- Raw materials
- Antihypertensive agents
- Diuretics
- Furosemide
- Quality & compliance
- CoA certified
Filters
Custom request?
Type
Production region
Qualifications
Country of origin
Furosemide API Manufacturers & Suppliers
16 verified results
Commercial-scale Suppliers
Employees: 10
All certificates
All certificates
Employees: 19
All certificates
Employees: 200+
All certificates
Employees: 50
All certificates
Employees: 200+
All certificates
Employees: 50+
All certificates
Employees: +250
All certificates
Employees: 25
All certificates
Employees: +250
All certificates
All certificates
All certificates
Employees: 3,500+
All certificates
All certificates
All certificates
All certificates
Total market transparency
Supplier trade data access
Buyer / supplier flow comparison
Furosemide | CAS No: 54-31-9 | GMP-certified suppliers
A medication that helps manage edema from heart, liver, and renal conditions, supports hypertension control, and aids rapid relief of fluid congestion in acute and chronic heart failure.
Therapeutic categories
Primary indications
- Furosemide is indicated for the treatment of edema associated with congestive heart failure, cirrhosis of the liver, and renal disease, including the nephrotic syndrome, in adults and pediatric patients
- Oral furosemide is indicated alone for the management of mild to moderate hypertension or severe hypertension in combination with other antihypertensive medications
Product Snapshot
- Furosemide is available as an oral small‑molecule formulation and as injectable and subcutaneous solutions for parenteral use
- It is used for fluid management in cardiac, hepatic, renal edema and for hypertension, with parenteral forms applied in acute volume‑overload settings
- It is approved for human and veterinary use in the US and Canada
Clinical Overview
Furosemide acts primarily by inhibiting sodium and chloride reabsorption in the proximal and distal tubules and the thick ascending limb of the loop of Henle. This effect is mediated by competitive blockade of the NKCC2 sodium‑potassium‑chloride cotransporter, increasing renal excretion of water, sodium, chloride, magnesium, calcium, hydrogen, and potassium. It also decreases uric acid excretion. Additional vasodilatory activity contributes to clinical benefit in acute pulmonary edema through reduced responsiveness to vasoconstrictors and increased prostaglandin production.
Pharmacodynamic onset following oral dosing occurs within about 1 to 1.5 hours, with peak effect around 2 hours and duration of 4 to 6 hours. Intravenous dosing produces onset within minutes and a shorter overall duration. Furosemide is highly protein bound and reaches the tubular lumen via active secretion by organic anion transporters.
Safety considerations include risks of electrolyte depletion, dehydration, volume contraction, ototoxicity, and photosensitivity. Renal function, serum electrolytes, and volume status require close monitoring, particularly during rapid diuresis or parenteral administration. Furosemide’s diuretic effect may be attenuated in severe renal impairment.
Common global brand contexts include oral tablets, oral solutions, and injectable formulations used in both acute care and chronic disease management.
For API procurement, suppliers should demonstrate control of polymorphic form, impurity profile, and residual solvents, with full compliance to relevant pharmacopoeial monographs and GMP standards to support formulation consistency and regulatory submissions.
Identification & chemistry
| Generic name | Furosemide |
|---|---|
| Molecule type | Small molecule |
| CAS | 54-31-9 |
| UNII | 7LXU5N7ZO5 |
| DrugBank ID | DB00695 |
Pharmacology
| Summary | Furosemide is a loop diuretic that increases urinary excretion of water and electrolytes by inhibiting the NKCC2 sodium‑potassium‑chloride cotransporter in the thick ascending limb of the loop of Henle and, to a lesser extent, other nephron segments. This blockade reduces tubular sodium and chloride reabsorption, driving diuresis and altering renal handling of additional ions. Furosemide also produces vasodilatory effects through reduced sensitivity to vasoconstrictors and increased prostaglandin activity, contributing to its therapeutic utility in fluid‑overload states. |
|---|---|
