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Atenolol: Drug information

Atenolol: Drug information
(For additional information see "Atenolol: Patient drug information" and see "Atenolol: Pediatric drug information")

For abbreviations, symbols, and age group definitions used in Lexicomp (show table)
ALERT: US Boxed Warning
Cessation of therapy:

Advise patients with coronary artery disease who are being treated with atenolol against abrupt discontinuation of therapy. Severe exacerbation of angina and the occurrence of myocardial infarction (MI) and ventricular arrhythmias have been reported in patients with angina following the abrupt discontinuation of therapy with beta-blockers. The last 2 complications may occur with or without preceding exacerbation of the angina pectoris. As with other beta-blockers, when discontinuation of atenolol is planned, observe the patient carefully and advise the patient to limit physical activity to a minimum. If the angina worsens or acute coronary insufficiency develops, it is recommended that atenolol be promptly reinstituted, at least temporarily. Because coronary artery disease is common and may be unrecognized, it may be prudent not to discontinue atenolol therapy abruptly, even in patients treated only for hypertension.

Brand Names: US
  • Tenormin
Brand Names: Canada
  • ACT Atenolol [DSC];
  • AG-Atenolol;
  • APO-Atenol;
  • DOM-Atenolol;
  • GMD-Atenolol;
  • JAMP-Atenolol;
  • Mar-Atenolol;
  • MINT-Atenol;
  • PMS-Atenolol;
  • RIVA-Atenolol;
  • TARO-Atenolol;
  • Tenormin;
  • TEVA-Atenolol;
  • TRIA-Atenolol
Pharmacologic Category
  • Antianginal Agent;
  • Antihypertensive;
  • Beta-Blocker, Beta-1 Selective
Dosing: Adult
Angina

Angina:

Note: For vasospastic angina, beta-blockers are not recommended; calcium channel blockers and nitrates are preferred. For nonvasospastic angina, guidelines recommend titrating dose to a resting heart rate of 55 to 60 beats per minute (ACCF/AHA [Fihn 2012]), while other experts recommend a target of 60 to 70 beats per minute (Kannam 2021).

Oral: Initial: 50 mg once daily; may increase dose at weekly intervals based on frequency and severity of anginal symptoms and tolerability; usual dosage range: 50 to 100 mg once daily.

Atrial fibrillation/flutter, maintenance of ventricular rate control

Atrial fibrillation/flutter, maintenance of ventricular rate control (off-label use):

Oral: Initial: 25 mg once daily; increase dose gradually as tolerated to achieve ventricular rate control up to 100 mg once daily (AHA/ACC/HRS [January 2014]).

Hypertension

Hypertension (alternative agent):

Note: Recommended only in patients with specific comorbidities (eg, myocardial infarction [MI], arrhythmia) (ACC/AHA [Whelton 2018]).

Oral: Initial: 25 mg once or twice daily; titrate at ≥1 week intervals as needed based on response and tolerability up to 100 mg/day in 1 or 2 divided doses (ACC/AHA [Whelton 2018]; manufacturer's labeling).

Marfan syndrome with aortic aneurysm

Marfan syndrome with aortic aneurysm (off-label use):

Note : Data for specific dosing are limited but a beta-blocker is recommended to slow aortic dilatation (ACCF/AHA/AATS [Hiratzka 2010]).

Oral: Initial: 0.5 mg/kg once daily; titrate to maintain heart rate <100 beats per minute after submaximal exercise (eg, running up and down 2 flights of stairs); doses should be rounded to the nearest 25 mg increment; usual dosage range: 25 to 100 mg/day; maximum dose: 200 mg/day (Wright 2020).

Migraine, prevention

Migraine, prevention (alternative agent) (off-label use):

Note: An adequate trial for assessment of effect is considered to be at least 2 to 3 months at a therapeutic dose (EHF [Steiner 2019]).

Oral: Initial: 25 mg once daily; titrate gradually (eg, every 1 to 2 weeks) based on response and tolerability up to 100 mg once daily (AAN/AHS [Silberstein 2012]; Edvardsson 2013; Ha 2019; Schwedt 2022; Silberstein 2015).

