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Azilsartan (Monograph)

Brand name: Edarbi
Drug class: Angiotensin II Receptor Antagonists
VA class: CV805
Chemical name: (5-methyl-2-oxo-1,3-dioxol-4-yl)methyl ester-1-[[2′-(2,5-Dihydro-5-oxo-1,2,4-oxadiazol-3-yl)[1,1′-biphenyl]-4-yl]methyl]-2-ethoxy-1H-benzimidazole-7-carboxylic acid, potassium salt
Molecular formula: C30H23KN4O8
CAS number: 863031-24-7

Medically reviewed by on Nov 23, 2023. Written by ASHP.


  • May cause fetal and neonatal morbidity and mortality if used during pregnancy. (See Fetal/Neonatal Morbidity and Mortality under Cautions.)

  • If pregnancy is detected, discontinue as soon as possible.


Angiotensin II receptor (AT1) antagonist (i.e., angiotensin II receptor blocker, ARB).

Uses for Azilsartan


Management of hypertension (alone or in combination with other classes of antihypertensive agents).

Angiotensin II receptor antagonists are recommended as one of several preferred agents for the initial management of hypertension according to current evidence-based hypertension guidelines; other preferred options include ACE inhibitors, calcium-channel blockers, and thiazide diuretics. While there may be individual differences with respect to recommendations for initial drug selection and use in specific patient populations, current evidence indicates that these antihypertensive drug classes all generally produce comparable effects on overall mortality and cardiovascular, cerebrovascular, and renal outcomes.

Individualize choice of therapy; consider patient characteristics (e.g., age, ethnicity/race, comorbidities, cardiovascular risk) as well as drug-related factors (e.g., ease of administration, availability, adverse effects, cost).

A 2017 ACC/AHA multidisciplinary hypertension guideline classifies BP in adults into 4 categories: normal, elevated, stage 1 hypertension, and stage 2 hypertension. (See Table 1.)

Whelton PK, Carey RM, Aronow WS et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018;71:e13-115.

Individuals with SBP and DBP in 2 different categories (e.g., elevated SBP and normal DBP) should be designated as being in the higher BP category (i.e., elevated BP).

Table 1. ACC/AHA BP Classification in Adults1200


SBP (mm Hg)

DBP (mm Hg)









Hypertension, Stage 1




Hypertension, Stage 2




The goal of hypertension management and prevention is to achieve and maintain optimal control of BP. However, the BP thresholds used to define hypertension, the optimum BP threshold at which to initiate antihypertensive drug therapy, and the ideal target BP values remain controversial.

The 2017 ACC/AHA hypertension guideline generally recommends a target BP goal (i.e., BPs to achieve with drug therapy and/or nonpharmacologic intervention) <130/80 mm Hg in all adults regardless of comorbidities or level of atherosclerotic cardiovascular disease (ASCVD) risk. In addition, an SBP goal of <130 mm Hg is recommended for noninstitutionalized ambulatory patients ≥65 years of age with an average SBP of ≥130 mm Hg. These BP goals are based upon clinical studies demonstrating continuing reduction of cardiovascular risk at progressively lower levels of SBP.

Previous hypertension guidelines generally have based target BP goals on age and comorbidities. Guidelines such as those issued by the JNC 8 expert panel generally have targeted a BP goal of <140/90 mm Hg regardless of cardiovascular risk and have used higher BP thresholds and target BPs in elderly patients compared with those recommended by the 2017 ACC/AHA hypertension guideline.

Some clinicians continue to support previous target BPs recommended by JNC 8 due to concerns about the lack of generalizability of data from some clinical trials (e.g., SPRINT study) used to support the current ACC/AHA hypertension guideline and potential harms (e.g., adverse drug effects, costs of therapy) versus benefits of BP lowering in patients at lower risk of cardiovascular disease.

Consider potential benefits of hypertension management and drug cost, adverse effects, and risks associated with the use of multiple antihypertensive drugs when deciding a patient’s BP treatment goal.