| Mechanism of action | Furosemide promotes diuresis by blocking tubular reabsorption of sodium and chloride in the proximal and distal tubules, as well as in the thick ascending loop of Henle. This diuretic effect is achieved through the competitive inhibition of sodium-potassium-chloride cotransporters (NKCC2) expressed along these tubules in the nephron, preventing the transport of sodium ions from the lumenal side into the basolateral side for reabsorption. This inhibition results in increased excretion of water along with sodium, chloride, magnesium, calcium, hydrogen, and potassium ions.As with other loop diuretics, furosemide decreases the excretion of uric acid. Furosemide exerts direct vasodilatory effects, which results in its therapeutic effectiveness in the treatment of acute pulmonary edema. Vasodilation leads to reduced responsiveness to vasoconstrictors, such as angiotensin II and noradrenaline, and decreased production of endogenous natriuretic hormones with vasoconstricting properties. It also leads to increased production of prostaglandins with vasodilating properties. Furosemide may also open potassium channels in resistance arteries.The main mechanism of action of furosemide is independent of its inhibitory effect on carbonic anhydrase and aldosterone. |
| Pharmacodynamics | Furosemide manages hypertension and edema associated with congestive heart failure, cirrhosis, and renal disease, including the nephrotic syndrome. Furosemide is a potent loop diuretic that works to increase the excretion of Na+ and water by the kidneys by inhibiting their reabsorption from the proximal and distal tubules, as well as the loop of Henle.It works directly acts on the cells of the nephron and indirectly modifies the content of the renal filtrate.Ultimately, furosemide increases the urine output by the kidney. Protein-bound furosemide is delivered to its site of action in the kidneys and secreted via active secretion by nonspecific organic transporters expressed at the luminal site of action. Following oral administration, the onset of the diuretic effect is about 1 and 1.5 hours , and the peak effect is reached within the first 2 hours.The duration of effect following oral administration is about 4-6 hours but may last up to 8 hours.Following intravenous administration, the onset of effect is within 5 minutes, and the peak effect is reached within 30 minutes. The duration of action following intravenous administration is approximately 2 hours. Following intramuscular administration, the onset of action is somewhat delayed. |
Targets
| Target | Organism | Actions |
|---|---|---|
| Solute carrier family 12 member 1 | Humans | inhibitor |
| Carbonic anhydrase 2 | Humans | inhibitor |
| G-protein coupled receptor 35 | Humans | agonist |
ADME / PK
| Absorption | Following oral administration, furosemide is absorbed from the gastrointestinal tract.It displays variable bioavailability from oral dosage forms, ranging from 10 to 90%.The oral bioavailability of furosemide from oral tablets or oral solution is about 64% and 60%, respectively, of that from an intravenous injection of the drug. |
|---|---|
| Half-life | The half-life from the dose of 40 mg furosemide was 4 hours following oral administration and 4.5 hours following intravenous administration. The terminal half-life of furosemide is approximately 2 hours following parenteral administration.The terminal half-life may be increased up to 24 hours in patients with severe renal failure. |
| Protein binding | Plasma concentrations ranging from 1 to 400 mcg/mL are about 91-99% bound in healthy individuals. The unbound fraction is about 2.3-4.1% at therapeutic concentrations.Furosemide mainly binds to serum albumin. |
| Metabolism | The metabolism of furosemide occurs mainly in the kidneys and the liver, to a smaller extent. The kidneys are responsible for about 85% of total furosemide total clearance, where about 40% involves biotransformation.Two major metabolites of furosemide are furosemide glucuronide, which is pharmacologically active, and saluamine (CSA) or 4-chloro-5-sulfamoylanthranilic acid. |
| Route of elimination | The kidneys are responsible for 85% of total furosemide total clearance, where about 43% of the drug undergoes renal excretion.Significantly more furosemide is excreted in urine following the I.V. injection than after the tablet or oral solution. Approximately 50% of the furosemide load is excreted unchanged in urine, and the rest is metabolized into glucuronide in the kidney. |
| Volume of distribution | The volume of distribution following intravenous administration of 40 mg furosemide were 0.181 L/kg in healthy subjects and 0.140 L/kg in patients with heart failure. |
| Clearance | Following intravenous administration of 400 mg furosemide, the plasma clearance was 1.23 mL/kg/min in patients with heart failure and 2.34 mL/kg/min in healthy subjects, respectively. |
Formulation & handling
- Oral formulations face low aqueous solubility, often requiring pH adjustment or solubilizing excipients to enhance dissolution.
- Parenteral solutions are typically alkaline for solubility; handling requires attention to precipitation risks upon dilution.
- Small‑molecule solid API is stable under normal conditions but should be protected from moisture to prevent degradation and flowability issues.
