BUMETANIDE

Main information

  • Trade name:
  • BUMETANIDE- bumetanide tablet
  • Composition:
  • BUMETANIDE 2 mg
  • Administration route:
  • ORAL
  • Prescription type:
  • PRESCRIPTION DRUG
  • Medicine domain:
  • Humans
  • Medicine type:
  • Allopathic drug

Documents

Localization

  • Available in:
  • BUMETANIDE- bumetanide tablet
    United States
  • Language:
  • English

Therapeutic information

  • Therapeutic indications:
  • Bumetanide tablets, USP are indicated for the treatment of edema associated with congestive heart failure, hepatic and renal disease, including the nephrotic syndrome. Almost equal diuretic response occurs after oral and parenteral administration of bumetanide. Therefore, if impaired gastrointestinal absorption is suspected or oral administration is not practical, bumetanide should be given by the intramuscular or intravenous route. Successful treatment with bumetanide tablets, USP following instances of allergic reactions to furosemide suggests a lack of cross-sensitivity. Bumetanide is contraindicated in anuria. Although bumetanide can be used to induce diuresis in renal insufficiency, any marked increase in blood urea nitrogen or creatinine, or the development of oliguria during therapy of patients with progressive renal disease, is an indication for discontinuation of treatment with bumetanide. Bumetanide is also contraindicated in patients in hepatic coma or in states of severe electrolyte depletion unti
  • Product summary:
  • Bumetanide Tablets, USP, for oral administration, are available as 0.5 mg Green, round, biconvex, bisected and debossed “E” above and “128” below the bisect on one side and plain on the reverse side and supplied as: NDC 0185-0128-01 bottles of 100 NDC 0185-0128-05 bottles of 500 1 mg Yellow, round, biconvex, bisected and debossed “E” above and “129” below the bisect on one side and plain on the reverse side and supplied as: NDC 0185-0129-01 bottles of 100 NDC 0185-0129-05 bottles of 500 2 mg Beige to light brown, round, biconvex, bisected and debossed “E” above and “130” below the bisect on one side and plain on the reverse side and supplied as: NDC 0185-0130-01 bottles of 100 NDC 0185-0130-05 bottles of 500 Storage Store at 20° to 25°C (68° to 77°F) [see USP Controlled Room Temperature]. Dispense contents in a tight, light-resistant container as defined in the USP with a child-resistant closure, as required. KEEP TIGHTLY CLOSED. To report SUSPECTED ADVERSE REACTIONS, contact Sandoz Inc. at 1-800-525-8747 or FDA at 1-800-FDA-1088 or www.fda.gov/ medwatch. Manufactured by Sandoz Inc. Princeton, NJ 08540 46192277 Rev. September 2016 MF0128REV09/ 16

Status

  • Source:
  • DailyMed - NLM - National Library of Medicine
  • Authorization status:
  • Abbreviated New Drug Application
  • Authorization number:
  • 43353-292-51
  • Last update:
  • 26-05-2019

Summary of Product characteristics: dosage, interactions, side effects

BUMETANIDE- bumetanide tablet

Aphena Pharma Solutions - Tennessee, LLC

----------

Bumetanide Tablets, USP

Rx Only

WARNING

Bumetanide is a potent diuretic which, if given in excessive amounts, can lead to a 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 AND ADMINISTRATION).

DESCRIPTION

Bumetanide is a loop diuretic, available as scored tablets. Each tablet for oral administration contains

0.5 mg, 1 mg or 2 mg of bumetanide. In addition, each tablet contains the following inactive ingredients:

anhydrous lactose, corn starch, magnesium stearate, microcrystalline cellulose, pregelatinized starch

(corn), talc, with the following dye systems: 0.5 mg- D&C yellow No. 10 aluminum lake, FD&C blue

No. 1 aluminum lake and FD&C red No. 40 aluminum lake; 1 mg- D&C yellow No. 10 aluminum lake; 2

mg- synthetic black iron oxide, synthetic red iron oxide and synthetic yellow iron oxide.

