Demadex (Torsemide)

DEMADEX®

Roche

Torsemide

Diuretic – Antihypertensive

Action And Clinical Pharmacology: 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 NaK2Clcarrier 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.

Pharmacokinetics: The bioavailability of torsemide tablets is approximately 80%, with little intersubject variation; the 90% confidence interval is 75 to 89%. The drug is absorbed with little first-pass metabolism, and the serum concentration reaches its peak (Cmax) within 1 hour after oral administration. Cmax and area under the serum concentration-time curve (AUC) after oral administration are proportional to dose over the range of 2.5 to 200 mg. Simultaneous food intake delays the time to Cmax by about 30 minutes, but overall bioavailability (AUC) and diuretic activity are unchanged. Absorption is essentially unaffected by renal or hepatic dysfunction.

The volume of distribution of torsemide is 12 to 15 L 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.

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). The major metabolite in humans is the carboxylic acid derivative, which is biologically inactive. Two of the lesser metabolites possess some diuretic activity, but for practical purposes metabolism terminates the action of the drug.

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.

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 congestive heart failure than in normal subjects.

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 response in renal failure may still be achieved if patients are given higher doses. The total plasma clearance and elimination half-life of torsemide remain normal under the conditions of impaired renal function because metabolic elimination by the liver remains intact.

In patients with hepatic cirrhosis, the volume of distribution, plasma half-life, and renal clearance are all increased, but total clearance is unchanged.

The pharmacokinetic profile of torsemide in healthy elderly subjects is similar to that in young subjects except for a decrease in renal clearance related to the decline in renal function that commonly occurs with aging. However, total plasma clearance and elimination half-life remain unchanged.

The pharmacokinetics of torsemide after i.v. administration were studied in normal volunteers at doses of 5, 10 and 20 mg. The pharmacokinetics did not seem to be dependent upon dose, indicating that, over the dose range of 5 to 20 mg, torsemide obeys linear pharmacokinetics. The pharmacokinetic parameters of torsemide following i.v. administration are summarized in Table I.

Clinical Effects: The diuretic effects of torsemide begin within 10 minutes of i.v. dosing and peak within the first hour. With oral dosing, the onset of diuresis occurs within 1 hour and the peak effect occurs during the first or second hour. Independent of the route of administration, diuresis lasts about 6 to 8 hours. In healthy subjects given single doses, the dose-response relationship for sodium excretion is linear over the dose range of 2.5 to 20 mg. The increase in potassium excretion is negligible after a single dose of up to 10 mg and only slight (5 to 15 mEq) after a single dose of 20 mg.

Torsemide has been studied in controlled trials in patients with New York Heart Association Class II to Class IV congestive heart failure. Patients who received 10 to 20 mg of daily torsemide in these studies achieved significantly greater reductions in weight and edema than did patients who received placebo.

In single-dose studies in patients with nonanuric renal failure, high doses of torsemide (20 to 200 mg) caused marked increases in water and sodium excretion. In patients with nonanuric 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. Chronic use of any diuretic in renal disease has not been studied in adequate and well-controlled trials.

When given with aldosterone antagonists, torsemide also caused increases in sodium and fluid excretion in patients with edema or ascites due to hepatic cirrhosis. Urinary sodium excretion rate relative to the urinary excretion rate of torsemide is less in cirrhotic patients than in healthy subjects (possibly because of the hyperaldosteronism and resultant sodium retention that are characteristic of portal hypertension and ascites). However, because of the increased renal clearance of torsemide in patients with hepatic cirrhosis, these factors tend to balance each other, and the result is an overall natriuretic response that is similar to that seen in healthy subjects. Chronic use of any diuretic in hepatic disease has not been studied in adequate and well-controlled trials.

In patients with essential hypertension, torsemide has been shown in controlled studies to lower blood pressure when administered once a day at doses of 5 to 10 mg. The antihypertensive effect is near maximal after 4 to 6 weeks of treatment, but it may continue to increase for up to 12 weeks. Systolic and diastolic supine and standing blood pressures are all reduced. There is no significant orthostatic effect, and there is only a minimal peak-trough difference in blood-pressure reduction.