Regulatory status
| Lifecycle | The API remains in a mid‑to‑late protected phase in the US, with key patents expiring in 2034. Given current marketing only in the US and Canada, broader generic entry is unlikely before these expiries, indicating a relatively mature but still patent‑protected market. |
|---|
| Markets | US, Canada |
|---|
Supply Chain
| Supply chain summary | The market for furosemide is dominated by numerous generic manufacturers and repackagers, with no single originator company driving supply, reflecting its long-standing status as a widely produced diuretic. Branded and unbranded products are well established in the US and Canada, supported by a large network of formulators and distributors. Although several patents remain active to 2034, these appear to relate to specific products or uses rather than the core API, and extensive generic competition is already present. |
|---|
Safety
| Toxicity | Clinical consequences from overdose depend on the extent of electrolyte and fluid loss and include dehydration, blood volume reduction, hypotension, electrolyte imbalance, hypokalemia, hypochloremic alkalosis,hemoconcentration, cardiac arrhythmias (including A-V block and ventricular fibrillation).Symptoms of overdose include acute renal failure, thrombosis, delirious states, flaccid paralysis, apathy and confusion. In cirrhotic patients, overdosage might precipitate hepatic coma. In rats, the oral LD<sub>50</sub>, intraperitoneal LD<sub>50</sub>, and subcutaneous LD<sub>50</sub> is 2600 mg/kg, 800 mg/kg, and 4600 mg/kg, respectively. The Lowest published toxic dose (TDLo) in a female is 6250 μg/kg. |
|---|
- Overexposure may lead to significant electrolyte and fluid imbalance, with reported outcomes including hypokalemia, hypochloremic alkalosis, hemoconcentration, and associated cardiac arrhythmias
- Severe overdose has been linked to acute renal failure, thrombosis, neurocognitive disturbances, and in cirrhotic subjects, risk of hepatic coma
- Animal toxicity data indicate LD50 values of 2600 mg/kg (oral, rat), 800 mg/kg (intraperitoneal, rat), and 4600 mg/kg (subcutaneous, rat), supporting standard industrial controls to limit accidental high‑dose exposure
Certificate of Analysis
A CoA is a document issued by a companies’ QA/QC-department that confirms that a product meets its product specification and is part of the quality control of a product batch. The CoA commonly contains results obtained from laboratory tests of an individual batch of a product. There are different international standards to which a product can be tested, for example: Ph. Eur. | EP – (European Pharmacopoeia) USP – (United States Pharmacopeia)
Furosemide is a type of Diuretics
Diuretics, a subcategory of pharmaceutical active pharmaceutical ingredients (APIs), are compounds commonly used in the treatment of conditions such as hypertension, congestive heart failure, and edema. Diuretics, also known as water pills, function by increasing the production of urine, thereby promoting the excretion of excess water and electrolytes from the body.
There are several types of diuretics, including thiazide diuretics, loop diuretics, and potassium-sparing diuretics. Thiazide diuretics, such as hydrochlorothiazide, work by inhibiting the reabsorption of sodium and chloride in the kidneys, leading to increased urine production. Loop diuretics, such as furosemide, act on the loop of Henle in the kidneys to block the reabsorption of sodium and chloride, resulting in a more potent diuretic effect. Potassium-sparing diuretics, like spironolactone, help retain potassium in the body while still promoting diuresis.
These diuretic APIs are widely used in the pharmaceutical industry to formulate medications that effectively manage fluid retention and related conditions. They are available in various forms, including tablets, capsules, and intravenous formulations. Diuretics are often prescribed as part of combination therapies to enhance their effectiveness and minimize adverse effects.
It is important to note that the use of diuretics should be closely monitored by healthcare professionals due to potential side effects such as electrolyte imbalances, dehydration, and hypotension. Proper dosage and patient-specific considerations are crucial to ensure optimal therapeutic outcomes.
In conclusion, diuretics are a vital subcategory of pharmaceutical APIs used to treat conditions characterized by fluid retention. Their mechanisms of action vary, but they all facilitate increased urine production, assisting the body in eliminating excess fluids. The proper use of diuretics, in combination with medical supervision, can effectively manage various cardiovascular and renal conditions.
Furosemide (Diuretics), classified under Antihypertensive agents
Antihypertensive agents are a crucial category of pharmaceutical active pharmaceutical ingredients (APIs) used to treat high blood pressure, also known as hypertension. These medications are designed to lower blood pressure and reduce the risk of associated cardiovascular complications.
Antihypertensive agents function by targeting various mechanisms involved in blood pressure regulation. Some common classes of antihypertensive agents include angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), beta-blockers, calcium channel blockers (CCBs), and diuretics.
ACE inhibitors work by inhibiting the enzyme responsible for converting angiotensin I to angiotensin II, a hormone that constricts blood vessels. ARBs, on the other hand, block the receptors to which angiotensin II binds, thereby preventing its vasoconstrictive effects.