Chemically, bumetanide is 3-(butylamino)-4-phenoxy-5-sulfamoylbenzoic acid. It is a practically white

powder having a calculated molecular weight of 364.42, and the following structural formula:

H N O S

CLINICAL PHARMACOLOGY

Bumetanide is a loop diuretic with a rapid onset and short duration of action. Pharmacological and

clinical studies have shown that 1 mg bumetanide has a diuretic potency equivalent to approximately 40

mg furosemide. The major site of bumetanide action is the ascending limb of the loop of Henle.

The mode of action has been determined through various clearance studies in both humans and

experimental animals. Bumetanide inhibits sodium reabsorption in the ascending limb of the loop of

Henle, as shown by marked reduction of free-water clearance ( H O) during hydration and tubular free-

water reabsorption (T H O) during hydropenia. Reabsorption of chloride in the ascending limb is also

blocked by bumetanide, and bumetanide is somewhat more chloruretic than natriuretic.

Potassium excretion is also increased by bumetanide, in a dose-related fashion.

Bumetanide may have an additional action in the proximal tubule. Since phosphate reabsorption takes

place largely in the proximal tubule, phosphaturia during bumetanide-induced diuresis is indicative of

this additional action. This is further supported by the reduction in the renal clearance of bumetanide by

probenecid, associated with diminution in the natriuretic response. This proximal tubular activity does

not seem to be related to an inhibition of carbonic anhydrase. Bumetanide does not appear to have a

noticeable action on the distal tubule.

Bumetanide decreases uric acid excretion and increases serum uric acid. Following oral administration

of bumetanide the onset of diuresis occurs in 30 to 60 minutes. Peak activity is reached between 1 and 2

hours. At usual doses (1 mg to 2 mg) diuresis is largely complete within 4 hours; with higher doses, the

diuretic action lasts for 4 to 6 hours. Diuresis starts within minutes following an intravenous injection

and reaches maximum levels within 15 to 30 minutes.

Several pharmacokinetic studies have shown that bumetanide, administered orally or parenterally, is

eliminated rapidly in humans, with a half-life of between 1 and 1½ hours. Plasma protein-binding is in

the range of 94% to 96%.

Oral administration of carbon-14 labeled bumetanide to human volunteers revealed that 81% of the

administered radioactivity was excreted in the urine, 45% of it as unchanged drug. Urinary and biliary

metabolites identified in this study were formed by oxidation of the N-butyl side chain. Biliary

excretion of bumetanide amounted to only 2% of the administered dose.

Pediatric Pharmacology

Elimination of bumetanide appears to be considerably slower in neonatal patients compared with adults,

possibly because of immature renal and hepatobiliary function in this population. Small pharmacokinetic

studies of intravenous bumetanide in preterm and full-term neonates with respiratory disorders have

reported an apparent half-life of approximately 6 hours, with a range up to 15 hours and a serum

clearance ranging from 0.2 mL/min/kg to 1.1 mL/min/kg. In a population of neonates receiving

bumetanide for volume overload, mean serum clearance rates were 2.17 mL/min/kg in patients less than 2

months of age and 3.8 mL/min/kg in patients aged 2 to 6 months. Mean serum half-life of bumetanide was

2.5 hours and 1.5 hours in patients aged less than 2 months and those aged 2 to 6 months, respectively.

Elimination half-life decreased considerably during the first month of life, from a mean of

approximately 6 hours at birth to approximately 2.4 hours at 1 month of age.

In preterm neonates, mean serum concentrations following a single 0.05 mg/kg dose ranged from 126

mcg/L at 1 hour to 57 mcg/L at 8 hours. In another study, mean serum concentrations following a single

0.05 mg/kg dose were 338 ng/mL at 30 minutes and 176 ng/mL after 4 hours. A single dose of 0.1 mg/kg

produced mean serum levels of 314 ng/mL at 1 hour, and 195 ng/mL at 6 hours. Mean volume of

distribution in neonates and infants has been reported to range from 0.26 L/kg to 0.39 L/kg.