The antihypertensive effects of torsemide are, like those of other diuretics, on the average greater in black patients (a low-renin population) than in nonblack patients.

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 b-adrenergic blocking agents, ACE inhibitors, and calcium-channel blockers. Adverse drug interactions have not been observed, and special dosage adjustment has not been necessary.

Indications And Clinical Uses: For the treatment of edema associated with congestive heart failure, renal disease, or hepatic disease. Chronic use of any diuretic in renal or hepatic disease has not been studied in adequate and well-controlled trials.

Torsemide is indicated for the treatment of mild to moderate essential hypertension alone or in combination with other antihypertensive agents.

Torsemide i.v. injection is indicated when a rapid onset of diuresis is desired or when oral administration is impractical.

Contra-Indications: In patients with known hypersensitivity to torsemide or to sulfonylureas.

Torsemide is contraindicated in patients who are anuric and in cases of hepatic coma and states of severe electrolyte depletion until the condition is improved or corrected.

Manufacturers’ Warnings In Clinical States: Torsemide is a potent diuretic which, if given in excessive amounts, can lead to profound diuresis with water and electrolyte depletion. Therefore, careful medical supervision is required and dose and dosage schedule have to be adjusted to the individual patient’s needs (see Dosage).

Hepatic Disease with Cirrhosis and Ascites: Torsemide should be used with caution in patients with hepatic disease with cirrhosis and ascites, since sudden alterations of fluid and electrolyte balance may precipitate hepatic coma. In these patients, diuresis with torsemide is best initiated in the hospital. To prevent hypokalemia and metabolic alkalosis, an aldosterone antagonist or potassium-sparing drug should be used concomitantly with torsemide.

Ototoxicity: Tinnitus and hearing loss (usually reversible) have been observed after rapid i.v. injection of other loop diuretics and have also been observed after oral torsemide. Ototoxicity has also been seen in animal studies when very high plasma levels of torsemide were induced. Administered i.v., torsemide should be injected slowly over 2 minutes, and single doses should not exceed 200 mg.

Volume and Electrolyte Depletion: Patients receiving diuretics should be observed for clinical evidence of electrolyte imbalance, hypovolemia, or prerenal azotemia. Symptoms of these disturbances may include one or more of the following: dryness of the mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pain or cramps, muscular fatigue, hypotension, oliguria, tachycardia, nausea, and vomiting. Excessive diuresis may cause dehydration, blood-volume reduction, and possibly thrombosis and embolism, especially in elderly patients. In patients who develop fluid and electrolyte imbalances, hypovolemia, or prerenal azotemia, the observed laboratory changes may include hyper- or hyponatremia, hyper- or hypochloremia, hyper- or hypokalemia, acid-base abnormalities, and increased blood urea nitrogen. If any of these occur, torsemide should be discontinued until the situation is corrected; torsemide may be restarted at a lower dose.

In controlled studies in the United States, torsemide was administered to hypertensive patients at doses of 5 or 10 mg daily. After 6 weeks at these doses, the mean decrease in serum potassium was approximately 0.1 mEq/L. In patients with congestive heart failure, hepatic cirrhosis, or renal disease treated with torsemide at doses higher than those studied in U.S. antihypertensive trials (i.e., 10 mg daily), hypokalemia was observed with greater frequency, in a dose-related manner.

In patients with cardiovascular disease, especially those receiving digitalis glycosides, diuretic-induced hypokalemia may be a risk factor for the development of arrhythmias. The risk of hypokalemia is greatest in patients with cirrhosis of the liver, in patients experiencing a brisk diuresis, in patients who are receiving inadequate oral intake of electrolytes, and in patients receiving concomitant therapy with corticosteroids or ACTH.

Periodic monitoring of serum potassium and other electrolytes is advised in patients treated with torsemide.