Beta-blockers reduce blood pressure by blocking the effects of adrenaline and noradrenaline, which are responsible for increasing heart rate and constricting blood vessels. CCBs inhibit calcium from entering the smooth muscles of blood vessels, resulting in relaxation and vasodilation. Diuretics promote the elimination of excess fluid and sodium from the body, reducing blood volume and thereby lowering blood pressure.
Antihypertensive agents are typically prescribed based on the individual patient's condition and specific needs. They can be used alone or in combination to achieve optimal blood pressure control. It is important to note that antihypertensive agents should be taken regularly as prescribed by a healthcare professional and may require periodic monitoring to ensure their effectiveness and manage any potential side effects.
In summary, antihypertensive agents play a vital role in the management of hypertension by targeting various mechanisms involved in blood pressure regulation. These medications offer significant benefits in reducing the risk of cardiovascular complications associated with high blood pressure.
Furosemide API manufacturers & distributors
Compare qualified Furosemide API suppliers worldwide. We currently have 15 companies offering Furosemide API, with manufacturing taking place in 3 different countries. Use the table below to review supplier type, countries of origin, certifications, product portfolio and GMP audit availability.
| Supplier | Type | Country | Product origin | Certifications | Portfolio |
|---|---|---|---|---|---|
| Amri India | Producer | India | India | CEP, CoA, USDMF, WC | 2 products |
| Aquatic Remedies Pvt Ltd | Producer | India | India | CoA | 35 products |
| Arshine Pharmaceutical Co... | Distributor | China | China | BSE/TSE, CEP, CoA, FDA, GMP, MSDS, USDMF | 176 products |
| AXXO GmbH | Distributor | Germany | World | CoA, GMP, GDP, MSDS, USDMF | 243 products |
| Curia | Producer | United States | India | CEP, CoA, EDMF/ASMF, GMP, MSDS, USDMF | 106 products |
| Duchefa Farma B.V. | Distributor | Netherlands | India | CoA, GMP, ISO9001, MSDS | 170 products |
| Global Pharma Tek | Distributor | India | India | BSE/TSE, CoA, FDA, GMP, ISO9001, MSDS | 484 products |
| Ipca Labs. | Producer | India | India | CEP, CoA, FDA, GMP, JDMF, USDMF, WC | 69 products |
| Kromozome | Distributor | India | India | CoA, FDA, GMP, MSDS | 17 products |
| LGM Pharma | Distributor | United States | World | BSE/TSE, CEP, CoA, GMP, MSDS, USDMF | 441 products |
| Mangalam Drugs & Organics... | Producer | India | India | CoA, GMP, WC | 10 products |
| Prachi Pharmaceuticals | Producer | India | India | CoA, FDA, GMP, ISO9001, USDMF, WHO-GMP | 12 products |
| SEDANAH | Distributor | Jordan | World | CoA, GMP | 70 products |
| SETV Global | Producer | India | India | CoA, FDA, GMP | 515 products |
| Tenatra Exports Private L... | Distributor | India | India | BSE/TSE, CoA, FDA, GMP, MSDS | 263 products |
When sending a request, specify which Furosemide API quality you need: for example EP (Ph. Eur.), USP, JP, BP, or another pharmacopoeial standard, as well as the required grade (base, salt, micronised, specific purity, etc.).
Use the list above to find high-quality Furosemide API suppliers. For example, you can select GMP, FDA or ISO certified suppliers. Visit our help page to learn more about sourcing APIs via Pharmaoffer.
Frequently asked questions about Furosemide API
Sourcing
What matters most when sourcing GMP-grade Furosemide?
Which documents are typically required when sourcing Furosemide API?
Which manufacturers are known to produce Furosemide API?
How can I request quotes for Furosemide API from GMP suppliers?
Is a GMP audit report available for Furosemide manufacturers?
How many suppliers offer Furosemide API on Pharmaoffer?
Which countries are known to manufacture Furosemide API?
Which certifications do suppliers of Furosemide usually hold?
Technical
What is Furosemide (CAS 54-31-9) used for?
Which therapeutic class does Furosemide fall into?
What conditions is Furosemide mainly prescribed for?
How does Furosemide work?
What should someone know about the safety or toxicity profile of Furosemide?
What are important formulation and handling considerations for Furosemide as an API?
Is Furosemide a small molecule?
Are there special stability concerns for oral Furosemide?
Regulatory
Where is Furosemide approved or in use globally?
What’s the regulatory and patent landscape for Furosemide right now?
Pharmaoffer
How does Pharmaoffer’s Smart Sourcing Service help with Furosemide procurement?
Is Furosemide included in the PRO Data Insights coverage?
Where can I access the API market report for Furosemide?
