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Systematic (IUPAC) name
4-chloro-2-(furan-2-ylmethylamino)- 5-sulfamoylbenzoic acid
CAS number 54-31-9
ATC code C03CA01
PubChem CID 162482
DrugBank APRD00608
ChemSpider 3322
Chemical data
Formula Template:OrganicBox atomTemplate:OrganicBox atomTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBox atomTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBox atomTemplate:OrganicBoxTemplate:OrganicBox atomTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBox atomTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBox 
Mol. mass 330.745 g/mol
SMILES eMolecules & PubChem
Pharmacokinetic data
Bioavailability 43-69%
Metabolism hepatic and renal glucuronidation
Half-life up to 100 minutes
Excretion renal 66%, biliary 33%
Therapeutic considerations
Licence data

US Daily Med:link

Pregnancy cat. C(AU) C(US)
Legal status Prescription only
Routes Oral, IV, IM
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Furosemide (INN) or frusemide (former BAN) is a loop diuretic used in the treatment of congestive heart failure and edema. It is most commonly marketed by Sanofi-Aventis under the brand name Lasix. It has also been used to prevent thoroughbred and standardbred race horses from bleeding through the nose during races.

Along with some other diuretics, furosemide is also included on the World Anti-Doping Agency's banned drug list due to its alleged use as a masking agent for other drugs.


Mechanism of action

The name Lasix is derived from the phrase "lasts six (hours)" referring to its duration of action.[citation needed] Like other loop diuretics, furosemide acts by inhibiting the Na-K-2Cl symporter in the thick ascending limb of the loop of Henle. The action on the distal tubules is independent of any inhibitory effect on carbonic anhydrase or aldosterone; it also abolishes the corticomedullary osmotic gradient and blocks negative as well as positive free water clearance.

Due to the large NaCl absorptive capacity of the Loop of Henle, diuresis is not limited by development of acidosis, as it is with the carbonic anhydrase inhibitors.

By inhibiting the transporter, the loop diuretics reduce the reabsorption of NaCl and also diminish the lumen-positive potential that derives from K+ recycling. This electrical potential normally drives divalent cation reabsorbtion in the loop, and by reducing this potential loop diuretics cause an increase in Mg2+ and Ca2+ excretion. Prolonged use can cause significant hypomagnesemia in some patients. Since Ca2+ is actively reabsorbed in the distal convoluted tubule, loop diuretics do not generally cause hypocalcemia.

Additionally, furosemide is a noncompetitive subtype-specific blocker of GABA-A receptors [1][2][3]. Furosemide has been reported to reversibly antagonize GABA-evoked currents of alpha6 beta2 gamma2 receptors at microM concentrations, but not alpha1 beta2 gamma2 receptors [1][3]. During development, the alpha6 beta2 gamma2 receptor increases in expression in cerebellar granule neurons, corresponding to increased sensitivity to furosemide[2].

Clinical use in humans

Furosemide, as a loop diuretic, is principally used in the following indications (Aventis, 1998):

  • Edema associated with heart failure, hepatic cirrhosis, renal impairment, nephrotic syndrome
  • Hypertension
  • Adjunct in cerebral/pulmonary edema where rapid diuresis is required (IV injection)

It is also sometimes used in the management of severe hypercalcemia in combination with adequate rehydration [4].

Although disputed,[5] it is considered ototoxic: "usually with large parenteral doses and rapid administration and in renal impairment"[6]

The tendency, as for all loop diuretics, to cause low potassium levels (hypokalemia) has given rise to combination products, either with potassium itself (e.g. Lasix-K) or with the potassium sparing diuretic of amiloride (Co-amilofruse).

Use in research

Furosemide has been used in research on the inner-ear. It's known to decrease temporarily the response to sound by reducing the mobility of the basilar membrane of the cochlea and by reducing the transduction that normally results from the bending of stereocilia on hair cells. (demonstrated in 1991 by Mario Ruggero and Nola Rich from the University of Minnesota)

Use in horses

The diuretic-effects are put to use most commonly in horses to prevent "bleeding" during a race. Sometime in the early 1970s, furosemide's ability to prevent, or at least greatly reduce, the incidence of "bleeding" (EIPH) by horses during races was discovered accidentally. Pursuant to the racing rules of most states, horses that bleed from the nostrils three times are permanently barred from racing (for their own protection). Clinical trials followed, and by decade's end, racing commissions in some states began legalizing its use on race horses. On September 1, 1995, New York became the last state in the United States to approve such use, after years of refusing to consider doing so. Some states allow its use for all racehorses; some allow it only for confirmed "bleeders." However, its use for this purpose is still prohibited in many other countries, and veterinarians dispute its use for this problem.