Torsemide is not removed from circulation by hemodialysis.

Precautions: Laboratory Values: Potassium: See Warnings, Volume and Electrolyte Depletion.

Calcium: Single doses of torsemide increased the urinary excretion of calcium by normal subjects, but serum calcium levels were slightly increased in 4- to 6-week hypertension trials. In long-term hypertension studies, the average 1-year change in serum calcium was a decrease of 0.1 mg/dL (0.02 mmol/L). Among 426 patients treated with torsemide for an average of 11 months, hypocalcemia was not reported as an adverse event.

Magnesium: Single doses of torsemide caused healthy volunteers to increase their urinary excretion of magnesium, but serum magnesium levels were slightly increased in 4- to 6-week hypertension trials. In long-term hypertension studies, the average 1-year change in serum magnesium was an increase of 0.03 mg/dL (0.01 mmol/L). Among 426 patients treated with torsemide for an average of 11 months, 1 case of hypomagnesemia (1.3 mg/dL (0.53 mmol/L)) was reported as an adverse event.

In long-term open clinical study of torsemide in patients with congestive heart failure, who received magnesium supplements, an increase in serum magnesium of 0.2 mg/dL (0.08 mmol/L) was observed. In a 4-week study in which magnesium supplementation was not given, the rate of occurrence of serum magnesium levels below 1.7 mg/dL (0.7 mmol/L) was 6 and 9% in the groups receiving 5 and 10 mg of torsemide, respectively.

Blood Urea Nitrogen (BUN), Creatinine, and Uric Acid: Torsemide produces small dose-related increases in each of these laboratory values. In hypertensive patients who received 10 mg of torsemide daily for 6 weeks, the mean increase in blood urea nitrogen was 1.8 mg/dL (0.6 mmol/L), the mean increase in serum creatinine was 0.05 mg/dL (4 mol/L), and the mean increase in serum uric acid was 1.2 mg/dL (70 mol/L).

Little further change occurred with long-term treatment, and all changes reversed when treatment was discontinued.

Symptomatic gout has been reported in patients receiving torsemide.

Glucose: Hypertensive patients who received 10 mg of daily torsemide experienced a mean increase in serum glucose concentration of 5.5 mg/dL (0.3 mmol/L) after 6 weeks of therapy, with a further increase of 1.8 mg/dL (0.1 mmol/L) during the subsequent year. In long-term studies in diabetics, mean fasting glucose values were not significantly changed from baseline. Cases of hyperglycemia have been reported but are uncommon.

Serum Lipids: In controlled hypertension studies of 4- to 6-weeks’ duration, daily doses of 5, 10, and 20 mg of torsemide were associated with increases in total plasma cholesterol of 4, 4 and 8 mg/dL (0.1 to 0.2 mmol/L), respectively. The increase with 20 mg of torsemide was statistically significant.

In the same studies, mean increases in plasma triglycerides of 16, 13, and 71 mg/dL (0.15 to 0.8 mmol/L), respectively were observed. The increase with 20 mg was statistically significant.

Other: In long-term studies in hypertensive patients, torsemide has been associated with small mean decreases in hemoglobin, hematocrit, and erythrocyte count and small mean increases in white blood cell count, platelet count, and serum alkaline phosphatase. Although statistically significant, all of these changes were medically inconsequential. No significant trends have been observed in any liver enzyme tests other than alkaline phosphatase.

Drug Interactions: In patients with essential hypertension, torsemide has been administered together with b-blockers, ACE inhibitors, and calcium-channel blockers. In patients with congestive heart failure, torsemide has been administered together with digitalis glycosides, ACE inhibitors, and organic nitrates. None of these combined uses were associated with new or unexpected adverse events.

Glyburide and Warfarin: Torsemide does not affect the protein binding of glyburide or warfarin.

Digoxin: Torsemide does not affect the pharmacokinetics of digoxin. Coadministration of digoxin is reported to increase the area under the curve for torsemide by 50%, but dose adjustment of torsemide is not necessary.