The degree of protein binding of bumetanide in cord sera from healthy neonates was approximately

97%, suggesting the potential for bilirubin displacement. A study using pooled sera from critically ill

neonates found that bumetanide at concentrations of 0.5 µg/mL to 50 mcg/mL, but not 0.25 mcg/mL,

caused a linear increase in unbound bilirubin concentrations.

In 56 infants aged 4 days to 6 months, bumetanide doses ranging from 0.005 mg/kg to 0.1 mg/kg were

studied for pharmacodynamic effect. Peak bumetanide excretion rates increased linearly with increasing

doses of drug. Maximal diuretic effect was observed at a bumetanide excretion rate of about 7

mcg/kg/hr, corresponding to doses of 0.035 mg/kg to 0.040 mg/kg. Higher doses produced a higher

bumetanide excretion rate but no increase in diuretic effect. Urine flow rate peaked during the first hour

after drug administration in 80% of patients and by 3 hours in all patients.

Geriatric Pharmacology

In a group of ten geriatric subjects between the ages of 65 and 73 years, total bumetanide clearance was

significantly lower (1.8 ± 0.3 mL/minkg) compared with younger subjects (2.9 ± 0.2 mL/minkg) after a

single oral bumetanide 0.5 mg dose. Maximum plasma concentrations were higher in geriatric subjects

(16.9 ± 1.8 ng/mL) compared with younger subjects (10.3 ± 1.5 ng/mL). Urine flow rate and total

excretion of sodium and potassium were increased less in the geriatric subjects compared with younger

subjects, although potassium excretion and fractional sodium excretion were similar between the two

age groups. Nonrenal clearance, bioavailability, and volume of distribution were not significantly

different between the two groups.

INDICATIONS AND USAGE

Bumetanide tablets, USP are indicated for the treatment of edema associated with congestive heart

failure, hepatic and renal disease, including the nephrotic syndrome.

Almost equal diuretic response occurs after oral and parenteral administration of bumetanide.

Therefore, if impaired gastrointestinal absorption is suspected or oral administration is not practical,

bumetanide should be given by the intramuscular or intravenous route.

Successful treatment with bumetanide tablets, USP following instances of allergic reactions to

furosemide suggests a lack of cross-sensitivity.

CONTRAINDICATIONS

Bumetanide is contraindicated in anuria. Although bumetanide can be used to induce diuresis in renal

insufficiency, any marked increase in blood urea nitrogen or creatinine, or the development of oliguria

during therapy of patients with progressive renal disease, is an indication for discontinuation of

treatment with bumetanide. Bumetanide is also contraindicated in patients in hepatic coma or in states of

severe electrolyte depletion until the condition is improved or corrected. Bumetanide is contraindicated

in patients hypersensitive to this drug.

WARNINGS

Volume and Electrolyte Depletion

The dose of bumetanide should be adjusted to the patient’s need. Excessive doses or too frequent

administration can lead to profound water loss, electrolyte depletion, dehydration, reduction in blood

volume and circulatory collapse with the possibility of vascular thrombosis and embolism, particularly

in elderly patients.

Hypokalemia

Hypokalemia can occur as a consequence of bumetanide administration. Prevention of hypokalemia

requires particular attention in the following conditions: patients receiving digitalis and diuretics for

congestive heart failure, hepatic cirrhosis and ascites, states of aldosterone excess with normal renal

function, potassium-losing nephropathy, certain diarrheal states, or other states where hypokalemia is

thought to represent particular added risks to the patient, i.e., history of ventricular arrhythmias.

In patients with hepatic cirrhosis and ascites, sudden alterations of electrolyte balance may precipitate

hepatic encephalopathy and coma. Treatment in such patients is best initiated in the hospital with small

doses and careful monitoring of the patient’s clinical status and electrolyte balance. Supplemental

potassium and/or spironolactone may prevent hypokalemia and metabolic alkalosis in these patients.

