Losartan is a prescription blood pressure drug from the angiotensin II receptor blocker class (ARBs, the “sartans”). The FDA approved it as Cozaar on April 14, 1995, and the brand is now sold by Organon. It is widely available as a generic tablet, alone or combined with the diuretic hydrochlorothiazide (Hyzaar).
US labeling covers three uses: high blood pressure, lowering stroke risk in people with high blood pressure and an enlarged heart muscle (based on the LIFE trial), and slowing kidney disease in type 2 diabetes (based on the RENAAL trial). The label carries a boxed warning for fetal toxicity. Losartan is sometimes discussed as a blood pressure option for anabolic steroid users, but no trials have tested it in people using anabolic steroids.
This page summarizes what the FDA label and the major outcome trials report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Drug class | Angiotensin II type 1 (AT1) receptor blocker (ARB) |
| Brand / approval | Cozaar (Organon), NDA 020386, approved April 14, 1995; AB-rated generics available |
| Route | Oral tablet (the label also describes a pharmacy-prepared suspension for children) |
| Strengths | 25 mg, 50 mg, 100 mg |
| Labeled adult dose | Usually 50 mg once daily; maximum 100 mg once daily; 25 mg start if volume-depleted or with mild-to-moderate liver impairment |
| Half-life (label) | Losartan ≈2 h; its active metabolite 6–9 h |
| Key mechanism fact | About 14% of a dose becomes an active metabolite that is 10–40 times more potent and produces most of the effect |
| Boxed warning | Fetal toxicity: stop as soon as pregnancy is detected |
| US status | Prescription only |
| WADA status | Not named on the 2026 Prohibited List; combination tablets with hydrochlorothiazide contain a prohibited diuretic |
What it is
Losartan potassium is a non-peptide molecule with the formula C₂₂H₂₂ClKN₆O and a molecular weight of 461.01, and it is freely soluble in water (Cozaar label). Each tablet contains a small amount of potassium: 2.12 mg in the 25 mg tablet, 4.24 mg in the 50 mg and 8.48 mg in the 100 mg.
The FDA approved Cozaar under NDA 020386 as a new molecular entity on April 14, 1995. Drugs@FDA lists the brand tablets with an “AB” therapeutic equivalence code, meaning approved generics are rated interchangeable (Drugs@FDA).
How it lowers blood pressure
Angiotensin II is the main blood-pressure-raising hormone of the renin-angiotensin system. It narrows blood vessels and triggers the release of aldosterone (a hormone that makes the kidneys retain salt and water). Losartan and its active metabolite stop angiotensin II from binding the AT1 receptor. Per the label:
- Both bind AT1 with about 1,000-fold greater affinity than the AT2 receptor, and neither acts as a partial agonist.
- Losartan itself is a reversible, competitive blocker. The active metabolite is 10–40 times more potent by weight and blocks in a non-competitive way.
- A 100 mg dose blocks about 85% of the blood pressure response to infused angiotensin II at peak, with 25–40% still blocked at 24 hours.
- Plasma renin activity rises 2–3 fold as feedback is removed, and aldosterone falls. Despite the drop in aldosterone, the label reports that very little effect on serum potassium was observed.
- Losartan does not inhibit ACE (angiotensin-converting enzyme), so unlike ACE inhibitors it does not increase the response to bradykinin, a peptide linked to ACE-inhibitor cough.
The effect is mostly present within one week; in some studies the maximum took 3–6 weeks. The label reports no rebound rise in blood pressure after abrupt withdrawal and essentially no change in average heart rate.
Uric acid: a losartan-specific effect
Losartan increases uric acid excretion in urine. In a small randomized, double-blind crossover trial in 13 hypertensive patients with high uric acid and gout, losartan 50 mg daily lowered serum uric acid from 538 to 491 µmol/L (≈9.0 to ≈8.3 mg/dL), while irbesartan had no effect; doubling the losartan dose did not lower it further (Würzner et al., J Hypertens 2001). A review of ARB studies concluded that only losartan has clear evidence of lowering serum uric acid, so this is not a class effect (Sutton Burke et al., J Pharm Pract 2020). Losartan is not approved to treat gout or high uric acid.
