Support compounds

Furosemide (Lasix)

Furosemide, sold as Lasix, is a prescription “loop” diuretic: a drug that makes the kidneys excrete more salt and water. Doctors use it to clear fluid buildup (edema) in heart failure, liver cirrhosis and kidney disease, and sometimes to treat high blood pressure. It has been FDA approved since 1966 and is the most commonly used loop diuretic in heart failure (Mentz et al., JAMA 2023).

Outside medicine, furosemide is misused by bodybuilders to shed water before a contest and by weight-class athletes to “make weight” quickly. It has been one of the most frequently detected diuretics in anti-doping tests (Cadwallader et al., Br J Pharmacol 2010), and the World Anti-Doping Agency (WADA) bans it at all times. Its own label opens with a boxed warning: given in excessive amounts, it can cause profound loss of water and electrolytes.

This page summarizes what the FDA labels, clinical trials and anti-doping literature report. It is for education only and is not medical advice.

Property Detail
Drug class Loop diuretic (anthranilic acid derivative with a sulfonamide group)
Brands / approval Lasix tablets, NDA 016273, approved 1966; generics; subcutaneous Furoscix (2022) and Lasix ONYU (2025)
Routes Oral tablet; injection (IV/IM); subcutaneous on-body infusor or autoinjector
Lasix strengths 20, 40 and 80 mg tablets
Labeled oral dose (edema, adults) 20–80 mg as a single starting dose, titrated as needed up to 600 mg/day in severe edema
Half-life (label) About 2 hours (terminal); diuresis lasts 6–8 hours after an oral dose
Oral bioavailability 64% vs IV in fasted healthy men (label); highly variable between people
US status Prescription only (Rx)
WADA status Prohibited at all times (S5 Diuretics and masking agents); a Specified Substance

What it is

Chemically, furosemide is 4-chloro-N-furfuryl-5-sulfamoylanthranilic acid, formula C₁₂H₁₁ClN₂O₅S, molecular weight 330.7 g/mol (Lasix label; PubChem). It is a white, practically water-insoluble powder. The molecule carries a sulfonamide group, which is why the label warns that people allergic to sulfonamides may also react to it.

Lasix tablets were first approved by the FDA in 1966 under NDA 016273 (Drugs@FDA). Two newer products deliver furosemide under the skin for heart failure patients at home: Furoscix, approved in 2022, and Lasix ONYU, approved in 2025 (Furoscix label; Lasix ONYU label).

How it works

Furosemide blocks the Na-K-2Cl cotransporter (NKCC2) in the thick ascending limb of the loop of Henle, the kidney segment that reabsorbs a large share of filtered salt (Huang et al., Am J Physiol Renal Physiol 2016). Salt that is not reabsorbed stays in the urine and pulls water with it. The label adds that its effect does not depend on carbonic anhydrase or aldosterone.

Because the drug works from inside the tubule, the response tracks the amount of furosemide reaching the urine rather than its blood level (Ponto and Schoenwald, Clin Pharmacokinet 1990). Loop diuretics also markedly raise urinary losses of potassium, magnesium and calcium (Cadwallader et al., Br J Pharmacol 2010). This is the root of most of its side effects.

How it compares with other diuretics

Furosemide acts at a different site from the other diuretics in this library, which changes its strength and its effect on potassium (Cadwallader et al., Br J Pharmacol 2010).

Drug Class Main site of action Effect on potassium
Furosemide Loop diuretic Loop of Henle (NKCC2) Lowers it
Hydrochlorothiazide (HCTZ) Thiazide Early distal convoluted tubule Lowers it
Spironolactone Potassium-sparing (mineralocorticoid receptor blocker) Collecting duct Raises it

The Lasix label describes furosemide as “particularly useful when an agent with greater diuretic potential is desired.” In heart failure care, 40 mg of furosemide is treated as roughly equal to 1 mg of bumetanide or 20 mg of torsemide (Ellison and Felker, NEJM 2017).