Ototoxicity

In cats, dogs and guinea pigs, bumetanide has been shown to produce ototoxicity. In these test animals

bumetanide was 5 to 6 times more potent than furosemide and, since the diuretic potency of bumetanide

is about 40 to 60 times furosemide, it is anticipated that blood levels necessary to produce ototoxicity

will rarely be achieved. The potential exists, however, and must be considered a risk of intravenous

therapy, especially at high doses, repeated frequently in the face of renal excretory function impairment.

Potentiation of aminoglycoside ototoxicity has not been tested for bumetanide. Like other members of

this class of diuretics, bumetanide probably shares this risk.

Allergy to Sulfonamides

Patients allergic to sulfonamides may show hypersensitivity to bumetanide.

Thrombocytopenia

Since there have been rare spontaneous reports of thrombocytopenia from postmarketing experience,

patients should be observed regularly for possible occurrence of thrombocytopenia.

PRECAUTIONS

General

Serum potassium should be measured periodically and potassium supplements or potassium-sparing

diuretics added if necessary. Periodic determinations of other electrolytes are advised in patients

treated with high doses or for prolonged periods, particularly in those on low-salt diets.

Hyperuricemia may occur; it has been asymptomatic in cases reported to date. Reversible elevations of

the BUN and creatinine may also occur, especially in association with dehydration and particularly in

patients with renal insufficiency. Bumetanide may increase urinary calcium excretion with resultant

hypocalcemia.

Diuretics have been shown to increase the urinary excretion of magnesium; this may result in

hypomagnesemia.

Laboratory Tests

Studies in normal subjects receiving bumetanide revealed no adverse effects on glucose tolerance,

plasma insulin, glucagon and growth hormone levels, but the possibility of an effect on glucose

metabolism exists. Periodic determinations of blood sugar should be done, particularly in patients with

diabetes or suspected latent diabetes.

Patients under treatment should be observed regularly for possible occurrence of blood dyscrasias,

liver damage or idiosyncratic reactions, which have been reported occasionally in foreign marketing

experience. The relationship of these occurrences to bumetanide use is not certain.

Drug Interactions

Drugs with Ototoxic Potential

(See WARNINGS)

Especially in the presence of impaired renal function, the use of parenterally administered bumetanide in

patients to whom aminoglycoside antibiotics are also being given should be avoided, except in life-

threatening conditions.

Drugs with Nephrotoxic Potential

There has been no experience with the concurrent use of bumetanide with drugs known to have a

nephrotoxic potential. Therefore, the simultaneous administration of these drugs should be avoided.

Lithium

Lithium should generally not be given with diuretics (such as bumetanide) because they reduce its renal

clearance and add a high risk of lithium toxicity.

Probenecid

Pretreatment with probenecid reduces both the natriuresis and hyperreninemia produced by bumetanide.

This antagonistic effect of probenecid on bumetanide natriuresis is not due to a direct action on sodium

excretion but is probably secondary to its inhibitory effect on renal tubular secretion of bumetanide.

Thus, probenecid should not be administered concurrently with bumetanide.

Indomethacin

Indomethacin blunts the increases in urine volume and sodium excretion seen during bumetanide

treatment and inhibits the bumetanide-induced increase in plasma renin activity. Concurrent therapy with

bumetanide is thus not recommended.

Antihypertensives

Bumetanide may potentiate the effect of various antihypertensive drugs, necessitating a reduction in the

dosage of these drugs.

Digoxin

Interaction studies in humans have shown no effect on digoxin blood levels.

Anticoagulants

Interaction studies in humans have shown bumetanide to have no effect on warfarin metabolism or on

plasma prothrombin activity.

Carcinogenesis, Mutagenesis and Impairment of Fertility

Bumetanide was devoid of mutagenic activity in various strains of Salmonella typhimurium when tested

in the presence or absence of an in vitro metabolic activation system. An 18-month study showed an

increase in mammary adenomas of questionable significance in female rats receiving oral doses of 60

mg/kg/day (2000 times a 2-mg human dose). A repeat study at the same doses failed to duplicate this

finding.