For decisions regarding when to initiate drug therapy (BP threshold), the 2017 ACC/AHA hypertension guideline incorporates underlying cardiovascular risk factors. ASCVD risk assessment recommended by ACC/AHA for all adults with hypertension.

ACC/AHA currently recommend initiation of antihypertensive drug therapy in addition to lifestyle/behavioral modifications at an SBP ≥140 mm Hg or DBP ≥90 mm Hg in adults who have no history of cardiovascular disease (i.e., primary prevention) and a low ASCVD risk (10-year risk <10%).

For secondary prevention in adults with known cardiovascular disease or for primary prevention in those at higher risk for ASCVD (10-year risk ≥10%), ACC/AHA recommend initiation of antihypertensive drug therapy at an average SBP ≥130 mm Hg or an average DBP ≥80 mm Hg.

Adults with hypertension and diabetes mellitus, chronic kidney disease (CKD), or age ≥65 years are assumed to be at high risk for cardiovascular disease; ACC/AHA state that such patients should have antihypertensive drug therapy initiated at a BP ≥130/80 mm Hg.

In stage 1 hypertension, experts state that it is reasonable to initiate drug therapy using the stepped-care approach in which one drug is initiated and titrated and other drugs are added sequentially to achieve the target BP. Initiation of antihypertensive therapy with 2 first-line agents from different pharmacologic classes recommended in adults with stage 2 hypertension and average BP >20/10 mm Hg above BP goal.

Black hypertensive patients generally tend to respond better to monotherapy with calcium-channel blockers or thiazide diuretics than to angiotensin II receptor antagonists. However, the combination of an ACE inhibitor or an angiotensin II receptor antagonist with a calcium-channel blocker or thiazide diuretic produces similar BP lowering in black patients as in other racial groups.

Angiotensin II receptor antagonists or ACE inhibitors may be particularly useful in hypertensive patients with diabetes mellitus or CKD; angiotensin II receptor antagonists also may be preferred, as an alternative to ACE inhibitors, in hypertensive patients with heart failure or ischemic heart disease and/or post-MI.

Diabetic Nephropathy

A recommended agent in the management of patients with diabetes mellitus and persistent albuminuria [off-label] who have modestly elevated (30–300 mg/24 hours) or higher (>300 mg/24 hours) levels of urinary albumin excretion; slows rate of progression of renal disease in such patients.

Heart Failure

Angiotensin II receptor antagonists have been used in the management of heart failure [off-label].

Because of their established benefits, ACE inhibitors have been the preferred drugs for inhibition of the renin-angiotensin-aldosterone (RAA) system in patients with heart failure and reduced left ventricular ejection fraction (LVEF); however, some evidence indicates that therapy with an ACE inhibitor (enalapril) may be less effective than angiotensin receptor-neprilysin inhibitor (ARNI) therapy (e.g., sacubitril/valsartan) in reducing cardiovascular death and heart failure-related hospitalization.

Angiotensin II receptor antagonists considered reasonable alternative therapy for those patients in whom an ACE inhibitor or ARNI is inappropriate. (See Sensitivity Reactions under Cautions.)

No additional therapeutic benefit when angiotensin II receptor antagonist used in combination with an ACE inhibitor.

ACCF, AHA, and the Heart Failure Society of America (HFSA) recommend that patients with chronic symptomatic heart failure and reduced LVEF (NYHA class II or III) who are able to tolerate an ACE inhibitor or angiotensin II receptor antagonist be switched to therapy containing an ARNI to further reduce morbidity and mortality.

Azilsartan Dosage and Administration


BP Monitoring and Treatment Goals


Oral Administration

Administer orally once daily without regard to meals.

Must be dispensed and stored in the original manufacturer’s container.


Available as azilsartan kamedoxomil (the potassium salt of azilsartan medoxomil); dosage expressed in terms of azilsartan medoxomil.



Usual dosage: Manufacturer states 80 mg once daily. Some experts state 40–80 mg once daily. Consider initial dosage of 40 mg once daily in patients receiving high dosages of diuretics.