Spironolactone: In healthy subjects, coadministration of torsemide was associated with signficant reduction in the renal clearance of spironolactone, with corresponding increases in the AUC. The pharmacokinetic profile and diuretic activity of torsemide are not altered by spironolactone. Clinical experience indicates that dosage adjustment of either agent is not required.

Cimetidine: The pharmacokinetic profile and diuretic activity of torsemide are not altered by cimetidine.

Salicylates: Because torsemide and salicylates compete for secretion by renal tubules, patients receiving high doses of salicylates may experience salicylate toxicity when torsemide is concomitantly administered. Also, although possible interactions between torsemide and nonsteroidal anti-inflammatory agents (including ASA) have not been studied, coadministration of these agents with another loop diuretic (furosemide) has occasionally been associated with renal dysfunction.

Indomethacin: The natriuretic effect of torsemide is partially inhibited by the concomitant administration of indomethacin. This effect 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).

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 torsemide and cholestyramine are used concomitantly, simultaneous administration is not recommended.

Probenecid: Coadministration of probenecid reduces secretion of torsemide into the proximal tubule and thereby decreases the diuretic activity of torsemide.

Lithium: Other diuretics are known to reduce the renal clearance of lithium, inducing a high risk of lithium toxicity, so coadministration of lithium and diuretics should be undertaken with great caution, if at all. Coadministration of lithium and torsemide has not been studied.

Aminoglycoside Antibiotics and Ethacrynic Acid: Other diuretics have been reported to increase the ototoxic potential of aminoglycoside antibiotics and of ethacrynic acid, especially in the presence of impaired renal function. These potential interactions with torsemide have not been studied. In clinical trials tinnitus and hearing loss, usually reversible, have been reported after oral torsemide, therefore, concomitant administration of these products with torsemide is not recommended (see Warnings).

Pregnancy: There was no fetotoxicity or teratogenicity in rats treated with up to 5 mg/kg/day of torsemide or in rabbits treated with 1.6 mg/kg/day. 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.

No studies were carried out in pregnant women.

Torsemide should be given to pregnant women only if the potential benefit justifies the potential risk to the fetus.

Labor and Delivery: The effect of torsemide on labor and delivery is unknown.

Lactation: It should be noted that diuretics may partially inhibit lactation. It is not known whether torsemide is excreted in human milk. However, other diuretics do appear in human milk. If the use of torsemide is considered essential the patient should stop nursing.

Children: Safety and effectiveness in children have not been established.

Administration of another loop diuretic to severely premature infants with edema due to patent ductus arteriosus and hyaline membrane disease has occasionally been associated with renal calcifications, sometimes barely visible on x-ray but sometimes in staghorn form, filling the renal pelves. Some of these calculi have been dissolved, and hypercalciuria has been reported to have decreased, when chlorothiazide has been coadministered along with the loop diuretic. In other premature neonates with hyaline membrane disease, another loop diuretic has been reported to increase the risk of persistent patent ductus arteriosus, possibly through a prostaglandin-E-mediated process. The use of torsemide in such patients has not been studied.

Geriatrics: Of the total number of patients who received torsemide in U.S. clinical studies, 24% (198/843) were 65 or older while about 4% (34/843) were 75 or older. Decrease in renal clearance, related to the decline in renal function that commonly occurs with aging, has been observed. However, total plasma clearance and elimination half-life remain unchanged as compared to young healthy subjects (see Pharmacology and Dosage).

Adverse Reactions: Torsemide had been evaluated for safety in approximately 3 400 patients. Over 800 of these patients received torsemide for at least 6 months, and over 380 for more than 1 year.

In all North American studies, in which patients were treated for up to one year, 75.6% (536/709) of patients with hypertension, 67.3% (74/110) of patients with congestive heart failure and 54.2% (13/24) of patients with renal disease reported adverse events. Discontinuation of therapy due to adverse events occurred in 9.0% (76/843) of patients treated with torsemide.