Furosemide is also used in horses for pulmonary edema, congestive heart failure (in combination with other drugs), and allergic reactions. Despite the fact that it increases circulation to the kidneys, it does not help kidney function, and is not recommended for kidney disease.

Precautions, side-effects, and administration

Furosemide is injected either intramuscularly (IM) or intravenously (IV), usually 0.5-1.0 mg/kg 2x/day, although less before a horse is raced. As with many diuretics, it can cause dehydration and electrolyte imbalance, including loss of potassium, calcium, sodium, and magnesium. It is especially important to prevent potassium loss. Excessive use of Furosemide will most likely lead to a metabolic alkalosis due to hypochloremia and hypokalemia. The drug should therefore not be used in horses that are dehydrated or experiencing kidney failure. It should be used with caution in horses with liver problems or electrolyte abnormalities. Overdose may lead to dehydration, change in drinking patterns and urination, seizures, GI problems, kidney damage, lethargy, collapse, and coma.

Furosemide should be used with caution when combined with corticosteroids (as this increases the risk of electrolyte imbalance), aminoglycoside antibiotics (increases risk of kidney or ear damage), and trimethoprim sulfa (causes decreased platelet count). It may also cause interactions with anesthesics, so its use should be related to the veterinarian if the animal is going into surgery, and it decreases the kidney's ability to excrete aspirin, so dosages will need to be adjusted if combined with that drug

Furosemide may cause digoxin toxicity due to hypokalemia.

The drug is best not used during pregnancy or in a lactating mare, as it has been shown to be passed through the placenta and milk in studies with other species. It should not be used in horses with pituitary pars intermedia dysfunction (Cushings).

Furosemide is detectable in urine 36–72 hours following injection. Its use is prohibited by most equestrian organizations.

Drug Interactions

Furosemide has potential interactions with the following medications:[7]

  • Other diuretics (e.g. ethacrynic acid, hydrochlorothiazide)
  • Indomethacin
  • Lithium
  • Synergistic effects with other antihypertensives (e.g. Doxazosin)

Brand names

Some of the brand names under which furosemide is marketed include: Aisemide, Apo-Furosemide, Beronald, Desdemin, Discoid, Diural, Diurapid, Dryptal, Durafurid, Errolon, Eutensin, Flusapex, Frusetic, Frusid, Fulsix, Fuluvamide, Furesis, Furix, Furo-Puren, Furosedon, Hydro-rapid, Impugan, Katlex, Lasilix, Lasix, Lodix, Lowpston, Macasirool, Mirfat, Nicorol, Odemase, Oedemex, Profemin, Rosemide, Rusyde, Salix, Trofurit, Uremide, Urex, Frudix, Fusid.frusone


  1. 1.0 1.1 Korpi ER, Kuner T, Seeburg PH, Lüddens H (1995). "Selective antagonist for the cerebellar granule cell-specific gamma-aminobutyric acid type A receptor". Mol. Pharmacology. 47 (2): 283–9. PMID 7870036. 
  2. 2.0 2.1 Tia S, Wang JF, Kotchabhakdi N, Vicini S (1996). "Developmental changes of inhibitory synaptic currents in cerebellar granule neurons: role of GABA(A) receptor alpha 6 subunit". J. Neurosci. 16 (11): 3630–40. PMID 8642407. http://www.jneurosci.org/cgi/content/full/16/11/3630. 
  3. 3.0 3.1 Wafford KA, Thompson SA, Thomas D, Sikela J, Wilcox AS, Whiting PJ (1996). "Functional characterization of human gamma-aminobutyric acidA receptors containing the alpha 4 subunit". Mol. Pharmacol. 50 (3): 670–8. PMID 8794909. 
  4. Rossi S, ed (2004). Australian Medicines Handbook 2004 (5th ed.). Adelaide, S.A.: Australian Medicines Handbook Pty Ltd. ISBN 0-9578521-4-2. http://www.amh.net.au/. 
  5. Rais-Bahrami K, Majd M, Veszelovszky E, Short B (2004). "Use of furosemide and hearing loss in neonatal intensive care survivors". Am J Perinatol 21 (6): 329–32. doi:10.1055/s-2004-831887. PMID 15311369. 
  6. BNF 45 March 2003
  7. Brand name:Lasix - Generic name: Furosemide Prescription Drug Information, Side Effects - PDRHealth

Further reading

  • Aventis Pharma (1998). Lasix Approved Product Information. Lane Cove: Aventis Pharma Pty Ltd.
  • Barbara Forney (2007). Understanding Equine Medications, Revised Edition (Horse Health Care Library). Eclipse Press. ISBN 1-58150-151-X. 

External links


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