
PRINCIPAL DISPLAY PANEL - 40 mg Tablet Blister Pack Label NDC 73502-287-12 SOAANZ ® (torsemide) Tablets 40 mg Manufactured for: Sarfez Pharmaceuticals Inc. KR/DRUGS/KTK/25/460/2001 LOT: EXP: PRINCIPAL DISPLAY PANEL - 40 mg Tablet Blister Pack Label
PRINCIPAL DISPLAY PANEL - 40 mg Tablet Blister Pack Carton NDC 73502-287-16 SOAANZ ® (torsemide) Tablets 40 mg per tablet 30 Tablets (5 blister cards x 6 tablets each) Rx only SARFEZ ® PRINCIPAL DISPLAY PANEL - 40 mg Tablet Blister Pack Carton
PRINCIPAL DISPLAY PANEL - 60 mg Tablet Blister Pack Label NDC 73502-288-15 SOAANZ ® (torsemide) Tablets 60 mg Manufactured for: Sarfez Pharmaceuticals Inc. KR/DRUGS/KTK/25/460/2001 LOT: EXP: PRINCIPAL DISPLAY PANEL - 60 mg Tablet Blister Pack Label
PRINCIPAL DISPLAY PANEL - 60 mg Tablet Blister Pack Carton NDC 73502-288-17 SOAANZ ® (torsemide) Tablets 60 mg per tablet 30 Tablets (5 blister cards x 6 tablets each) Rx only SARFEZ ® PRINCIPAL DISPLAY PANEL - 60 mg Tablet Blister Pack Carton
Spl unclassified section
Information not classified as belonging to one of the other fields. Approximately 40% of labeling with effective_time between June 2009 and August 2014 have information in this field.SARFEZ and SOAANZ are registered trademarks of Sarfez. Any other trademarks are the property of their respective owners. Manufactured For: Sarfez Pharmaceuticals Inc. Vienna, VA 22182 © 2021 Sarfez Pharmaceuticals Inc.
SOAANZ: Information for patients
Information necessary for patients to use the drug safely and effectively, such as precautions concerning driving or the concomitant use of other substances that may have harmful additive effects.17 PATIENT COUNSELING INFORMATION Symptomatic Hypotension: Advise patients receiving SOAANZ that lightheadedness can occur, especially during the first days of therapy, and that it should be reported to the prescribing physician. Patients should be told that if syncope occurs, SOAANZ should be discontinued until the physician has been consulted. All patients should be cautioned that inadequate fluid intake, excessive perspiration, diarrhea, or vomiting can lead to an excessive fall in blood pressure, with the same consequences of lightheadedness and possible syncope [see Warnings and Precautions (5.1) ] . Non-Steroidal Anti-inflammatory Drugs (NSAID): Advise patients to discuss with their physician before taking NSAID medications concomitantly [see Drug Interactions (7.1) ] .
Geriatric use
Information about any limitations on any geriatric indications, needs for specific monitoring, hazards associated with use of the drug in the geriatric population.8.5 Geriatric Use Of the total number of patients who received torsemide in United States clinical studies, 24% were 65 or older and about 4% were 75 or older. No specific age-related differences in effectiveness or safety were observed between younger patients and elderly patients.
Pediatric use
Information about any limitations on any pediatric indications, needs for specific monitoring, hazards associated with use of the drug in any subsets of the pediatric population (such as neonates, infants, children, or adolescents), differences between pediatric and adult responses to the drug, and other information related to the safe and effective pediatric use of the drug.8.4 Pediatric Use The safety and effectiveness of SOAANZ in pediatric patients have not been established. Administration of a loop diuretic to premature infants has been associated with the precipitation of nephrocalcinosis/nephrolithiasis. Nephrocalcinosis/nephrolithiasis has also been observed in children under 4 years of age with no history of prematurity who have been treated chronically with a loop diuretic. A loop diuretic, when administered during the first weeks of life, has also been reported to increase the risk of persistent patent ductus arteriosus.
Pregnancy
Information about effects the drug may have on pregnant women or on a fetus. This field may be ommitted if the drug is not absorbed systemically and the drug is not known to have a potential for indirect harm to the fetus. It may contain information about the established pregnancy category classification for the drug. (That information is nominally listed in the teratogenic_effects field, but may be listed here instead.)8.1 Pregnancy Risk Summary There are no available data on use of SOAANZ in pregnant women and the risk of major birth defects or miscarriage. In pregnant rats and rabbits dosed, on a mg/m 2 basis, with 2.4 and 1.6 times a human starting dose of 20 mg/day, respectively, there was no fetotoxicity or teratogenicity. However, in pregnant rats and rabbits administered 50 and 6.8 times the human dose, respectively, decreases in body weight, decreased fetal resorption and delayed fetal ossification was observed. The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. All pregnancies have a background risk of birth defect, loss, or other adverse outcomes. In the U.S. general population, the estimated background risk of major malformations and miscarriage in clinically recognized pregnancies is 2-4%, and 15-20%, respectively. Animal Data There was no fetotoxicity or teratogenicity in rats treated with up to 5 mg/kg/day of torsemide (on a mg/m 2 basis, the animal dose is 2.4 times the human starting dose of 20 mg/day), or in rabbits, treated with 1.6 mg/kg/day (on a mg/m 2 basis, the animal dose is 1.6 times the human starting dose of 20 mg/day dose). Fetal and maternal toxicity (decrease in average body weight, increase in fetal resorption and delayed fetal ossification) occurred in rabbits and rats given doses 4 (rabbits) and 5 (rats) times larger.