Pharmacokinetics
Most of losartan’s effect comes from an active carboxylic acid metabolite, formed during first-pass metabolism mainly by the enzyme CYP2C9. From the FDA label (Cozaar label):
| Parameter | Losartan | Active metabolite |
|---|---|---|
| Oral bioavailability | ≈33% (large first-pass metabolism) | — |
| Share of dose converted | — | ≈14% |
| Time to peak | 1 h | 3–4 h |
| Exposure (AUC) | Reference | ≈4 times that of losartan |
| Terminal half-life | ≈2 h | ≈6–9 h |
| Volume of distribution | ≈34 L | ≈12 L |
| Free (unbound) fraction in plasma | 1.3% | 0.2% |
| Total plasma clearance | ≈600 mL/min | ≈50 mL/min |
| Unchanged in urine (single dose) | ≈4% | ≈6% |
Other label points:
- Food: a meal slows absorption and lowers peak levels, but total exposure falls only about 10%. It can be taken with or without food.
- Linearity: kinetics are linear up to 200 mg, and neither compound accumulates with once-daily dosing.
- Excretion: after an oral radiolabeled dose, about 35% is recovered in urine and 60% in feces, with bile contributing.
- Sex: losartan levels were about twice as high in women with hypertension as in men, but metabolite levels were similar; no dose change is needed.
- Kidney impairment: levels of both compounds rise 50–90% in mild to moderate kidney impairment. Neither is removed by hemodialysis.
- Liver impairment: in mild to moderate alcoholic cirrhosis, losartan levels were 5 times and metabolite levels about 1.7 times those of healthy volunteers, which is why the label recommends a 25 mg starting dose.
- Genetics: people with a rare CYP2C9 defect do not convert losartan to its active metabolite.
The short half-life of the parent drug is offset by the longer-lived metabolite. In the hypertension trials, twice-daily dosing at the same total dose gave consistently larger trough (24-hour) responses than once-daily dosing.
Approved medical use
| Indication | Labeled dosing |
|---|---|
| Hypertension, adults | Start 50 mg once daily; up to 100 mg once daily. Start 25 mg with possible volume depletion (e.g., on diuretics) |
| Hypertension, children 6–16 years | Start 0.7 mg/kg once daily (up to 50 mg); doses above 1.4 mg/kg or 100 mg daily not studied. Not recommended under age 6 or with GFR under 30 mL/min/1.73 m² |
| Stroke risk reduction in hypertension with left ventricular hypertrophy | Start 50 mg; add hydrochlorothiazide 12.5 mg and/or raise losartan to 100 mg, then hydrochlorothiazide to 25 mg as needed |
| Diabetic nephropathy in type 2 diabetes with a history of hypertension | Start 50 mg; raise to 100 mg based on blood pressure |
The stroke indication carries a caveat: the label states there is evidence the benefit does not apply to Black patients (see LIFE below). The nephropathy indication applies to patients with raised serum creatinine and a urine albumin-to-creatinine ratio of at least 300 mg/g (Cozaar label).
A fixed combination of losartan and hydrochlorothiazide is sold as Hyzaar (DailyMed).
What the research shows
Blood pressure lowering
The label’s main efficacy evidence comes from 4 placebo-controlled trials lasting 6–12 weeks, with 1,075 patients on losartan and 334 on placebo (Cozaar label):
| Regimen | Placebo-subtracted reduction (systolic / diastolic) |
|---|---|
| 10 mg or 25 mg once daily | Some effect at peak; small, inconsistent effect at 24 h |
| 50–150 mg once daily | 5.5–10.5 / 3.5–7.5 mmHg |
| 150 mg once daily | No greater effect than 50–100 mg |
| 50 mg plus hydrochlorothiazide 12.5 mg | 15.5 / 9.2 mmHg |
The effect was similar in men and women and in patients over and under 65. It was somewhat smaller in Black patients, who more often have low-renin hypertension.
Stroke and heart outcomes: the LIFE trial
LIFE was a double-blind randomized trial in 9,193 people aged 55–80 with hypertension (160–200/95–115 mmHg) and left ventricular hypertrophy (LVH, a thickened heart muscle) on ECG. It compared losartan-based with atenolol-based treatment (atenolol is a beta-blocker), adding hydrochlorothiazide and other drugs as needed. Mean follow-up was 4.8 years (Dahlöf et al., Lancet 2002; Cozaar label).