Pharmacokinetics

From the Lasix tablet label:

Parameter Value
Onset of diuresis (oral) Within 1 hour
Peak effect First or second hour
Duration of diuresis 6–8 hours
Bioavailability vs IV (fasted healthy men) 64% (tablet), 60% (oral solution)
Mean absorption time 87 min (tablet) vs 50 min (oral solution)
Protein binding 91–99%, mainly to albumin
Terminal half-life About 2 hours
Metabolism Furosemide glucuronide is the main or only metabolite
Excretion Mostly unchanged in urine; hemodialysis does not speed removal

Oral absorption is the drug’s weak point. A review in the New England Journal of Medicine puts oral bioavailability at a mean of about 50% with a range of 10–90%, notes that food delays absorption, and reports a half-life of about 2.7 hours in heart failure (Ellison and Felker, NEJM 2017). The same review states that in people with normal kidney function, IV furosemide is about twice as potent per milligram as oral.

In a crossover study of 16 patients with compensated heart failure, oral furosemide reached its peak at 2.4 ± 2.5 hours, slower than in healthy volunteers, while torsemide peaked at 1.1 hours and was absorbed more completely and consistently (Vargo et al., Clin Pharmacol Ther 1995).

The body pushes back against repeated doses. After a dose wears off, the kidney retains extra sodium, and as fluid volume drops each dose produces a smaller response, a pattern called the “braking phenomenon” (Ellison and Felker, NEJM 2017).

Approved medical use

The Lasix tablet label lists two indications:

  • Edema in adults and children with congestive heart failure, cirrhosis of the liver, or kidney disease including nephrotic syndrome.
  • Hypertension in adults, alone or with other blood pressure drugs. The label notes that patients not controlled by thiazides will probably not be controlled by furosemide alone.
Use Labeled oral dosing
Edema, adults 20–80 mg as a single dose; may repeat or raise by 20–40 mg no sooner than 6–8 hours later; maintenance once or twice daily; up to 600 mg/day in severe edema
Edema, children 2 mg/kg as a single dose; may raise by 1–2 mg/kg no sooner than 6–8 hours later; doses over 6 mg/kg not recommended
Hypertension, adults 80 mg/day, usually as 40 mg twice daily; other blood pressure drugs reduced by at least 50% when furosemide is added
Elderly Start at the low end of the range

The label says edema “may be most efficiently and safely mobilized” by dosing on 2–4 consecutive days each week. It advises closer clinical and laboratory monitoring when doses over 80 mg/day are used for long periods.

The subcutaneous products are fixed-dose (80 mg delivered over about 5 hours by an on-body infusor, or in about 10 seconds by the Furoscix ReadyFlow autoinjector). They are labeled for short-term treatment of edema in heart failure (and, for Furoscix, chronic kidney disease) and should be replaced with oral diuretics as soon as practical (Furoscix label).

What the research shows

Heart failure

Loop diuretics are a cornerstone of heart failure treatment, yet a 2020 review notes that robust trial evidence guiding their use is sparse (Felker et al., JACC 2020). Two large randomized trials stand out.

The DOSE trial randomized 308 patients with acute decompensated heart failure, in a double-blind 2 × 2 design, to IV furosemide by bolus every 12 hours or continuous infusion, and at a low dose (equal to their home oral dose) or a high dose (2.5 times it) (Felker et al., NEJM 2011):

Comparison Symptom score (AUC over 72 h) Change in creatinine at 72 h
Bolus vs continuous infusion 4236 vs 4373 (p = 0.47) +0.05 vs +0.07 mg/dL (p = 0.45)
High vs low dose 4430 vs 4171 (p = 0.06) +0.08 vs +0.04 mg/dL (p = 0.21)

Neither comparison reached significance on its primary endpoints. The high-dose strategy produced more fluid removal but also transient worsening of kidney function.

TRANSFORM-HF randomized 2,859 patients hospitalized for heart failure at 60 US hospitals to torsemide or furosemide after discharge, in an open-label pragmatic design (Mentz et al., JAMA 2023). Over a median 17.4 months, death occurred in 26.1% on torsemide and 26.2% on furosemide (HR 1.02, 95% CI 0.89–1.18). Despite torsemide’s better absorption, it did not lower mortality. The authors note that loss to follow-up, crossover and nonadherence limit interpretation.

