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Torsemide 20 mg Tablet, 100-count — NDC 71335-2841-1 (Billing 71335-2841-01)

by Bryant Ranch Prepack · 100 TABLET in 1 BOTTLE

This is a package of 100 tablets of Torsemide 20 mg Tablet from Bryant Ranch Prepack, marketed since Jul 2023 and currently FDA-listed. It is this product's only package size.

NDC 71335-2841-01
🏷️ FDA NDC (as labeled) 71335-2841-1 billing pads the package segment with a zero
Rx only Generic On market Non-controlled ⇄ Compare with another NDC
🗂️ FDA directory synced Oct 1, 2026 · this listing last changed Jul 24, 2026 · sources: openFDA · FDA label (DailyMed) · FDA Orange & Purple Book · First Databank · CMS NADAC, ASP, Medicare & Medicaid · RxNorm
📋 All sources & update times →

This page is curated, coded, and maintained by

Compiled from public FDA, CMS, DailyMed, NADAC, and related drug data sources. Editorial policy

Identity & classification

Regulatory identifiers FDA, NLM and CMS codes for this package

FDA NDC (as labeled) 71335-2841-1
Product NDC 71335-2841
11-digit billing NDC 71335284101
NCPDP billing unit EA — each (per item)
RxCUI 198371
UNII W31X2H97FB
Application # ANDA076894
SPL Set ID e707eda7-4bde-4944-ae19-1b4fa35b6a3c
Established class (EPC) Loop Diuretic
Physiologic effect Increased Diuresis at Loop of Henle
DEA schedule Non-controlled
Marketing category ANDA
Marketing status On market
FDA listing status Listed (active directory)
Marketing start 2023-07-24
Route ORAL
Dosage form TABLET
Substance TORSEMIDE
TE code (Orange Book) AB · RLD · RS

Drug-database identifiers Medi-Span GPI and First Databank GCN / HICL / AHFS classification

GCN Seq No 021408
GCN 21132
HICL code 008829
Ingredient (HICL) Torsemide
HIC1 code R
Therapeutic class — broad (HIC1) Kidney/Urinary Tract
HIC2 code R1
Therapeutic class — intermediate (HIC2) Affect Primarily Kidneys/Urinary Tract
HIC3 code R1M
Therapeutic class — specific (HIC3) Loop Diuretics
AHFS code 24:36.08.00
AHFS class Loop Diuretics (24:36)
FDB label name TORSEMIDE 20 MG TABLET
FDB brand name Torsemide
Legend status F — Federal legend — prescription drug or device
Quick answers
  • GSN (GCN sequence number): 021408
  • GCN: 21132
  • HICL (First Databank): 008829
  • AHFS class code: 24:36.08.00
  • RxCUI (RxNorm): 198371
Why two NDCs? The FDA registers this code as 71335-2841-1 — a 5-4-1 layout, and that's what's printed on the package and shown on DailyMed. For insurance claims, every NDC is standardized to a uniform 11-digit 5-4-2 format by adding a zero to the package segment → 71335-2841-01. Same drug, same package — only the format differs.
Where does this data come from?
Identifiers from the FDA openFDA NDC Directory and Structured Product Labeling; RxCUI from RxNorm (NLM); GPI from Medi-Span; GCN / HIC / AHFS / legend from First Databank.

RxNorm drug class

This medicine belongs to the Loop Diuretic class.

Pharmacologic class Loop Diuretic
Drug family (ATC) Sulfonamides, plain
Where does this data come from?
Therapeutic classes from RxNorm RxClass (U.S. National Library of Medicine) — Established Pharmacologic Class (FDA), ATC drug family (WHO) and mechanism of action, matched by this product’s RxCUI.

Clinical

Label name TORSEMIDE 20 MG TABLET Ingredient Torsemide
📗 Our plain-language guide HelloPharmacist
  • Yes, increased urination is the whole point — but it's doing so for a reason. Torsemide blocks your kidneys from reabsorbing sodium and water, so your body flushes out extra fluid....
  • What exactly is torsemide doing for me — is it just making me urinate more?
  • Most people take it in the morning, and that's the practical advice. Because it causes increased urination for several hours, taking it at night can disrupt your sleep. You can tak...
  • When should I take torsemide — does it matter what time of day?
📖 Read our full Torsemide guide →
8
Nutrient depletion considerations

Torsemide may be associated with lower levels of 8 nutrients — worth a chat with your pharmacist, not a cause for alarm.