Use in specific populations
Information about use of the drug by patients in specific populations, including pregnant women and nursing mothers, pediatric patients, and geriatric patients.8 USE IN SPECIFIC POPULATIONS 8.1 Pregnancy Risk Summary There are no available data on use of SOAANZ in pregnant women and the risk of major birth defects or miscarriage. In pregnant rats and rabbits dosed, on a mg/m 2 basis, with 2.4 and 1.6 times a human starting dose of 20 mg/day, respectively, there was no fetotoxicity or teratogenicity. However, in pregnant rats and rabbits administered 50 and 6.8 times the human dose, respectively, decreases in body weight, decreased fetal resorption and delayed fetal ossification was observed. The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. All pregnancies have a background risk of birth defect, loss, or other adverse outcomes. In the U.S. general population, the estimated background risk of major malformations and miscarriage in clinically recognized pregnancies is 2-4%, and 15-20%, respectively. Animal Data There was no fetotoxicity or teratogenicity in rats treated with up to 5 mg/kg/day of torsemide (on a mg/m 2 basis, the animal dose is 2.4 times the human starting dose of 20 mg/day), or in rabbits, treated with 1.6 mg/kg/day (on a mg/m 2 basis, the animal dose is 1.6 times the human starting dose of 20 mg/day dose). Fetal and maternal toxicity (decrease in average body weight, increase in fetal resorption and delayed fetal ossification) occurred in rabbits and rats given doses 4 (rabbits) and 5 (rats) times larger. 8.2 Lactation Risk Summary There are no data regarding the presence of torsemide in human milk or the effects of torsemide on the breastfed child. Diuretics can suppress lactation. 8.4 Pediatric Use The safety and effectiveness of SOAANZ in pediatric patients have not been established. Administration of a loop diuretic to premature infants has been associated with the precipitation of nephrocalcinosis/nephrolithiasis. Nephrocalcinosis/nephrolithiasis has also been observed in children under 4 years of age with no history of prematurity who have been treated chronically with a loop diuretic. A loop diuretic, when administered during the first weeks of life, has also been reported to increase the risk of persistent patent ductus arteriosus. 8.5 Geriatric Use Of the total number of patients who received torsemide in United States clinical studies, 24% were 65 or older and about 4% were 75 or older. No specific age-related differences in effectiveness or safety were observed between younger patients and elderly patients. 8.6 Use in Renal Impairment In patients with non-anuric renal failure, high doses of torsemide (20 mg to 200 mg) caused marked increases in water and sodium excretion. In patients with non-anuric renal failure, severe enough to require hemodialysis, chronic treatment with up to 200 mg of daily torsemide has not been shown to change steady-state fluid retention. When patients in a study of acute renal failure received total daily doses of 520 mg to 1200 mg of torsemide, 19% experienced seizures. Ninety-six patients were treated in this study; 6/32 treated with torsemide experienced seizures, 6/32 treated with comparably high doses of furosemide experienced seizures, and 1/32 treated with placebo experienced a seizure. [see Dosage and Administration (2.1)].
How supplied
Information about the available dosage forms to which the labeling applies, and for which the manufacturer or distributor is responsible. This field ordinarily includes the strength of the dosage form (in metric units), the units in which the dosage form is available for prescribing, appropriate information to facilitate identification of the dosage forms (such as shape, color, coating, scoring, and National Drug Code), and special handling and storage condition information.16 HOW SUPPLIED/STORAGE AND HANDLING SOAANZ tablets are available as round, film-coated, debossed on one side in the following configurations: Strength Color Debossing Bottle of 30 tablets Bottle of 90 Tablets 20 mg Yellow T20 NDC 73502-786-07 NDC 73502-786-08 40 mg Orange T40 NDC 73502-586-10 NDC 73502-586-11 60 mg Pink T60 NDC 73502-687-13 NDC 73502-687-14 Strength Color Debossing Tablets per Card Carton of 30 Tablets 20 mg Yellow T20 6 NDC 73502-286-09 40 mg Orange T40 6 NDC 73502-288-15 60 mg Pink T60 6 NDC 73502-287-12 Store between 20°C and 25°C (68°F and 77°F). Excursions permitted between 15°C and 30°C (59° F and 86°F).
| Strength | Color | Debossing | Bottle of 30 tablets | Bottle of 90 Tablets |
|---|---|---|---|---|
| 20 mg | Yellow | T20 | NDC 73502-786-07 | NDC 73502-786-08 |
| 40 mg | Orange | T40 | NDC 73502-586-10 | NDC 73502-586-11 |
| 60 mg | Pink | T60 | NDC 73502-687-13 | NDC 73502-687-14 |
| Strength | Color | Debossing | Tablets per Card | Carton of 30 Tablets |
|---|---|---|---|---|
| 20 mg | Yellow | T20 | 6 | NDC 73502-286-09 |
| 40 mg | Orange | T40 | 6 | NDC 73502-288-15 |
| 60 mg | Pink | T60 | 6 | NDC 73502-287-12 |
Storage and handling
Information about safe storage and handling of the drug product.Store between 20°C and 25°C (68°F and 77°F). Excursions permitted between 15°C and 30°C (59° F and 86°F).
Disclaimer: Do not rely on openFDA or Phanrmacy Near Me to make decisions regarding medical care. While we make every effort to ensure that data is accurate, you should assume all results are unvalidated. Source: OpenFDA, Healthporta Drugs API