Reproduction studies were performed to evaluate general reproductive performance and fertility in rats

at oral dose levels of 10 mg/kg/day, 30 mg/kg/day, 60 mg/kg/day or 100 mg/kg/day. The pregnancy rate

was slightly decreased in the treated animals; however, the differences were small and not statistically

significant.

Pregnancy

Teratogenic Effects

Pregnancy Category C

Bumetanide is neither teratogenic nor embryocidal in mice when given in doses up to 3400 times the

maximum human therapeutic dose.

Bumetanide has been shown to be nonteratogenic, but it has a slight embryocidal effect in rats when

given in doses of 3400 times the maximum human therapeutic dose and in rabbits at doses of 3.4 times

the maximum human therapeutic dose. In one study, moderate growth retardation and increased incidence

of delayed ossification of sternebrae were observed in rats at oral doses of 100 mg/kg/day, 3400 times

the maximum human therapeutic dose. These effects were associated with maternal weight reductions

noted during dosing. No such adverse effects were observed at 30 mg/kg/day (1000 times the maximum

human therapeutic dose). No fetotoxicity was observed at 1000 to 2000 times the human therapeutic

dose.

In rabbits, a dose-related decrease in litter size and an increase in resorption rate were noted at oral

doses of 0.1 mg/kg/day and 0.3 mg/kg/day (3.4 and 10 times the maximum human therapeutic dose). A

slightly increased incidence of delayed ossification of sternebrae occurred at 0.3 mg/kg/day; however,

no such adverse effects were observed at the dose of 0.03 mg/kg/day. The sensitivity of the rabbit to

bumetanide parallels the marked pharmacologic and toxicologic effects of the drug in this species.

Bumetanide was not teratogenic in the hamster at an oral dose of 0.5 mg/kg/day (17 times the maximum

human therapeutic dose). Bumetanide was not teratogenic when given intravenously to mice and rats at

doses up to 140 times the maximum human therapeutic dose.

There are no adequate and well-controlled studies in pregnant women. A small investigational

experience in the United States and marketing experience in other countries to date have not indicated

any evidence of adverse effects on the fetus, but these data do not rule out the possibility of harmful

effects. Bumetanide should be given to a pregnant woman only if the potential benefit justifies the

potential risk to the fetus.

Nursing Mothers

It is not known whether this drug is excreted in human milk. As a general rule, nursing should not be

undertaken while the patient is on bumetanide since it may be excreted in human milk.

Pediatric Use

Safety and effectiveness in pediatric patients below the age of 18 have not been established.

In vitro studies using pooled sera from critically ill neonates have shown bumetanide to be a potent

displacer of bilirubin (see CLINICAL PHARMACOLOGY, Pediatric Pharmacology). The

administration of bumetanide could present a particular concern if given to critically ill or jaundiced

neonates at risk for kernicterus.

Geriatric Use

Clinical studies of bumetanide did not include sufficient numbers of subjects aged 65 and over to

determine whether they responded differently from younger subjects. Other reported clinical

experience has not identified differences in responses between the elderly and younger patients. In

general, dose selection for an elderly patient should be cautious, usually starting at the low end of the

dosing range, reflecting the greater frequency of decreased hepatic, renal or cardiac function, and of

concomitant disease or other drug therapy.

This drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug

may be greater in patients with impaired renal function. Because elderly patients are more likely to have

decreased renal function, care should be taken in dose selection, and it may be useful to monitor renal

function.

ADVERSE REACTIONS

The most frequent clinical adverse reactions considered probably or possibly related to bumetanide are

muscle cramps (seen in 1.1% of treated patients), dizziness (1.1%), hypotension (0.8%), headache

(0.6%), nausea (0.6%) and encephalopathy (in patients with preexisting liver disease) (0.6%). One or

more of these adverse reactions have been reported in approximately 4.1% of patients treated with

bumetanide.