🧪 Full Torsemide nutrient depletion report →
An association is not a deficiency. Educational only — don't start or stop anything without professional guidance.
Where does this data come from?
Plain-language summary from MedlinePlus (U.S. National Library of Medicine); supplement & herbal interactions and nutrient depletion data from the Natural Medicines database; our full guide is HelloPharmacist editorial content.

Pricing

A drug doesn't have one price. Each row is a different public payment system, and none is what you'd pay at the counter — that depends on your insurance. The ⓘ on each row explains what it measures.

Price systemPer eachPer package
Retail pharmacies payNADAC · weekly Not in the retail survey — common for institutional, discontinued, or low-volume packs.
Medicaid paysCMS SDUD · 12 mo No recent Medicaid claims on file for this NDC — rare and low-volume NDCs are suppressed in the public data.
Medicare drug plans payPart D · Q2 2026 $0.1821 $18.21 / 100 tablets
Where does this data come from?
NADAC (National Average Drug Acquisition Cost) is the CMS weekly pharmacy-acquisition-cost survey — what pharmacies pay. ASP (Average Sales Price) is the CMS Medicare Part B drug-payment file, published quarterly. Medicaid pays is computed by us from CMS State Drug Utilization Data (total reimbursed ÷ units, trailing 12 months) — gross of rebates and inclusive of dispensing fees, so it reflects what Medicaid paid, not an acquisition cost. Medicare drug plans pay is the median negotiated point-of-sale unit cost across plans listing this NDC in the CMS quarterly Prescription Drug Plan pricing files, before rebates. The VA pays is the federal contract price (FSS, and the statutory Big 4 ceiling where listed) from the VA National Acquisition Center pharmaceutical price file. All are free public government data; each measures a different payer, so the figures are not directly comparable.

Packaging — all sizes for this product

Package NDCDescription Marketing startMarketing endStatus
71335-2841-01 You're viewing this Main listing 100 TABLET in 1 BOTTLE 2025-10-22 — Active

Therapeutic equivalents

ProductLabelerPackNADAC/unitTEStatusPrice vs. this
Torsemide 20 mg 00054-0077-25 Hikma 100 tablets $0.064 AB Availability likely —
Torsemide 20 mg 00904-7283-06 Major 50 tablets $0.064 AB Availability likely —
Torsemide 20 mg 23155-0873-01 Heritage 100 tablets $0.064 AB Availability likely —
Torsemide 20 mg 31722-0531-01 Camber 100 tablets $0.064 AB Availability likely —
Torsemide 20 mg 50111-0917-01 Teva 100 tablets $0.064 AB Availability likely —
Torsemide 20 mg 50268-0756-15 AvPAK 50 tablets $0.064 AB Availability likely —
Torsemide 20 mg 62135-0820-90 Chartwell 90 tablets $0.064 AB Availability likely —
Torsemide 20 mg 65862-0127-01 Aurobindo 100 tablets $0.064 AB Availability likely —
Torsemide 20 mg 68084-0539-01 American 100 tablets $0.064 AB Availability likely —
Torsemide 20 mg 00615-7997-05 NCS 15 tablets — AB FDA listed —
Torsemide 20 mg 42291-0818-90 AvKARE 90 tablets — AB FDA listed —
Torsemide 20 mg 43353-0315-16 Aphena 6000 tablets — AB FDA listed —
Torsemide 20 mg 50090-6499-00 A-S 90 tablets — AB FDA listed —
Torsemide 20 mg 50090-7261-00 A-S 90 tablets — AB FDA listed —
Torsemide 20 mg 51407-0362-90 Golden 90 tablets — AB FDA listed —
Torsemide 20 mg 57237-0140-01 Rising 100 tablets — AB FDA listed —
Torsemide 20 mg 67296-2190-03 Redpharm 30 tablets — AB FDA listed —
Torsemide 20 mg 70518-2195-01 REMEDYREPACK 90 tablets — AB FDA listed —
Torsemide 20 mg 70518-4139-00 REMEDYREPACK 30 tablets — AB FDA listed —
Torsemide 20 mg 71335-2663-01 Bryant 100 tablets — AB FDA listed —
Torsemide 20 mgthis 71335-2841-01 Bryant 100 tablets — AB FDA listed —
Torsemide 20 mg 71335-2962-01 Bryant 500 tablets — AB FDA listed —
Torsemide 20 mg 71610-0819-22 Aphena 1170 tablets — AB FDA listed —
Torsemide 20 mg 72162-2412-01 Bryant 100 tablets — AB FDA listed —
Torsemide 20 mg 72865-0260-01 XLCare 100 tablets — AB FDA listed —
About this product: this is a generic version of the medicine. FDA equivalence ratings are shown when available, and other versions are listed above, least expensive first.
Where does this data come from?
Equivalents are other NDCs of the same ingredient, form and route from the openFDA NDC Directory, ranked least-expensive-first by NADAC. Therapeutic-equivalence (AB) ratings come from the FDA Orange Book; biologics use the FDA Purple Book for biosimilar & interchangeable status.