Special Populations

Hepatic Impairment

No adjustment of initial azilsartan medoxomil dosage necessary in patients with mild to moderate hepatic impairment. Not studied in patients with severe hepatic impairment.

Renal Impairment

No adjustment of initial azilsartan medoxomil dosage necessary in patients with mild to severe renal impairment or end-stage renal disease.

Geriatric Patients

No adjustment of initial azilsartan medoxomil dosage is necessary.

Volume- and/or Salt-depleted Patients

Correct volume and/or salt depletion prior to initiation of azilsartan therapy or initiate therapy using lower initial dosage (40 mg once daily).

Cautions for Azilsartan




Fetal/Neonatal Morbidity and Mortality

Possible fetal and neonatal morbidity and mortality when drugs that act directly on the renin-angiotensin system (e.g., angiotensin II receptor antagonists, ACE inhibitors) are used during the second and third trimesters of pregnancy. Resulting oligohydramnios can be associated with fetal lung hypoplasia and skeletal deformations. ACE inhibitors also reported to increase the risk of major congenital malformations when administered during the first trimester of pregnancy. Potential neonatal effects include skull hypoplasia, anuria, hypotension, renal failure, and death.

Discontinue azilsartan as soon as possible when pregnancy is detected, unless continued use is considered life-saving. Nearly all women can be transferred successfully to alternative therapy for the remainder of their pregnancy.

Sensitivity Reactions

Angioedema, pruritus, and rash reported during postmarketing experience.

Other Warnings and Precautions


Possible symptomatic hypotension, particularly in volume- and/or salt-depleted patients (e.g., those treated with diuretics). (See Volume- and/or Salt-depleted Patients under Dosage and Administration.)

Transient hypotension is not a contraindication to additional doses; may reinstate therapy cautiously after BP is stabilized (e.g., with volume expansion).


In July 2010, FDA initiated a safety review of angiotensin II receptor antagonists after a published meta-analysis found a modest but statistically significant increase in risk of new cancer occurrence in patients receiving an angiotensin II receptor antagonist compared with control. However, subsequent studies, including a larger meta-analysis conducted by FDA, have not shown such risk. Based on currently available data, FDA has concluded that angiotensin II receptor antagonists do not increase the risk of cancer.

Renal Effects

Possible oliguria, progressive azotemia and, rarely, acute renal failure and/or death in patients with severe heart failure, renal artery stenosis, or volume depletion.

Increases in BUN and SCr possible in patients with renal artery stenosis.

Specific Populations


Category D.

Can cause fetal and neonatal morbidity and death when administered to a pregnant woman. (See Boxed Warning.)


Azilsartan is distributed into milk in rats; not known whether azilsartan is distributed into human milk. Discontinue nursing or the drug.

Pediatric Use

Neonates with history of in utero exposure to azilsartan: If oliguria or hypotension occurs, support BP and renal function; exchange transfusions or dialysis may be required. (See Fetal/Neonatal Morbidity and Mortality under Warnings/Precautions: Warnings, in Cautions.)

Safety and efficacy of azilsartan not established in pediatric patients.

Geriatric Use

Increased incidence of elevated SCr in patients ≥75 years of age. No other differences in safety or efficacy relative to younger adults, but increased sensitivity cannot be ruled out.

Hepatic Impairment

Data lacking in patients with severe hepatic impairment.

Renal Impairment

Increased incidence of abnormally high SCr in patients with moderate to severe renal impairment.

Deterioration of renal function may occur. (See Renal Effects under Cautions.)

Black Patients

BP reduction with azilsartan monotherapy decreased by about 50% in black patients compared with patients of other races. (See Hypertension under Uses.)

Common Adverse Effects

Diarrhea; less common adverse effects include hypotension/orthostatic hypotension, nausea, asthenia, fatigue, muscle spasm, dizziness, postural dizziness, cough.

Drug Interactions

Metabolized principally by CYP2C9.