Rapid weight loss and exercise performance

Small human studies have tested furosemide as a way to drop body water quickly, as weight-class athletes do:

Study Design Furosemide dose Water loss Performance effect
Caldwell et al., 1984 62 non-endurance athletes; sauna vs diuretic vs exercise vs control 1.7 mg/kg in two doses About 3.1 kg body mass; plasma volume −14.1% Lower peak oxygen uptake and peak workload than the exercise group
Armstrong et al., 1985 8 men; crossover track races 40 mg Body mass −1.6% to −2.1%; plasma volume −9.9% to −12.3% 5,000 m slower by 1.31 min and 10,000 m by 2.62 min (both significant); 1,500 m not significantly changed
Watson et al., 2005 9 former sprinters; crossover 40 mg Body mass −2.2% to −2.5%; plasma volume about −7% No change in 50, 200 or 400 m times or vertical jump

The Caldwell weight and plasma-volume figures are as reported in a later review of the study (Cadwallader et al., Br J Pharmacol 2010). Taken together, furosemide-induced dehydration hurt endurance and maximal aerobic performance. It did not help sprinting, and the lighter body did not translate into faster times.

Bodybuilding and “drying out”

Bodybuilders use diuretics before contests to try to reduce water under the skin and look more defined. A 2021 evidence review found a “dearth of evidence” supporting common peak-week practices, and reported that self-prescribed diuretic use by enhanced bodybuilders has led to dangerous outcomes (Escalante et al., BMC Sports Sci Med Rehabil 2021). No controlled study has shown that furosemide improves how a physique looks on stage.

What the literature does contain is case reports of harm (see below).

Masking other drugs

WADA groups diuretics with “masking agents” because diluting the urine could, in theory, hide other banned drugs. A 2021 pharmacology review concluded that furosemide’s masking effect is limited and that it is mainly relevant to weight-class sports (Brinkman et al., Ned Tijdschr Geneeskd 2021). Furosemide itself is short-lived and is routinely screened for by WADA-accredited labs (Cadwallader et al., Br J Pharmacol 2010).

Side effects and risks

Boxed warning: fluid and electrolyte loss

The Lasix label’s boxed warning states that furosemide is a potent diuretic which, in excessive amounts, can cause profound diuresis with water and electrolyte depletion, so careful medical supervision is required. Excessive diuresis can cause dehydration, low blood volume and circulatory collapse, and possibly blood clots, especially in older people.

The label lists these warning signs of fluid or electrolyte imbalance:

  • dry mouth, thirst, weakness, lethargy, drowsiness, restlessness;
  • muscle pains, cramps or fatigue;
  • low blood pressure, low urine output, fast heart rate or arrhythmia;
  • nausea and vomiting.

The specific disturbances include low potassium (hypokalemia), low sodium, low magnesium, low calcium (rarely with tetany) and a metabolic alkalosis. Hypokalemia is more likely with brisk diuresis, poor intake, cirrhosis, or use with corticosteroids, large amounts of licorice or laxatives. In people with cirrhosis, sudden fluid shifts can trigger hepatic coma.

Hearing loss

The label reports tinnitus and reversible or irreversible hearing loss and deafness. These were usually linked to rapid injection, severe kidney impairment, higher than recommended doses, low blood protein, or use with aminoglycoside antibiotics, ethacrynic acid or other ear-toxic drugs. For high-dose IV therapy the label cites an infusion rate not exceeding 4 mg per minute in adults.

Metabolic and other effects

From the label:

  • Blood sugar: raised glucose and abnormal glucose tolerance; rarely, new diabetes.
  • Uric acid: asymptomatic hyperuricemia; gout rarely.
  • Lipids: increased cholesterol and triglycerides.
  • Hypersensitivity: possible cross-reaction in people allergic to sulfonamides; severe skin reactions (Stevens-Johnson syndrome, toxic epidermal necrolysis, DRESS) and anaphylaxis are listed.
  • Other: orthostatic hypotension (worse with alcohol), photosensitivity, pancreatitis, cholestatic jaundice, blood disorders, possible worsening of lupus, and acute urinary retention in men with prostate enlargement.