Myocardial infarction, early treatment and secondary prevention

Myocardial infarction, early treatment and secondary prevention:

Note: An oral beta-blocker is recommended within the first 24 hours for most patients. Patients who did not receive a beta-blocker within 24 hours of MI should be reevaluated for secondary prevention at a later date (ACCF/AHA [O'Gara 2013]).

Oral: Initial: 25 to 50 mg twice daily; some experts suggest a starting dose of 12.5 mg once daily when there is concern for adverse effects; titrate as tolerated based on heart rate and BP up to a usual maximum dose of 100 mg/day administered in 1 or 2 divided doses (ISIS-1 1986; Rosenson 2020; Simons 2020; manufacturer's labeling). Optimal duration of therapy is unknown; treat for a minimum of 3 years (ACC/AHA [Amsterdam 2014]; ACCF/AHA [O'Gara 2013]).

Supraventricular tachycardia, maintenance of ventricular rate control

Supraventricular tachycardia (eg, atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, focal atrial tachycardia, multifactorial atrial tachycardia), maintenance of ventricular rate control (off-label use):

Oral: Initial: 25 to 50 mg once daily; titrate based on response and tolerability; maximum recommended dose: 100 mg once daily (ACC/AHA/HRS [Page 2016]).

Thyrotoxicosis

Thyrotoxicosis (off-label use):

Note: For control of adrenergic symptoms until euthyroidism is established (ATA [Ross 2016]).

Oral: Initial: 25 to 50 mg once daily; titrate as needed to control symptoms (eg, tachycardia, palpitations, tremulousness) up to a maximum of 200 mg/day in 2 divided doses. Doses ≥50 mg/day can be administered in 2 divided doses if adrenergic symptoms become noticeable toward the end of the dosing interval with once daily dosing (ATA [Ross 2016]; Ross 2022).

Ventricular arrhythmia or ventricular premature beats, prevention

Ventricular arrhythmia or ventricular premature beats (symptomatic), prevention (off-label use):

Oral: Initial: 25 mg once daily; titrate dose as needed based on response and tolerability up to a maximum dose of 200 mg/day in 1 or 2 divided doses; usual dosage range: 25 to 100 mg/day (AHA/ACC/HRS [Al-Khatib 2017]; Krittayaphong 2002; Manolis 2020).

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing: Kidney Impairment: Adult

The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.

Altered kidney function (Kirch 1981; McAinsh 1980):

CrCl >30 mL/minute: No dosage adjustment necessary.

CrCl 10 to 30 mL/minute: Maximum dose: 50 mg daily.

CrCl <10 mL/minute: Maximum dose: 25 mg daily.

Hemodialysis, intermittent (thrice weekly): Moderately dialyzable (20% to 50%) (Campese 1985; Flouvat 1980; Tieu 2018):

Daily dosing: 25 to 50 mg daily; when scheduled dose falls on a dialysis day, administer post dialysis (Golightly 2013).

Three times weekly (post dialysis) dosing: Initial: 25 to 50 mg 3 times weekly administered post dialysis on dialysis days; titrate based on patient response to a maximum of 100 mg 3 times weekly administered post dialysis on dialysis days (Agarwal 2014; Kirch 1981).

Peritoneal dialysis: Not significantly dialyzed (Salahudeen 1984): Maximum: 25 mg daily (Golightly 2013).

Dosing: Hepatic Impairment: Adult

There are no dosage adjustments provided in the manufacturer’s labeling; however, atenolol undergoes minimal hepatic metabolism.

Dosing: Pediatric

(For additional information see "Atenolol: Pediatric drug information")

Note: Dosage should be individualized based on patient response.

Hemangioma, infantile

Hemangioma, infantile: Limited data available: Infants and Children <2 years: Oral: 1 mg/kg/dose once daily for 6 months; dosing based on a randomized, controlled noninferiority trial compared to propranolol (n=23 total, atenolol treatment group: n=13); atenolol was found to be as effective as propranolol; no significant adverse effects were reported in either group (Abarzua-Araya 2014).

Hypertension

Hypertension: Children and Adolescents: Oral: Initial: 0.5 to 1 mg/kg/day either once daily or divided in doses twice daily; titrate dose to effect; usual range: 0.5 to 1.5 mg/kg/day; maximum daily dose: 2 mg/kg/day not to exceed 100 mg/day (NHBPEP 2004; NLHBI 2011).