Availability & generic status

🏛️
2023
On the market since
Jul 2023
📍
2026
Currently FDA-listed
3 years listed
🔓
·
Generic on the market
this product is a generic
✅This is a generic drug

This product is an FDA-approved generic. Other versions of the same drug are listed under Therapeutic equivalents, least expensive first.

Where does this data come from?
Patents and exclusivity from the FDA Orange Book (small-molecule drugs), refreshed from public FDA data. Generic launch timing is an estimate, not a guarantee.

Inactive Ingredients / Excipients

Inactive ingredients, also called excipients, are components of the drug product other than the active ingredient. They may include fillers, dyes, coatings, preservatives, flavors, or other formulation ingredients.

Loading inactive ingredients from the official FDA label in the background. No external source is being called by this page request.
Where does this data come from?
Source: official FDA Structured Product Labeling (SPL) via DailyMed and the openFDA label index. Structured IACT rows and label-wide narrative are kept separate; availability and product-level specificity depend on the submitted label.

Inactive ingredient FAQ

Are inactive ingredients the same for every manufacturer?
No. Inactive ingredients can differ by manufacturer, dosage form, strength, and package / product version.
Why might an inactive ingredient be missing?
Some SPLs do not provide a complete structured inactive-ingredient list, and older or unusual labels may only include the information in narrative text.
Can inactive ingredients matter?
Yes. They can matter for allergies, intolerances, dyes, gluten / lactose concerns, preservatives, and formulation differences — but confirm with a pharmacist or the manufacturer when it’s clinically important.

Manufacturer & labeler

LabelerBryant Ranch Prepack
Application holderCOREPHARMA LLC
FDA applicationANDA076894 (ANDA)
Labeler code71335
First marketedJul 2023
Product typeHuman Prescription Drug
Portfolio4,436 products on file
The labeler markets the product; the application holder owns the FDA approval. They’re often the same company but can differ (e.g. a repackager or an authorized generic). A mailing address / phone appears here when the manufacturer includes it in the product’s FDA label (not all do).
Where does this data come from?
Labeler, application holder and registered establishment from the FDA openFDA NDC Directory and Drugs@FDA; address/contact from the product’s FDA label.

Full prescribing information FDA SPL

The complete FDA label for this product — the official prescribing information, verbatim, section by section. Very long sections are excerpted here and marked; the full text is on DailyMed (linked in the sources below). Jump with a chip, search within the label, or expand everything.
🎯 Indications and Usage ⏱️ Dosage and Administration 💊 Dosage Forms and Strengths ⛔ Contraindications ⚠️ Warnings and Cautions 🤒 Adverse Reactions 🔄 Drug Interactions 👥 Use in Specific Populations 🤰 Pregnancy 🧒 Pediatric Use 🧓 Geriatric Use 🆘 Overdosage 🧬 Clinical Pharmacology 🧬 Mechanism of Action 📦 How Supplied / Storage and Handling 📋 Description 💬 Information for Patients 🍼 Nursing Mothers 🧬 Pharmacokinetics 🧬 Pharmacodynamics 🧪 Nonclinical Toxicology 📄 Carcinogenesis, Mutagenesis, Impairment of Fertility 📄 Package Label / Principal Display Panel
🎯 Indications and Usage ~2 min read ▾

1 INDICATIONS AND USAGE Torsemide is a loop diuretic indicated for: the treatment of edema associated with heart failure, renal disease or hepatic disease. ( 1.1 ) the treatment of hypertension, to lower blood pressure. Lowering blood pressure reduces the risk of fatal and nonfatal cardiovascular events, primarily strokes and myocardial infarctions. ( 1.2 )

1.1Edema Torsemide tablets are indicated for the treatment of edema associated with heart failure, renal disease or hepatic disease.