Serious skin reactions (i.e., Stevens-Johnson syndrome, toxic epidermal necrolysis) have been reported

in association with bumetanide use.

Less frequent clinical adverse reactions to bumetanide are impaired hearing (0.5%), pruritus (0.4%),

electrocardiogram changes (0.4%), weakness (0.2%), hives (0.2%), abdominal pain (0.2%), arthritic

pain (0.2%), musculoskeletal pain (0.2%), rash (0.2%) and vomiting (0.2%). One or more of these

adverse reactions have been reported in approximately 2.9% of patients treated with bumetanide.

Other clinical adverse reactions, which have each occurred in approximately 0.1% of patients, are

vertigo, chest pain, ear discomfort, fatigue, dehydration, sweating, hyperventilation, dry mouth, upset

stomach, renal failure, asterixis, itching, nipple tenderness, diarrhea, premature ejaculation and

difficulty maintaining an erection.

Laboratory abnormalities reported have included hyperuricemia (in 18.4% of patients tested),

hypochloremia (14.9%), hypokalemia (14.7%), azotemia (10.6%), hyponatremia (9.2%), increased serum

creatinine (7.4%), hyperglycemia (6.6%), and variations in phosphorus (4.5%), CO content (4.3%),

bicarbonate (3.1%) and calcium (2.4%). Although manifestations of the pharmacologic action of

bumetanide, these conditions may become more pronounced by intensive therapy.

Also reported have been thrombocytopenia (0.2%) and deviations in hemoglobin (0.8%), prothrombin

time (0.8%), hematocrit (0.6%), WBC (0.3%) and differential counts (0.1%). There have been rare

spontaneous reports of thrombocytopenia from post-marketing experience.

Diuresis induced by bumetanide may also rarely be accompanied by changes in LDH (1.0%), total serum

bilirubin (0.8%), serum proteins (0.7%), SGOT (0.6%), SGPT (0.5%), alkaline phosphatase (0.4%),

cholesterol (0.4%) and creatinine clearance (0.3%). Increases in urinary glucose (0.7%) and urinary

protein (0.3%) have also been seen.

OVERDOSAGE

Overdosage can lead to acute profound water loss, volume and electrolyte depletion, dehydration,

reduction of blood volume and circulatory collapse with a possibility of vascular thrombosis and

embolism. Electrolyte depletion may be manifested by weakness, dizziness, mental confusion, anorexia,

lethargy, vomiting and cramps. Treatment consists of replacement of fluid and electrolyte losses by

careful monitoring of the urine and electrolyte output and serum electrolyte levels.

DOSAGE AND ADMINISTRATION

Dosage should be individualized with careful monitoring of patient response.

Oral Administration

The usual total daily dosage of bumetanide tablets is 0.5 mg to 2 mg and in most patients is given as a

single dose.

If the diuretic response to an initial dose of bumetanide tablets is not adequate, in view of its rapid onset

and short duration of action, a second or third dose may be given at 4 to 5 hour intervals up to a

maximum daily dose of 10 mg. An intermittent dose schedule, whereby bumetanide tablets is given on

alternate days or for 3 to 4 days with rest periods of 1 to 2 days in between, is recommended as the

safest and most effective method for the continued control of edema. In patients with hepatic failure, the

dosage should be kept to a minimum, and if necessary, dosage increased very carefully.

Because cross-sensitivity with furosemide has rarely been observed, bumetanide tablets can be

substituted at approximately a 1:40 ratio of bumetanide tablets to furosemide in patients allergic to

furosemide.

Parenteral Administration

Bumetanide injection may be administered parenterally (IV or IM) to patients in whom gastrointestinal

absorption may be impaired or in whom oral administration is not practical.

Parenteral treatment should be terminated and oral treatment instituted as soon as possible.