Harms reported with non-medical use

Case reports describe serious electrolyte emergencies in people using furosemide to change their appearance:

  • A 26-year-old professional bodybuilder took 80 mg of furosemide 48 and 24 hours before a contest, lost 5–6 kg, and arrived at the emergency department the next day with palpitations and paralysis from severe hypokalemia (Mayr et al., Am J Emerg Med 2012; details as summarized by Escalante et al., 2021).
  • A 22-year-old woman who had taken 250 mg/day for four months “to improve the shape of her muscles” presented with a potassium of 1.1 mmol/L, low sodium, metabolic alkalosis, mild kidney impairment and muscle breakdown (Ruisz et al., BMC Womens Health 2013).
  • A 31-year-old bodybuilder using anabolic steroids, amphetamines, a furosemide–amiloride combination and potassium supplements had a heart attack with a potassium of 6.7 mmol/L (too high) and ventricular tachycardia (Appleby et al., Int J Cardiol 1994).

The last case shows that combining diuretics with potassium-sparing drugs or potassium supplements can swing potassium the other way. Both low and high potassium can cause dangerous heart rhythms.

Interactions

Key interactions from the Lasix label:

Combined with Risk
Aminoglycoside antibiotics, ethacrynic acid, cisplatin Increased ear toxicity; avoid except in life-threatening situations
Lithium Reduced lithium clearance and high risk of lithium toxicity
ACE inhibitors or ARBs Severe low blood pressure and worsening kidney function, including kidney failure
NSAIDs, indomethacin, high-dose aspirin Weaker diuretic effect; reports of rising creatinine and potassium; salicylate toxicity at lower doses
Sucralfate Reduced effect; separate doses by at least 2 hours
Corticosteroids, laxatives, licorice More potassium loss
Digoxin (digitalis) Low potassium makes digitalis effects on the heart worse
Cephalosporins, cyclosporine Kidney toxicity; gouty arthritis with cyclosporine

Who should not use it

The label contraindicates furosemide in people who cannot make urine (anuria) and in people with prior hypersensitivity to it. Other cautions:

  • Pregnancy: no adequate human studies. In rabbits, furosemide caused unexplained maternal deaths and abortions at 2 times the maximum human dose (animal data).
  • Breastfeeding: it passes into breast milk and may inhibit lactation.
  • Children: kidney calcium deposits (nephrocalcinosis) in premature infants and in some children under 4 on long-term treatment.
  • Older adults: reduced kidney clearance and a smaller diuretic response; start low.

Monitoring

The label recommends checking serum electrolytes (particularly potassium), CO₂, creatinine and BUN frequently during the first few months of therapy and periodically after. Calcium and magnesium should be checked periodically, and blood and urine glucose in people with diabetes.

In the US, furosemide is a prescription-only drug (Lasix label).

The WADA 2026 Prohibited List names furosemide under S5 Diuretics and masking agents, prohibited both in and out of competition. All S5 substances are Specified Substances. The list also states that finding a diuretic together with any amount of a threshold substance (such as salbutamol, ephedrine or pseudoephedrine) counts as an adverse analytical finding unless the athlete holds therapeutic use exemptions for both.

Diuretics have long been a common finding in doping tests. WADA laboratory data compiled in a 2010 review:

Year Diuretics, % of all positive samples Furosemide findings
2003 5.2% 48 (most common diuretic)
2005 5.7% 91 (most common)
2007 7.4% 111 (most common)
2008 7.9% 104 (second to hydrochlorothiazide)

Source: Cadwallader et al., Br J Pharmacol 2010.

Key takeaways

  • A potent loop diuretic. Furosemide blocks salt reabsorption in the loop of Henle, causing a large but short diuresis that starts within an hour and lasts 6–8 hours.
  • Short half-life, erratic absorption. The terminal half-life is about 2 hours, and oral bioavailability ranges from about 10% to 90% between people.
  • Approved for edema and hypertension. Labeled oral doses start at 20–80 mg for edema, titrated under supervision, with up to 600 mg/day in severe cases.
  • Trials refine, not replace, its use. In heart failure, bolus vs infusion and high vs low dose made no significant difference in DOSE, and torsemide did not beat it on mortality in TRANSFORM-HF.
  • Dehydration does not help performance. Furosemide-induced water loss slowed distance running and gave sprinters no benefit, and there is no controlled evidence it improves stage appearance.
  • Electrolyte loss is the central danger. The label carries a boxed warning, case reports describe paralysis and heart rhythm emergencies in bodybuilders, and WADA bans it at all times.