1.2Hypertension Torsemide tablets are indicated for the treatment of hypertension, to lower blood pressure. Lowering blood pressure reduces the risk of fatal and nonfatal cardiovascular events, primarily strokes and myocardial infarctions. These benefits have been seen in controlled trials of antihypertensive drugs from a wide variety of pharmacologic classes including the class to which this drug principally belongs.

There are no controlled trials demonstrating risk reduction with torsemide. Control of high blood pressure should be part of comprehensive cardiovascular risk management, including, as appropriate, lipid control, diabetes management, antithrombotic therapy, smoking cessation, exercise, and limited sodium intake. Many patients will require more than one drug to achieve blood pressure goals.

For specific advice on goals and management, see published guidelines, such as those of the National High Blood Pressure Education Program’s Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC). Numerous antihypertensive drugs, from a variety of pharmacologic classes and with different mechanisms of action, have been shown in randomized controlled trials to reduce cardiovascular morbidity and mortality, and it can be concluded that it is blood pressure reduction, and not some other pharmacologic property of the drugs, that is largely responsible for those benefits.

The largest and most consistent cardiovascular outcome benefit has been a reduction in the risk of stroke, but reductions in myocardial infarction and cardiovascular mortality also have been seen regularly. Elevated systolic or diastolic pressure causes increased cardiovascular risk, and the absolute risk increase per mmHg is greater at higher blood pressures, so that even modest reductions of severe hypertension can provide substantial benefit. Relative risk reduction from blood pressure reduction is similar across populations with varying absolute risk, so the absolute benefit is greater in patients who are at higher risk independent of their hypertension (for example, patients with diabetes or hyperlipidemia), and such patients would be expected to benefit from more aggressive treatment to a lower blood pressure goal.

The antihypertensive effects of torsemide are on the average greater in black patients than in nonblack patients [see Clinical Pharmacology (12.2) ]. Some antihypertensive drugs have smaller blood pressure effects (as monotherapy) in black patients, and many antihypertensive drugs have additional approved indications and effects (e.g., on angina, heart failure, or diabetic kidney disease). These considerations may guide selection of therapy.

Torsemide can be used alone or in combination with other antihypertensive agents.

⏱️ Dosage and Administration ~2 min read ▾

2 DOSAGE AND ADMINISTRATION Edema associated with: Heart failure: Initial dose is 10 or 20 mg once daily. Titrate by factors of two; doses above 200 mg have not been studied. ( 2.1 ) Chronic Renal Failure: Initial dose is 20 mg once daily.

Titrate by factors of two; doses above 200 mg have not been studied. ( 2.1 ) Hepatic Cirrhosis: Initial dose is 5 or 10 mg once daily. Titrate by factors of two; doses above 40 mg have not been studied.

( 2.1 ) Hypertension: The recommended initial dose is 5 mg once daily. After 4 to 6 weeks, increase to 10 mg once daily, if needed. If 10 mg is insufficient, consider adding another agent.

( 2.2 )

2.1Treatment of Edema Edema associated with heart failure The recommended initial dose is 10 mg or 20 mg oral torsemide 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.

Edema associated with chronic renal failure The recommended initial dose is 20 mg oral torsemide 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.

Edema associated with hepatic cirrhosis The recommended initial dose is 5 mg or 10 mg oral torsemide once daily, administered together with an aldosterone antagonist or a potassium-sparing diuretic. If the diuretic response is inadequate, titrate upward by approximately doubling until the desired diuretic response is obtained. Doses higher than 40 mg have not been adequately studied in this population.

2.2Treatment of Hypertension The recommended 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, increase to 10 mg once daily. If the response to 10 mg is insufficient, add another antihypertensive agent to the treatment regimen.

💊 Dosage Forms and Strengths 138 words ▾

3 DOSAGE FORMS AND STRENGTHS Torsemide tablets 5 mg, USP are available as white to off-white, capsule shaped, uncoated tablets, debossed with bisect between “C” and “40” on one side and plain on other side. Torsemide tablets 10 mg, USP are available as white to off-white, capsule shaped, uncoated tablets, debossed with bisect between “C” and “41” on one side and plain on other side. Torsemide tablets 20 mg, USP are available as white to off-white, capsule shaped, uncoated tablets, debossed with bisect between “C” and “42” on one side and plain on other side.