Tachycardia, supraventricular

Tachycardia, supraventricular: Limited data available: Infants, Children, and Adolescents: Oral: Usual range: 0.3 to 1 mg/kg/day either once daily or in divided doses every 12 hours (Kliegman 2011; Mehta 1996; Trippel 1989). In two separate trials, titration of the dose to >1.4 mg/kg/day did not show additional treatment successes and potentially increased the risk of adverse effects (Mehta 1996; Trippel 1989).

Thyrotoxicosis

Thyrotoxicosis: Limited data available: Children and Adolescents: Oral: 1 to 2 mg/kg once daily; may increase to twice daily if needed; maximum dose: 100 mg/dose (Bahn 2011; Kliegman 2011).

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing: Kidney Impairment: Pediatric

Altered kidney function: Infants, Children, and Adolescents: Oral:

GFR >50 mL/minute/1.73 m2: No dosage adjustment necessary (Aronoff 2007).

GFR 30 to 50 mL/minute/1.73 m2: Maximum dose: 1 mg/kg/dose every 24 hours; maximum adult daily dose: 50 mg/day (Aronoff 2007).

GFR 10 to <30 mL/minute/1.73 m2: Maximum dose: 1 mg/kg/dose every 48 hours (Aronoff 2007); based on adult information, maximum dose should not exceed 50 mg/dose (Kirch 1981).

GFR <10 mL/minute/1.73 m2: Maximum dose: 1 mg/kg/dose every 48 hours (Aronoff 2007); based on adult information, maximum dose should not exceed 25 mg/dose (Kirch 1981).

Intermittent hemodialysis: Infants, Children, and Adolescents: Oral: Moderately dialyzable (20% to 50%) (Tieu 2018): Maximum dose: 1 mg/kg/dose every 48 hours; give after hemodialysis (Aronoff 2007). Note: Usual adult dose is 25 to 50 mg/day (Golightly 2013).

Peritoneal dialysis: Infants, Children, and Adolescents: Oral: Not significantly dialyzed (Salahudeen 1984): Maximum dose: 1 mg/kg/dose every 48 hours (Aronoff 2007); based on adult information, maximum dose should not exceed 25 mg/dose (Golightly 2013).

Dosing: Hepatic Impairment: Pediatric

There are no dosage adjustments provided in the manufacturer's labeling; however, atenolol undergoes minimal hepatic metabolism.

Dosing: Older Adult

Refer to adult dosing. In the management of hypertension, consider lower initial doses and titrate to response (Aronow 2011).

Dosage Forms: US

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Tablet, Oral:

Tenormin: 25 mg, 50 mg, 100 mg

Generic: 25 mg, 50 mg, 100 mg

Generic Equivalent Available: US

Yes

Dosage Forms: Canada

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Tablet, Oral:

Tenormin: 50 mg, 100 mg [contains corn starch]

Generic: 25 mg, 50 mg, 100 mg

Administration: Adult

Oral: May be administered without regard to meals.

Administration: Pediatric

Oral: May be administered without regard to food

Use: Labeled Indications

Angina: Long-term management of patients with angina pectoris.

Hypertension: Management of hypertension. Note: Beta-blockers are not recommended as first-line therapy (ACC/AHA [Whelton 2018]).

Myocardial infarction, early treatment and secondary prevention: Management of hemodynamically stable patients with definite or suspected acute myocardial infarction to reduce cardiovascular mortality.

Use: Off-Label: Adult

Atrial fibrillation/flutter, maintenance of ventricular rate control; Marfan syndrome with aortic aneurysm; Migraine, prevention; Supraventricular tachycardia (atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, focal atrial tachycardia, multifactorial atrial tachycardia), maintenance of ventricular rate control; Thyrotoxicosis; Ventricular arrhythmias or ventricular premature beats (symptomatic), prevention

Medication Safety Issues
Sound-alike/look-alike issues:

Atenolol may be confused with albuterol, Altenol, timolol, Tylenol

Tenormin may be confused with Imuran, Norpramin, thiamine, Trovan

Adverse Reactions (Significant): Considerations
Bradyarrhythmias

Beta-blockers may cause bradycardia or first, second, or third-degree atrioventricular (AV) heart block (Ref). At maintenance dosing, second- or third-degree AV block are less likely (Ref). Beta-blocking agents with intrinsic sympathomimetic activity (eg, pindolol) may cause fewer AV conduction abnormalities than those without intrinsic sympathomimetic activity (eg, atenolol) due to their partial agonist effects (Ref). In most cases (up to 72%), AV block associated with a beta-blocker will resolve upon discontinuation; however, there are reported cases of recurrent AV block and nearly 50% of patients with more severe AV block may require a permanent pacemaker (Ref).