HOW SUPPLIED

Bumetanide Tablets, USP, for oral administration, are available as

0.5 mg

Green, round, biconvex, bisected and debossed “E” above and “128” below the bisect on one side and

plain on the reverse side and supplied as:

NDC 0185-0128-01 bottles of 100

NDC 0185-0128-05 bottles of 500

1 mg

Yellow, round, biconvex, bisected and debossed “E” above and “129” below the bisect on one side and

plain on the reverse side and supplied as:

NDC 0185-0129-01 bottles of 100

NDC 0185-0129-05 bottles of 500

2 mg

Beige to light brown, round, biconvex, bisected and debossed “E” above and “130” below the bisect on

one side and plain on the reverse side and supplied as:

NDC 0185-0130-01 bottles of 100

NDC 0185-0130-05 bottles of 500

Storage

Store at 20° to 25°C (68° to 77°F) [see USP Controlled Room Temperature].

Dispense contents in a tight, light-resistant container as defined in the USP with a child-resistant

closure, as required.

KEEP TIGHTLY CLOSED.

To report SUSPECTED ADVERSE REACTIONS, contact Sandoz Inc. at 1-800-525-8747 or

FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

Manufactured by

Sandoz Inc.

Princeton, NJ 08540

46192277

Rev. September 2016

MF0128REV09/16

Repackaging Information

Please reference the How Supplied section listed above for a description of individual tablets. This

drug product has been received by Aphena Pharma - TN in a manufacturer or distributor packaged

configuration and repackaged in full compliance with all applicable cGMP regulations. The package

configurations available from Aphena are listed below:

Count

2 mg

6000

43353-292-51

Store between 20°-25°C (68°-77°F). See USP Controlled Room Temperature. Dispense in a tight light-

resistant container as defined by USP. Keep this and all drugs out of the reach of children.

Repackaged by:

Cookeville, TN 38506

20171020DKJ

PRINCIPAL DISPLAY PANEL - 2mg

NDC 43353-292 Bumetanide 2mg - Rx Only

BUMETANIDE

bumetanide tablet

Product Information

Product T ype

HUMAN PRESCRIPTION DRUG

Ite m Code (Source )

NDC:43353-29 2(NDC:0 18 5-0 130 )

Route of Administration

ORAL

Active Ingredient/Active Moiety

Ingredient Name

Basis of Strength

Stre ng th

BUMETANIDE (UNII: 0 Y2S3XUQ5H) (BUMETANIDE - UNII:0 Y2S3XUQ5H)

BUMETANIDE

2 mg

Inactive Ingredients

Ingredient Name

Stre ng th

ANHYDRO US LACTO SE (UNII: 3SY5LH9 PMK)

STARCH, CO RN (UNII: O8 232NY3SJ)

MAGNESIUM STEARATE (UNII: 70 0 9 7M6 I30 )

CELLULO SE, MICRO CRYSTALLINE (UNII: OP1R32D6 1U)

FERRO SO FERRIC O XIDE (UNII: XM0 M8 7F357)

FERRIC O XIDE RED (UNII: 1K0 9 F3G6 75)

FERRIC O XIDE YELLO W (UNII: EX438 O2MRT)

TALC (UNII: 7SEV7J4R1U)

Product Characteristics

Color

BROWN

S core

2 pieces

Aphena Pharma Solutions - Tennessee, LLC

S hap e

ROUND

S iz e

10 mm

Flavor

Imprint Code

E;130

Contains

Packag ing

#

Item Code

Package Description

Marketing Start Date

Marketing End Date

1

NDC:43353-29 2-51

6 0 0 0 in 1 BOTTLE; Type 0 : No t a Co mbinatio n Pro duct

0 3/10 /20 17

Marketing Information

Marke ting Cate gory

Application Numbe r or Monograph Citation

Marke ting Start Date

Marke ting End Date

ANDA

ANDA0 7470 0

11/21/19 9 6

Labeler -

Aphena Pharma Solutions - T ennessee, LLC (128385585)

Establishment

Name

Ad d re s s

ID/FEI

Busine ss Ope rations

Aphena Pharma So lutio ns - Tennessee, LLC

128 38 558 5

REPACK(43353-29 2)

Revised: 10/2017