Torsemide tablets 100 mg, USP are available as white to off-white, capsule shaped, uncoated tablets, debossed with bisect between “C” and “43” on one side and plain on other side. Tablets: 5 mg, 10 mg, 20 mg and 100 mg ( 3 )

⛔ Contraindications 43 words ▾

4 CONTRAINDICATIONS Torsemide is contraindicated in patients with known hypersensitivity to torsemide or to povidone. Torsemide is contraindicated in patients who are anuric. Torsemide is contraindicated in patients with hepatic coma. Hypersensitivity to torsemide or povidone, anuria, and hepatic coma. ( 4 )

⚠️ Warnings and Cautions 179 words ▾

5 WARNINGS AND PRECAUTIONS Hypotension and worsening renal function: monitor volume status and renal function periodically ( 5.1 ) Electrolyte and metabolic abnormalities: monitor serum electrolytes and blood glucose periodically. ( 5.2 ) Ototoxicity ( 5.3 , 7.6 )

5.1Hypotension and Worsening Renal Function Excessive diuresis may cause potentially symptomatic dehydration, blood volume reduction and hypotension and worsening renal function, including acute renal failure particularly in salt-depleted patients or those taking renin-angiotensin aldosterone inhibitors. Worsening of renal function can also occur with concomitant use of nephrotoxic drugs (e.g., aminoglycosides, cisplatin, and NSAIDs). Monitor volume status and renal function periodically.

5.2Electrolyte and Metabolic Abnormalities Torsemide can cause potentially symptomatic hypokalemia, hyponatremia, hypomagnesemia, hypocalcemia, and hypochloremic alkalosis. Treatment with torsemide can cause an increase in blood glucose levels and hyperglycemia. Asymptomatic hyperuricemia can occur and gout may rarely be precipitated. Monitor serum electrolytes and blood glucose periodically.

5.3Ototoxicity Tinnitus and hearing loss (usually reversible) have been observed with loop diuretics, including torsemide. Higher than recommended doses, severe renal impairment, and hypoproteinemia, appear to increase the risk of ototoxicity.

🤒 Adverse Reactions ~3 min read ▾

6 ADVERSE REACTIONS The following risks are discussed in more detail in others 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) ] The most common adverse reaction is excessive urination (6.7%). ( 6.1 ) To report SUSPECTED ADVERSE REACTIONS, contact Avet Pharmaceuticals Inc. at 1-866-901-DRUG (3784) or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

6.1Clinical 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, torsemide has been evaluated for safety in approximately 4,000 subjects; over 800 of these subjects received torsemide for at least 6 months, and over 380 were treated for more than 1 year. Among these subjects were 564 who received torsemide during United States-based trials in which 274 other subjects received placebo.

Discontinuation of therapy due to adverse reactions occurred in 3.5% of United States patients treated with torsemide and in 4.4% of patients treated with placebo. In United States placebo-controlled trials excessive urination occurred in 6.7% of patients compared with 2.2% of patients receiving placebo. The daily doses of torsemide used in these trials ranged from 1.25 mg to 20 mg, with most patients receiving 5 mg to 10 mg; the duration of treatment ranged from 1 to 52 days, with a median of 41 days.

In the placebo-controlled hypertension studies excessive urination was dose related; 1% of patients receiving placebo, 4% of those treated with 5 mg of daily torsemide, and 15% of those treated with 10 mg. Excessive urination was generally not reported as an adverse event among patients who received torsemide for cardiac, renal, or hepatic failure. There was no effect of age or sex on the incidence of adverse reactions.

Laboratory Parameters Potassium In controlled studies in the United States, torsemide was administered to hypertensive patients at doses of 5 mg or 10 mg daily. After 6 weeks at these doses, the mean decrease in serum potassium was approximately 0.1 mEq/L. The percentage of patients who had a serum potassium level below 3.5 mEq/L at any time during the studies was 1.5% on torsemide and 3% on placebo.

In patients followed for 1 year, there was no progressive change in mean serum potassium levels. In patients with congestive heart failure, hepatic cirrhosis, or renal disease treated with torsemide at doses higher than those studied in United States antihypertensive trials, hypokalemia was observed with greater frequency, in a dose-related manner. 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 mmol/L), and the mean increase in serum uric acid was 1.2 mg/dL (70 mmol/L). Little further change occurred with long-term treatment, and all changes reversed when treatment was discontinued. 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. Serum Lipids Torsemide 20 mg caused small increases in total cholesterol and triglycerides in short term hypertension studies. The changes subsided with chronic therapy.

6.2Postmarketing Experience The following adverse reactions have been identified during… [Excerpted — this section continues on DailyMed.]