Mechanism: Dose-related; related to the pharmacologic action. Blockade of cardiac beta-1 adrenergic receptors results in slowed conduction and prolongation in the refractory period of the AV node. Slowing of AV conduction can lead to AV block (Ref).

Onset: Varied; one study included patients who were on beta-blocker for more than 1 month (Ref); however, other studies noted prolongation of the PR interval or AV nodal refractory period occurring anywhere from 1 dose to several days following treatment initiation (Ref).

Risk factors:

• Impaired AV node or sinus node conduction (Ref)

• Concurrent use of other agents that impair AV nodal conduction (eg, nondihydropyridine calcium channel blockers, digoxin, ivabradine, select antiarrhythmic agents) (Ref)

• Older patients (Ref)

• Hyperkalemia (Ref)

• Kidney impairment, including dialysis dependence (Ref)

Bronchospasm

Selective beta-blockers (eg, atenolol) have a lower risk of bronchospasm compared to non-cardioselective beta-blockers (Ref). While atenolol is associated with worsening bronchoconstriction and FEV1, there appears to be no change in overall day-to-day asthma control with use (Ref). Of the beta-blockers, atenolol has been associated with the least incidence of asthma attacks (Ref). Concurrent use of inhaled bronchodilators and/or corticosteroids are protective against beta-blocker–induced bronchospasm in patients with chronic obstructive pulmonary disease or asthma (Ref). Bronchospasm is reversible upon discontinuation or use of bronchodilators (Ref).

Mechanism: Dose-related; related to pharmacologic action. Beta-blocking agents can lead to airway smooth muscle constriction by antagonism of beta-2 receptors (Ref).

Onset: Rapid (Ref).

Risk factors:

• Acute use (reports suggest that single doses or acute use are more likely to cause changes in FEV1 compared to chronic use) (Ref)

CNS effects

Beta-blockers may cause reversible CNS effects such as fatigue, insomnia, vivid dreams, memory impairment, and sexual disorder (Ref). Sexual disorders may occur; however, patients who require beta-blocker therapy may have risk factors for erectile dysfunction (eg, coronary artery disease, heart failure) (Ref). In addition, there may be a psychosomatic component (Ref). Hydrophilic beta-blockers, such as atenolol, penetrate the blood-brain barrier to a lesser extent than lipophilic beta-blockers, possibly leading to a lower incidence of CNS effects; however, other studies have refuted this theory (Ref). CNS effects generally resolve with dose reduction or discontinuation (Ref).

Mechanism: Dose-related; exact mechanism is not fully understood. Proposed mechanisms include presence of beta receptors in the brain, affinity, and in some instances, inhibition of beta-blocking agents towards serotonin (5-HT) receptors in the brain (affecting mood and sleep), and beta-blocker–induced decreases in central sympathetic output (Ref). Beta-1 blockade may also impact sleep by blocking sympathetic signaling to the pineal gland, resulting in suppression of nighttime levels of melatonin (Ref). Beta-blockers may cause erectile dysfunction through decreased sympathetic nervous system output and subsequent decreases in luteinizing hormone secretion and testosterone stimulation (Ref).

Onset: Intermediate; CNS effects often occur within the first few weeks of treatment (Ref).

Risk factors:

• Older patients (Ref)

• Higher starting doses (Ref)

Potentiation/masking of hypoglycemia

Beta-blockers may worsen, prolong, or cause hypoglycemia (Ref). Additionally, beta-blockers may mask symptoms of hypoglycemia (tremor, irritability, palpitations), making diaphoresis the only symptom unaffected by beta-blockers (Ref). It is unclear if nonselective or selective beta-blockers are more likely to cause hypoglycemia as data are conflicting (Ref).