In controlled North American studies, in which 564 patients were treated for either hypertension or congestive heart failure, 50.5% (259/513) and 60.8% (31/51) respectively, reported adverse events. Discontinuation of therapy due to adverse events occurred in 3.5% (20/564) of patients treated with torsemide.

In studies conducted in North America and Europe, discontinuations due to adverse events were required in 3% of patients (38/1250) with congestive heart failure, 2% of patients (8/409) with renal disease, and 7.6% of patients (13/170) with liver cirrhosis. Reported adverse events were generally mild to moderate in severity.

The most common reasons for discontinuation of therapy with torsemide were (in descending order of frequency); dizziness, headache, nausea, weakness, vomiting, hyperglycemia, excessive urination, hyperuricemia, hypokalemia, excessive thirst, hypovolemia, impotence, esophageal hemorrhage, and dyspepsia. Discontinuation rates for these adverse events ranged from 0.1% to 0.5%.

Of the nearly 3 400 patients who received torsemide in clinical trials 1.7% experienced at least one serious adverse event. The incidence of these serious adverse events was 1.7% (27/1 595) in patients with hypertension, 1.5% (19/1 250) with congestive heart failure, 1.5% (6/409) with renal insufficiency and 4.1% (7/170) with liver cirrhosis.

Most of these serious adverse events were related to the cardiovascular system. Other frequently affected body systems included the body as a whole and the respiratory and digestive systems. Serious adverse events were atrial fibrillation, chest pain, diarrhea, digitalis intoxication, gastrointestinal hemorrhage, hyperglycemia, hyperuricemia, hypokalemia, hypotension, hypovolemia, shunt thrombosis, rash, rectal bleeding, syncope and ventricular tachycardia.

Angioedema has been reported in a patient exposed to torsemide who was later found to be allergic to sulfa drugs.

In studies using i.v. administered torsemide, the most frequently reported adverse events were dizziness and dehydration, which were probably associated with volume depletion. Otherwise, i.v. torsemide had an adverse event profile qualitatively similar to that observed for short-term orally administered torsemide.

In studies using orally and i.v. administered torsemide, adverse events which were reported with a frequency less than 1% include: anemia, angina pectoris, anxiety, arrhythmia, AV block, bradycardia, bundle branch block, cerebral ischemia, dry skin, dysuria, excessive thirst, flatulence, hematuria, hyperglycemia, hypovolemia, increased BUN, malaise, postural hypotension, rectal bleeding, somnolence, increased sweating, syncope, tachycardia, and vertigo.

Abnormal Laboratory Findings: Studies in hypertension showed a statistically significant decreasing trend for hemoglobin, hematocrit, erythrocyte count, lymphocytes, sodium, chloride, calcium, potassium and urine specific gravity. Statistically significant increasing trends were detected for platelets, white blood cells, neutrophils, alkaline phosphatase, magnesium glucose and creatinine. Although the trends were statistically significant, the magnitude of the changes were slight (see Warnings and Precautions).

In patients with congestive heart failure, a decreasing trend over time was observed for sodium, potassium, and chloride whereas an increasing trend was observed for magnesium. No significant trends were observed for other electrolytes. Hypomagnesemia was detected in 1 congestive heart failure study in which magnesium supplements were not given.

In studies of patients with renal insufficiency, statistically significant changes were observed for serum calcium and potassium.

In patients with congestive heart failure, renal disease and hepatic cirrhosis, the extent of hypokalemia was dose related and occurred with a greater frequency than in hypertensive patients (see Warnings).

Results of clinical laboratory tests are consistent with the effects anticipated with the use of a diuretic.

Post Marketing Surveillance: Presently available Post Marketing Surveillance (PMS) data would indicate that the adverse event profile observed during the marketing phase does not significantly differ in type or severity from the adverse event spectrum reported during the clinical development phase of torsemide.