Blood pressure fell almost equally: 30.2/16.6 mmHg on losartan and 29.1/16.8 mmHg on atenolol. Outcomes:
| Outcome | Losartan | Atenolol | Relative risk (95% CI) |
|---|---|---|---|
| Primary composite (CV death, stroke or heart attack) | 508 (23.8 per 1,000 patient-years) | 588 (27.9 per 1,000 patient-years) | 0.87 (0.77–0.98), p = 0.021 |
| Stroke, fatal or nonfatal | 232 | 309 | 0.75 (0.63–0.89), p = 0.001 |
| Heart attack, fatal or nonfatal | 198 | 188 | 1.07 (0.88–1.31), not significant |
| Cardiovascular death | 204 | 234 | 0.89 (0.73–1.07), not significant |
The benefit came mainly from fewer strokes. Total mortality and hospitalization for heart failure or angina did not differ significantly. The label notes that this result comes from a single trial against an active drug, so it is less compelling than a placebo comparison would be.
Black patients. In the subgroup of 533 Black patients (6% of LIFE), the primary outcome occurred in 17% on losartan vs 11% on atenolol. The label says it cannot be known whether this is chance, but that LIFE provides no evidence that the benefit applies to Black patients.
Heart muscle thickness. In an echocardiography substudy of 960 LIFE patients, losartan-based therapy reduced left ventricular mass index more than atenolol, by 21.7 vs 17.7 g/m² from baseline (p = 0.021), after adjusting for blood pressure (Devereux et al., Circulation 2004). These were older patients with hypertensive LVH, not athletes or steroid users.
Diabetic kidney disease: the RENAAL trial
RENAAL randomized 1,513 patients with type 2 diabetes and kidney disease (raised creatinine and heavy protein in the urine) to losartan 50–100 mg or placebo, on top of conventional blood pressure drugs other than ACE inhibitors or ARBs. Mean follow-up was 3.4 years, and 72% of patients took the 100 mg dose for most of the study (Brenner et al., NEJM 2001; Cozaar label):
| Outcome (any time in study) | Losartan | Placebo | Risk reduction (95% CI) |
|---|---|---|---|
| Primary composite (doubling of creatinine, end-stage kidney disease or death) | 43.5% | 47.1% | 16.1% (2.3–27.9%), p = 0.022 |
| Doubling of serum creatinine | 21.6% | 26.0% | 25.3% (7.8–39.4%), p = 0.006 |
| End-stage kidney disease (dialysis or transplant) | 19.6% | 25.5% | 28.6% (11.5–42.4%), p = 0.002 |
| Death | 21.0% | 20.3% | −1.7% (−26.9 to 18.6%), not significant |
Losartan cut proteinuria (protein in the urine) by about 35% and lowered the risk of a first hospitalization for heart failure by 32% (p = 0.005). The combined cardiovascular outcome did not differ between groups. Blood pressure ended at 143/76 mmHg on losartan and 146/77 mmHg on placebo; the authors concluded the kidney benefit exceeded what the blood pressure difference would explain.
Relevance to anabolic steroid use
High blood pressure and heart changes in anabolic-androgenic steroid (AAS) users are documented:
- In a cross-sectional study of men doing recreational strength training, 37 current AAS users had higher 24-hour systolic blood pressure than 30 controls (132 vs 124 mmHg), and systolic hypertension was more common (51% vs 17%). Current users also had higher aldosterone, and both current and former users had stiffer aortas (Rasmussen et al., J Hypertens 2018).
- In a cross-sectional study of 140 experienced male weightlifters, 86 long-term AAS users had lower left ventricular ejection fraction than 54 nonusers (52% vs 63%), worse diastolic function and more coronary plaque (Baggish et al., Circulation 2017). This study measured heart structure and arteries, not the effect of any blood pressure drug.
The only data linking losartan to steroid exposure come from animals. In rats given nandrolone decanoate, nandrolone raised cardiac angiotensin II and AT1 receptor expression and increased heart collagen; losartan given alongside prevented the collagen increase and the left ventricular hypertrophy (Rocha et al., Am J Physiol Heart Circ Physiol 2007). This is rat data and has not been tested in people.
We found no published human trials of losartan, or any ARB, in people using anabolic steroids. Whether it lowers blood pressure, reverses heart changes or reduces cardiovascular events in this group is unknown. Related library pages: telmisartan (another ARB), nebivolol and spironolactone.