Sources

  1. Validus Pharmaceuticals. Lasix (furosemide) tablets 20, 40 and 80 mg prescribing information. DailyMed.
  2. Food and Drug Administration. Drugs@FDA: Lasix, NDA 016273. FDA.
  3. scPharmaceuticals. Furoscix (furosemide injection) for subcutaneous use, prescribing information. DailyMed.
  4. SQ Innovation. Lasix ONYU (furosemide) injection for subcutaneous use, prescribing information. DailyMed.
  5. National Center for Biotechnology Information. PubChem Compound Summary for CID 3440, Furosemide. PubChem.
  6. Huang X, Dorhout Mees E, Vos P, et al. Everything we always wanted to know about furosemide but were afraid to ask. Am J Physiol Renal Physiol. 2016;310(10):F958–F971. PubMed.
  7. Ponto LL, Schoenwald RD. Furosemide (frusemide). A pharmacokinetic/pharmacodynamic review (Part I). Clin Pharmacokinet. 1990;18(5):381–408. PubMed.
  8. Ellison DH, Felker GM. Diuretic treatment in heart failure. N Engl J Med. 2017;377(20):1964–1975. PubMed; PMC.
  9. Vargo DL, Kramer WG, Black PK, et al. Bioavailability, pharmacokinetics, and pharmacodynamics of torsemide and furosemide in patients with congestive heart failure. Clin Pharmacol Ther. 1995;57(6):601–609. PubMed.
  10. Felker GM, Ellison DH, Mullens W, et al. Diuretic therapy for patients with heart failure: JACC state-of-the-art review. J Am Coll Cardiol. 2020;75(10):1178–1195. PubMed.
  11. Felker GM, Lee KL, Bull DA, et al. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med. 2011;364(9):797–805. PubMed.
  12. Mentz RJ, Anstrom KJ, Eisenstein EL, et al. Effect of torsemide vs furosemide after discharge on all-cause mortality in patients hospitalized with heart failure: the TRANSFORM-HF randomized clinical trial. JAMA. 2023;329(3):214–223. PubMed.
  13. Caldwell JE, Ahonen E, Nousiainen U. Differential effects of sauna-, diuretic-, and exercise-induced hypohydration. J Appl Physiol Respir Environ Exerc Physiol. 1984;57(4):1018–1023. PubMed.
  14. Armstrong LE, Costill DL, Fink WJ. Influence of diuretic-induced dehydration on competitive running performance. Med Sci Sports Exerc. 1985;17(4):456–461. PubMed.
  15. Watson G, Judelson DA, Armstrong LE, et al. Influence of diuretic-induced dehydration on competitive sprint and power performance. Med Sci Sports Exerc. 2005;37(7):1168–1174. PubMed.
  16. Cadwallader AB, de la Torre X, Tieri A, et al. The abuse of diuretics as performance-enhancing drugs and masking agents in sport doping: pharmacology, toxicology and analysis. Br J Pharmacol. 2010;161(1):1–16. PubMed; PMC.
  17. Brinkman DJ, Tichelaar J, Van Agtmael MA. Can furosemide mask the use of performance-enhancing drugs? [Article in Dutch]. Ned Tijdschr Geneeskd. 2021;165:D5915. PubMed.
  18. Escalante G, Stevenson SW, Barakat C, et al. Peak week recommendations for bodybuilders: an evidence based approach. BMC Sports Sci Med Rehabil. 2021;13(1):68. PubMed; PMC.
  19. Mayr FB, Domanovits H, Laggner AN. Hypokalemic paralysis in a professional bodybuilder. Am J Emerg Med. 2012;30(7):1324.e5–1324.e8. PubMed.
  20. Ruisz W, Stöllberger C, Finsterer J, et al. Furosemide-induced severe hypokalemia with rhabdomyolysis without cardiac arrest. BMC Womens Health. 2013;13:30. PubMed.
  21. Appleby M, Fisher M, Martin M. Myocardial infarction, hyperkalaemia and ventricular tachycardia in a young male body-builder. Int J Cardiol. 1994;44(2):171–174. PubMed.
  22. World Anti-Doping Agency. The 2026 Prohibited List. In effect January 1, 2026. WADA 2026 Prohibited List.