Symptoms And Treatment Of Overdose: Symptoms and Treatment: There is no human experience with overdoses of torsemide, but the signs and symptoms of overdosage can be anticipated to be those of excessive pharmacological 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 manoeuvres (e.g., manoeuvres 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.

Dosage And Administration: General: Dosage should be individualized with careful monitoring of patients’ response.

Simultaneous food intake has no overall effect on bioavailability of torsemide.

Because of the high bioavailability of torsemide, oral and i.v. doses are therapeutically equivalent, so patients may be switched to and from the i.v. form with no change in dose.

Torsemide i.v. injection should be administered slowly over a period of 2 minutes. Before administration, the solution of torsemide should be visually inspected for discoloration and particulate matter. If either is found, the ampul should not be used.

Geriatrics: Decrease in renal clearance related to a decrease in renal function has been observed. However, total plasma clearance and elimination half-life remain unchanged as compared to young healthy subjects. Therefore, special dose adjustment in the elderly with normal renal function is not necessary (see Pharmacology and Precautions).

Congestive Heart Failure: The usual initial dose is 10 or 20 mg of once-daily oral or i.v. torsemide. If the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained. A single dose of 200 mg should not be exceeded.

Chronic Renal Failure: The usual initial dose of torsemide is 20 mg of once-daily oral or i.v. torsemide. If the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained. A single dose of 200 mg should not be exceeded.

Hepatic cirrhosis: The usual initial dose is 5 or 10 mg of once-daily oral or i.v. torsemide, administered together with an aldosterone antagonist or a potassium-sparing diuretic. If the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained. A single dose of 40 mg should not be exceeded.

Hypertension: The usual initial dose is 5 mg once daily. If the 5 mg dose does not provide adequate reduction in blood pressure within 4 to 6 weeks, the dose may be increased to 10 mg once daily. If the response to 10 mg is insufficient, an additional antihypertensive agent should be added to the treatment regimen.

Reconstitution: For torsemide ampuls for i.v. injection, no dilution or reconstitution is required prior to use.

Availability And Storage: Ampuls: Each mL of sterile, colorless, clear liquid contains: torsemide 10 mg. Nonmedicinal ingredients: polyethylene glycol-400, sodium hydroxide (as needed to adjust pH), tromethamine in water for injection. Colorless glass ampuls of 2 and 5 mL, cartons of 10. Store at room temperature (15 to 30°C). Do not freeze.

Tablets: 5 mg: Each white to off-white, oval-shaped biconvex, scored tablet with “5” debossed on one side, and the logo and “102” debossed on the scored, opposite side, contains: torsemide 5 mg. Nonmedicinal ingredients: crospovidone, lactose, magnesium stearate, microcrystalline cellulose and povidone. Unit dose blister packs of 90. Store at room temperature (15 to 30°C).

10 mg: Each white to off-white, oval-shaped biconvex, scored tablet with “10” debossed on one side, and the logo and “103” debossed on the scored, opposite side, contains: torsemide 10 mg. Nonmedicinal ingredients: crospovidone, lactose, magnesium stearate, microcrystalline cellulose and povidone. Unit dose blister packs of 30. Store at room temperature (15 to 30°C).

20 mg: Each white to off-white, oval-shaped biconvex, scored tablet with “20” debossed on one side, and the logo and “104” debossed on the scored, opposite side, contains: torsemide 20 mg. Nonmedicinal ingredients: crospovidone, lactose, magnesium stearate, microcrystalline cellulose and povidone. Unit dose blister packs of 30. Store at room temperature (15 to 30°C).

100 mg: Each white to off-white, oval-shaped biconvex, scored tablet with “100” debossed on one side, and the logo and “105” debossed on the scored, opposite side, contains: torsemide 100 mg. Nonmedicinal ingredients: crospovidone, lactose, magnesium stearate, microcrystalline cellulose and povidone. Unit dose blister packs of 30. Store at room temperature (15 to 30°C).

DEMADEX® Roche Torsemide Diuretic – Antihypertensive

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