Side effects and risks
Boxed warning: fetal toxicity
Drugs that act on the renin-angiotensin system reduce fetal kidney function and increase fetal and newborn illness and death when used in the second and third trimesters. Reported harms include low amniotic fluid (oligohydramnios), underdeveloped lungs and skull, skeletal deformities, kidney failure, low blood pressure and death. The label says to stop losartan as soon as pregnancy is detected (Cozaar label).
It is not known whether losartan passes into human breast milk; it does in rats. The label advises choosing between nursing and the drug.
Common side effects
In hypertension trials (over 3,300 adults), overall adverse event rates were similar to placebo. Discontinuation for adverse events was 2.3% on losartan vs 3.7% on placebo. Events in at least 2% of patients and more often than placebo:
| Adverse event | Losartan | Placebo |
|---|---|---|
| Upper respiratory infection | 8% | 7% |
| Dizziness | 3% | 2% |
| Nasal congestion | 2% | 1% |
| Back pain | 2% | 1% |
In RENAAL, events at least 2 percentage points more common on losartan included fatigue, chest pain, low blood pressure (including on standing), diarrhea, anemia, hyperkalemia, low blood sugar, back pain, muscle weakness and urinary tract infection. The label also lists impotence among less common reactions.
Cough
Two double-blind trials enrolled patients who had developed cough on ACE inhibitors. Cough recurred at similar rates on losartan as on placebo or hydrochlorothiazide, and much more often on lisinopril (an ACE inhibitor):
| Trial | Comparator | Losartan 50 mg | Lisinopril 20 mg |
|---|---|---|---|
| Study 1 (n = 135) | Hydrochlorothiazide 25 mg: 25% | 17% | 69% |
| Study 2 (n = 97) | Placebo: 35% | 29% | 62% |
Cough, including recurrence on rechallenge, has still been reported after marketing.
Low blood pressure, kidney function and potassium
- Hypotension: more likely in people who are salt- or volume-depleted, such as those on high-dose diuretics. The label advises correcting depletion first.
- Kidney function: people whose kidney function depends on the renin-angiotensin system (narrowed renal arteries, chronic kidney disease, severe heart failure, dehydration) can develop acute kidney failure. The label advises periodic monitoring.
- Hyperkalemia (high blood potassium): the label advises periodic potassium checks and warns about other drugs that raise potassium. Patients are told not to use potassium supplements or potassium-containing salt substitutes without medical advice.
Rare and postmarketing reactions
Postmarketing reports include angioedema (swelling of the face, lips, throat or intestine, sometimes in people who had it before on ACE inhibitors), anaphylaxis, hepatitis, low platelets, low sodium, rhabdomyolysis (muscle breakdown) and vasculitis. Their frequency cannot be estimated from these reports.
Interactions
From the label (Cozaar label):
| Drug | Effect |
|---|---|
| Other drugs that raise potassium | Risk of hyperkalemia; monitor potassium |
| Lithium | Higher lithium levels and toxicity reported with ARBs; monitor lithium levels |
| NSAIDs, including COX-2 inhibitors | In older, volume-depleted or kidney-impaired patients, possible kidney deterioration including acute kidney failure (usually reversible); may blunt the blood pressure effect |
| ACE inhibitors or other ARBs (dual blockade) | More low blood pressure, fainting, hyperkalemia and kidney injury. In VA NEPHRON-D (1,448 patients), adding lisinopril to losartan gave no extra benefit but more hyperkalemia and acute kidney injury |
| Aliskiren | Contraindicated in diabetes; avoid if GFR is under 60 mL/min |
| Rifampin | Lowers exposure to losartan by 30% and to the active metabolite by 40% |
| Fluconazole (CYP2C9 inhibitor) | Raises losartan exposure ≈70% but lowers active metabolite ≈40%; clinical effect not studied |
| Erythromycin (CYP3A4 inhibitor) | Losartan exposure up 30%; metabolite unchanged |
| Hydrochlorothiazide, digoxin, warfarin, cimetidine, phenobarbital | No clinically significant interactions found |
Who should not take it
- People with hypersensitivity to any ingredient.
- People with diabetes taking aliskiren.
- Pregnancy (boxed warning).
The label has not established safety in children under 6, in children with GFR under 30 mL/min/1.73 m², or in severe liver impairment.