🔄 Drug Interactions ~2 min read ▾

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 torsemide. ( 7.3 ) Organic anion drugs: may decrease diuretic activity of torsemide. ( 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 )

7.1Nonsteroidal Anti-inflammatory Drugs 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. Concomitant use of nonsteroidal anti-inflammatory drugs (NSAIDs) and torsemide has been associated with the development of acute renal failure. The antihypertensive and 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).

7.2Cytochrome 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 torsemide 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.

7.3Cholestyramine 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 should be coadministered, administer torsemide at least one hour before or 4 to 6 h after cholestyramine administration.

7.4Organic 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 and thereby decreases the diuretic activity of torsemide. Monitor diuretic effect and blood pressure during coadministration.

7.5Lithium Like other diuretics, torsemide reduces the renal clearance of lithium, inducing a high risk of lithium toxicity. Monitor lithium levels periodically when torsemide is coadministered.

7.6Ototoxic 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 torsemide and aminoglycoside antibiotics, if possible.

7.7Renin-angiotensin Inhibitors Coadministration of torsemide with ACE inhibitors or angiotensin receptor blockers can increase the risk of hypotension and renal impairment.

7.8Radiocontrast Agents Torsemide can increase the risk of renal toxicity related to administration of radiocontrast agents.

7.9Corticosteroids and ACTH Concomitant use with torsemide may increase risk of hypokalemia

👥 Use in Specific Populations ~3 min read ▾

8 USE IN SPECIFIC POPULATIONS

8.1Pregnancy Risk Summary There are no available data on use of torsemide 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 10 and 1.7 times a human 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 to 4%, and 15 to 20%, respectively.

Data There was no fetotoxicity or teratogenicity in rats treated with up to 5 mg/kg/day of torsemide (on a mg/kg basis, this is 15 times a human dose of 20 mg/day; on a mg/m 2 basis, the animal dose is 10 times the human dose), or in rabbits, treated with 1.6 mg/kg/day (on a mg/kg basis, 5 times the human dose of 20 mg/kg/day; on a mg/m 2 basis, 1.7 times this 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.

8.2Lactation 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.

8.4Pediatric Use Safety and effectiveness in pediatric patients have not been established. Administration of another 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 the other loop diuretic.

The other loop diuretic, when administered during the first weeks of life, has also been reported to increase the risk of persistent patent ductus arteriosus. The use of torsemide in such patients has not been studied.

8.5Geriatric Use Of the total number of patients who received torsemide in United States clinical studies, 24% were 65 or older while about 4% were 75 or older. No specific age-related differences in effectiveness or safety were observed between younger patients and elderly patients.

8.6Use in Renal Impairment In single-dose studies 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.

8.7Use in Hepatic Impairment Torsemide can cause sudden alterations of fluid and electrolyte balance which may precipitate hepatic coma in patients with hepatic disease with cirrhosis and ascites. In these patients, diuresis with torsemide is best initiated in the hospital. Diuretic treatment can cause or contribute to the development of hypovolemia, hypokalemia, metabolic alkalosis, hyponatremia or azotemia which can lead to new or worsening hepatic encephalopathy.

Consider suspending or discontinuing torsemide [see Contraindications (4) ]. To prevent hypokalemia and metabolic alkalosis, use an aldosterone antagonist or potassium-sparing drug with tors… [Excerpted — this section continues on DailyMed.]

🤰 Pregnancy ~1 min read ▾

8.1Pregnancy Risk Summary There are no available data on use of torsemide 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 10 and 1.7 times a human 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 to 4%, and 15 to 20%, respectively.

Data There was no fetotoxicity or teratogenicity in rats treated with up to 5 mg/kg/day of torsemide (on a mg/kg basis, this is 15 times a human dose of 20 mg/day; on a mg/m 2 basis, the animal dose is 10 times the human dose), or in rabbits, treated with 1.6 mg/kg/day (on a mg/kg basis, 5 times the human dose of 20 mg/kg/day; on a mg/m 2 basis, 1.7 times this 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.

🧒 Pediatric Use 45 words ▾

8.5Geriatric Use Of the total number of patients who received torsemide in United States clinical studies, 24% were 65 or older while about 4% were 75 or older. No specific age-related differences in effectiveness or safety were observed between younger patients and elderly patients.

🧓 Geriatric Use 116 words ▾

8.6Use in Renal Impairment In single-dose studies 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.

🆘 Overdosage 87 words ▾

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.

🧬 Clinical Pharmacology ~3 min read ▾

12 CLINICAL PHARMACOLOGY

12.1Mechanism 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.