Specific Drugs




ACE inhibitors

Increased risk of renal impairment, hyperkalemia, and hypotension

Generally, avoid concomitant use; monitor BP, renal function, and electrolytes if used concomitantly


Increased risk of renal impairment, hyperkalemia, and hypotension

Generally, avoid concomitant use; monitor BP, renal function, and electrolytes if used concomitantly

Concomitant use contraindicated in patients with diabetes mellitus

Avoid concomitant use in patients with GFR <60 mL/minute


Pharmacokinetic interactions unlikely

Angiotensin II receptor antagonists

Increased risk of renal impairment, hyperkalemia, and hypotension

Generally, avoid concomitant use; monitor BP, renal function, and electrolytes if used concomitantly


Pharmacokinetic interactions unlikely


Pharmacokinetic interactions unlikely

Greater reversible increases in SCr possible


Pharmacokinetic interactions unlikely

Diuretics, potassium-sparing

Possible increase in serum potassium concentrations

Avoid concomitant administration


Pharmacokinetic interactions unlikely


Pharmacokinetic interactions unlikely


Greater reversible increases in SCr possible


Pharmacokinetic interactions unlikely


Increased serum lithium concentrations and lithium toxicity reported with concomitant angiotensin II receptor antagonist therapy

Monitor serum lithium concentrations during concomitant therapy


Pharmacokinetic interactions unlikely

NSAIAs, including selective cyclooxygenase-2 (COX-2) inhibitors

Possible deterioration of renal function, including possible acute renal failure, in patients who are geriatric, volume-depleted, or have compromised renal function; effects usually reversible

Possible attenuation of azilsartan antihypertensive effect

Periodically monitor renal function


Pharmacokinetic interactions unlikely

Potassium supplements and potassium-containing salt substitutes

Possible increase in serum potassium concentrations

Avoid concomitant administration


Pharmacokinetic interactions unlikely

Azilsartan Pharmacokinetics



Azilsartan medoxomil (prodrug) is rapidly and completely hydrolyzed to azilsartan during absorption in the GI tract.

Absolute bioavailability of azilsartan is about 60%.

Peak plasma azilsartan concentration generally reached 1.5–3 hours following oral administration.

Increases in AUC are dose proportional following single or multiple doses of azilsartan medoxomil in the range of 20–320 mg.

Steady-state concentrations of azilsartan are achieved within 5 days.


Most of the antihypertensive effect of azilsartan occurs within 2 weeks.


Food does not affect bioavailability of azilsartan.

Special Populations

Modest increases in peak plasma azilsartan concentration and AUC reported in geriatric patients and in patients with mild to severe renal impairment or mild to moderate hepatic impairment; no dosage adjustment required. Not studied in patients with severe hepatic impairment.



Azilsartan crosses the placenta and is distributed in the fetus in rats.

A minimal amount of azilsartan-associated radioactivity crosses the blood-brain barrier in rats.

Azilsartan is distributed into milk in rats; not known whether azilsartan is distributed into human milk.

Plasma Protein Binding




Azilsartan medoxomil undergoes rapid and complete hydrolysis to azilsartan.

Azilsartan is metabolized primarily by CYP2C9.

Azilsartan is metabolized to 2 primary metabolites, both of which are inactive; metabolite M-II (the major metabolite) is formed by O-dealkylation, and metabolite M-I (the minor metabolite) is formed by decarboxylation.

Systemic exposures to M-II and M-I are approximately 50% and <1%, respectively, that of azilsartan.

Elimination Route

Radiolabeled azilsartan medoxomil is eliminated mainly in feces (55%) and urine (42%, with 15% as azilsartan).


Approximately 11 hours.





25ºC (may be exposed to 15–30ºC). Dispense and store in tightly closed original container; protect from light and moisture.


Advice to Patients


Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

Azilsartan Kamedoxomil


Dosage Forms


Brand Names




40 mg (of azilsartan medoxomil)



80 mg (of azilsartan medoxomil)



AHFS DI Essentials™. © Copyright 2024, Selected Revisions December 3, 2018. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

† Off-label: Use is not currently included in the labeling approved by the US Food and Drug Administration.

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