Quality and contamination
In 2018–2019, several US manufacturers recalled lots of generic losartan and losartan/hydrochlorothiazide because they contained nitrosamine impurities above FDA’s interim acceptable intake limits. FDA bases these limits on a daily exposure that approximates a 1 in 100,000 cancer risk after 70 years. FDA reported the first losartan recall (one Sandoz lot, for NDEA) in November 2018, followed by larger recalls for NMBA traced to active ingredient made by Hetero Labs. FDA told patients to keep taking their medicine until a pharmacist or doctor provided a replacement (FDA).
Legal status and use in sport
In the US, losartan is a prescription-only drug (Cozaar label).
Losartan and ARBs as a class are not named on the WADA 2026 Prohibited List. Hydrochlorothiazide, the diuretic in combination tablets such as Hyzaar, is prohibited at all times under class S5 (diuretics and masking agents).
Key takeaways
- The first ARB. Losartan blocks the angiotensin II type 1 receptor, mostly through an active metabolite. The parent drug lasts ≈2 hours and the metabolite 6–9 hours.
- Modest blood pressure effect alone. At 50–150 mg it lowers blood pressure by 5.5–10.5/3.5–7.5 mmHg vs placebo; 50 mg plus hydrochlorothiazide 12.5 mg lowered it by 15.5/9.2 mmHg.
- Outcome data in two settings. In LIFE it reduced stroke by 25% vs atenolol in hypertension with LVH, and in RENAAL it slowed kidney disease progression in type 2 diabetes. Neither trial showed lower overall mortality.
- Lowers uric acid. Unlike other ARBs, losartan increases uric acid excretion, though it is not approved for gout.
- Untested in steroid users. AAS use is linked to higher blood pressure and heart changes, but evidence for losartan in this setting comes only from rats.
- Key risks. Fetal toxicity (boxed warning), low blood pressure, high potassium and kidney problems, especially with other renin-angiotensin blockers, aliskiren or NSAIDs.
Sources
- Organon LLC. Cozaar (losartan potassium) tablets prescribing information (revised June 2025). DailyMed.
- US Food and Drug Administration. Drugs@FDA: Cozaar (losartan potassium), NDA 020386, approval history. FDA.
- Organon LLC. Hyzaar (losartan potassium and hydrochlorothiazide) tablets prescribing information. DailyMed.
- Dahlöf B, Devereux RB, Kjeldsen SE, et al. Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol. Lancet. 2002;359(9311):995–1003. PubMed.
- Devereux RB, Dahlöf B, Gerdts E, et al. Regression of hypertensive left ventricular hypertrophy by losartan compared with atenolol: the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial. Circulation. 2004;110(11):1456–1462. PubMed.
- Brenner BM, Cooper ME, de Zeeuw D, et al. Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy. N Engl J Med. 2001;345(12):861–869. PubMed.
- Würzner G, Gerster JC, Chiolero A, et al. Comparative effects of losartan and irbesartan on serum uric acid in hypertensive patients with hyperuricaemia and gout. J Hypertens. 2001;19(10):1855–1860. PubMed.
- Sutton Burke EM, Kelly TC, Shoales LA, Nagel AK. Angiotensin receptor blockers effect on serum uric acid: a class effect? J Pharm Pract. 2020;33(6):874–881. PubMed.
- Rasmussen JJ, Schou M, Madsen PL, et al. Increased blood pressure and aortic stiffness among abusers of anabolic androgenic steroids: potential effect of suppressed natriuretic peptides in plasma? J Hypertens. 2018;36(2):277–285. PubMed.
- Baggish AL, Weiner RB, Kanayama G, et al. Cardiovascular toxicity of illicit anabolic-androgenic steroid use. Circulation. 2017;135(21):1991–2002. PubMed.
- Rocha FL, Carmo EC, Roque FR, et al. Anabolic steroids induce cardiac renin-angiotensin system and impair the beneficial effects of aerobic training in rats. Am J Physiol Heart Circ Physiol. 2007;293(6):H3575–H3583. PubMed.
- US Food and Drug Administration. FDA updates and press announcements on angiotensin II receptor blocker (ARB) recalls (valsartan, losartan, and irbesartan). FDA.
- World Anti-Doping Agency. The 2026 Prohibited List (in effect January 1, 2026). WADA 2026 Prohibited List.