12.2Pharmacodynamics With oral dosing, the onset of diuresis occurs within 1 hour and the peak effect occurs during the first or second hour and 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 mg to 20 mg. The increase in potassium excretion is negligible after a single dose of up to 10 mg and only slight (5 mEq to 15 mEq) after a single dose of 20 mg.

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. Hypertension 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 mg 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 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.

12.3Pharmacokinetics Absorption The bioavailability of torsemide tablets is approximately 80%, with small inter-subject 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 (C max ) within 1 hour after oral administration. C max and area under the serum concentration-time curve (AUC) after oral administration are proportional to dose over the range of 2.5 mg to 200 mg.

Simultaneous food intake delays the time to C max by about 30 minutes, but overall bioavailability (AUC) and diuretic activity are unchanged. 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 methyl-hydroxylation of torsemide, metabolite M3 is formed by ring hydroxylation of torsemide, and metabolite M5 is formed by oxidation of M1… [Excerpted — this section continues on DailyMed.]

🧬 Mechanism of Action 108 words ▾

12.1Mechanism 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.

📦 How Supplied / Storage and Handling 89 words ▾

16 HOW SUPPLIED/STORAGE AND HANDLING Torsemide tablets, USP 20 mg are available for oral administration as white to off-white, capsule shaped, uncoated tablets, debossed with bisect between “C” and “42” on one side and plain on other side. NDC: 71335-2841-1: 100 Tablets in a BOTTLE Storage Store at 20°C to 25°C (68°F to 77°F) [see USP Controlled Room Temperature]. Dispense in a tight, light-resistant container as defined in the USP with a child-resistant closure.

Keep out of reach of children. Repackaged/Relabeled by: Bryant Ranch Prepack, Inc. Burbank, CA 91504

📋 Description 96 words ▾

11 DESCRIPTION Torsemide, USP is 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 molecular formula is C 16 H 20 N 4 O 3 S, its pKa is 7.1, and its molecular weight is 348.43. Torsemide, USP is a white to off-white crystalline powder.

The tablet for oral administration contains 5 mg, 10 mg, 20 mg or 100 mg of torsemide. In addition, each tablet contains the following inactive ingredients: colloidal silicon dioxide, crospovidone, lactose monohydrate, magnesium stearate, and microcrystalline cellulose. Meets USP Dissolution Test 2.

💬 Information for Patients 121 words ▾

17 PATIENT COUNSELING INFORMATION Symptomatic Hypotension: Advise patients receiving torsemide that lightheadedness can occur, especially during the first days of therapy, and that it should be reported to the prescribing physician. The patients should be told that if syncope occurs, torsemide 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) ]. Distributed by: Avet Pharmaceuticals, Inc. East Brunswick, NJ 08816 40308 Revised: 05/2023

🍼 Nursing Mothers 92 words ▾

8.4Pediatric Use Safety and effectiveness in pediatric patients have not been established. Administration of another 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 the other loop diuretic.

The other loop diuretic, when administered during the first weeks of life, has also been reported to increase the risk of persistent patent ductus arteriosus. The use of torsemide in such patients has not been studied.

🧬 Pharmacokinetics ~3 min read ▾

12.3Pharmacokinetics Absorption The bioavailability of torsemide tablets is approximately 80%, with small inter-subject 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 (C max ) within 1 hour after oral administration. C max and area under the serum concentration-time curve (AUC) after oral administration are proportional to dose over the range of 2.5 mg to 200 mg.

Simultaneous food intake delays the time to C max by about 30 minutes, but overall bioavailability (AUC) and diuretic activity are unchanged. 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 methyl-hydroxylation 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 torsemide 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 an… [Excerpted — this section continues on DailyMed.]

🧬 Pharmacodynamics ~1 min read ▾

12.2Pharmacodynamics With oral dosing, the onset of diuresis occurs within 1 hour and the peak effect occurs during the first or second hour and 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 mg to 20 mg. The increase in potassium excretion is negligible after a single dose of up to 10 mg and only slight (5 mEq to 15 mEq) after a single dose of 20 mg.

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. Hypertension 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 mg 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 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.

🧪 Nonclinical Toxicology ~1 min read ▾

13 NONCLINICAL TOXICOLOGY

13.1Carcinogenesis, Mutagenesis and 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.

📄 Carcinogenesis, Mutagenesis, Impairment of Fertility ~1 min read ▾

13.1Carcinogenesis, Mutagenesis and 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 6 words ▾

Torsemide 20 mg Tablets #100 Label

Source: FDA Structured Product Labeling, mirrored from DailyMed / openFDA. Prefer the government’s original formatting? View this label on DailyMed ↗

Medicare Part D spend CMS · PART D · 2026 (Q1)

Medicare Part D (outpatient prescription) spending for Torsemide — the program that covers self-administered drugs. 11 manufacturers.
⚠️ Drug-level data: CMS publishes Part D spending by drug, not by NDC — these figures combine every manufacturer, strength and package size sold under the name Torsemide. That’s a different level of aggregation than the Medicaid card above, which is specific to this exact 11-digit NDC (pack size included), so the two aren’t directly comparable.
Period
Total Part D spend
$14.95M
Claims incl. refills
799.8K
Beneficiaries
504.2K
Spend / beneficiary
$29.66
Spend / claim
$18.70
Trend by period
💵 About the dollar figures: spending is what Part D plans paid before confidential manufacturer rebates, so the program’s real net cost is lower. A blank patient count means fewer than 11 people — CMS hides counts that small to protect privacy. Source: CMS Medicare Quarterly Part D Spending by Drug (data.cms.gov), updated quarterly.

About this NDC listing & data coverage

Finished prescription product
What data is (and isn’t) available for this NDC — tap to expand
NDC identity (package / product / labeler codes) ✓ Available
Labeler ✓ Available
Product & package description ✓ Available
Marketing category & status ✓ Available
Active ingredient / dosage form / route ✓ Available
FDA label (SPL via DailyMed) ✓ Available
Package photos — Not published for this NDC No photo available yet for this listing.
Inactive ingredients (structured) — Not published for this NDC The labeler did not submit a structured excipient list, or no SPL is available.
NADAC pharmacy acquisition price (CMS) — Not published for this NDC CMS publishes NADAC only for NDCs reported in its retail-pharmacy survey.
Orange Book / therapeutic-equivalence data ✓ Available
HCPCS J-code billing crosswalk — Not published for this NDC Most self-administered / retail products have no J-code — that is normal.
Medicaid utilization (CMS SDUD) — Not published for this NDC CMS reports utilization only for NDCs with Medicaid claims above its privacy threshold.
“Not published” reflects what the public FDA / CMS / NLM sources provide for this exact package code — it is a property of the data feeds, not a judgment about the product.

Questions about this listing

Why is there no price listed?
The pricing shown on our NDC pages comes from CMS NADAC, a voluntary survey of retail community pharmacy invoices. CMS does not publish a NADAC for every NDC — packages outside the retail survey (institutional and hospital products, bulk packages, discontinued items, and many OTC items) may never receive one. A missing price reflects the survey's scope, not this product's actual cost, and does not mean the product is free or unavailable.
Is the NDC printed on the package the same as the 11-digit billing NDC?
Yes, they identify this exact package in different formats. The form printed on the packaging and shown on DailyMed is the one the FDA registered. Insurance claims use a fixed 11-digit 5-4-2 format, so the short segment is padded with a leading zero and the dashes are dropped. The Identity section at the top of this page lists each form of this code.
Is this package still being marketed?
Yes, per the latest FDA NDC Directory data on this page: this package is listed as actively marketed, with no marketing end date reported by Bryant Ranch Prepack. Listing status can change — the directory data on this page refreshes weekly.
Who lists this product with the FDA?
Bryant Ranch Prepack is the labeler of record for this NDC — the company under whose FDA-assigned code the package is listed. The labeler may be the manufacturer itself or a distributor marketing the product under its own code.
Do I need a prescription for this product?
This NDC is listed with FDA as a prescription product, so it is dispensed under a prescriber's order. Your pharmacist can tell you whether any over-the-counter forms of the same medication exist.
This page identifies an FDA-listed package (the NDC) and reports public regulatory and pricing data about the listing. It is reference information, not a medical recommendation — talk to your pharmacist or prescriber about your own medication.
Where does this data come from?
Listing facts (marketing category, packager status, marketing dates) from the FDA openFDA NDC Directory; label availability from DailyMed; pricing coverage from CMS NADAC; equivalence scope from the FDA Orange Book.
← 71335-2840-01 · Bryant 71335-2842-01 · Bryant →
For educational and professional reference only — not medical advice. Pricing reflects published NADAC and CMS ASP (free public data) and may differ from your acquisition cost; always verify before billing or dispensing.