Mechanism: Dose-related; related to the pharmacologic action. Beta-blockers inhibit hepatic gluconeogenesis and glycogenolysis (Ref). Beta-blockers also reduce activation of the sympathetic nervous system, therefore masking hypoglycemic symptoms that are catecholamine-mediated (Ref).

Onset: Varied; data are limited for atenolol; onset is extrapolated from other beta blocking agents: Blood glucose recovery was significantly reduced following 1 dose or 1 day of therapy (Ref); in another study, episodes of severe hypoglycemia were reported over the course of 4 years (Ref).

Risk factors:

• Insulin-dependent diabetes (Ref)

• Type 2 diabetes mellitus (Ref)

• Hospitalized patients not requiring basal insulin (Ref)

Withdrawal

Beta-blocker therapy should not be withdrawn abruptly, but gradually tapered to avoid acute tachycardia, hypertension, and/or ischemia in patients with underlying cardiovascular disease (Ref). Some studies have found an increase in propensity-adjusted mortality and cardiovascular events; however, one study did not find changes in infarct size and left ventricular function when beta-blocker was abruptly withdrawn in patients with myocardial infarction (Ref). Additionally, another study assessing effects of abrupt withdrawal of atenolol in patients with severe angina did not show any catastrophic coronary events (Ref).

Mechanism: Dose dependent; related to the pharmacologic action. Beta blockade causes upregulation of beta-receptors, enhanced receptor sensitivity, and decreased sympathetic nervous system response (Ref). Abrupt withdrawal leads to a transient sympathetic hyper-response (Ref). Another proposed mechanism involves increased platelet aggregability to epinephrine and thrombin (Ref).

Onset: Rapid/varied and transient; increases in heart rate and blood pressure appear 24 hours after abrupt withdrawal, peak after 48 hours, and subside after 7 days (Ref).

Risk factors:

• Abrupt withdrawal in chronic users (Ref)

• Past medical history of coronary artery disease (including chronic stable angina) (Ref)

• Past medical history of hypertension (Ref)

Adverse Reactions

The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Incidence rates are from studies in hypertensive patients unless otherwise noted.

>10%:

Cardiovascular: Bradycardia (3%; acute myocardial infarction: 18%) (table 1), heart failure (acute myocardial infarction: 19%) (table 2), hypotension (acute myocardial infarction: 25%), supraventricular tachycardia (acute myocardial infarction: 12%), ventricular tachycardia (acute myocardial infarction: 16%)

Atenolol: Adverse Reaction: Bradycardia

Drug (Atenolol)

Conventional Therapy

Placebo

Indication

Number of Patients (Atenolol)

Number of Patients (Conventional Therapy)

Number of Patients (Placebo)

Comments

18%

10%

N/A

Acute myocardial infarction

244

233

N/A

Conventional therapy plus atenolol

3%

N/A

0%

Hypertension

164

N/A

206

N/A

Atenolol: Adverse Reaction: Heart Failure

Drug (Atenolol)

Conventional Therapy

Placebo

Indication

Number of Patients (Atenolol)

Number of Patients (Conventional Therapy)

Number of Patients (Placebo)

Comments

19%

24%

N/A

Acute myocardial infarction

244

233

N/A

Conventional therapy plus atenolol

1% to 10%:

Cardiovascular: Atrial fibrillation (acute myocardial infarction: 5%), atrial flutter (acute myocardial infarction: 2%), bundle branch block (acute myocardial infarction: 7%), heart block (acute myocardial infarction: 5%) (table 3), orthostatic hypotension (2%), pulmonary embolism (acute myocardial infarction: 1%)

Atenolol: Adverse Reaction: Heart Block

Drug (Atenolol)

Conventional Therapy

Placebo

Indication

Number of Patients (Atenolol)

Number of Patients (Conventional Therapy)

Number of Patients (Placebo)

Comments

5%

4%

N/A

Acute myocardial infarction

244

233

N/A

Conventional therapy plus atenolol

Gastrointestinal: Diarrhea (2%), nausea (4%)

Nervous system: Dizziness (1% to 4%), fatigue (≤3%) (table 4), lethargy (1%), vertigo (2%)

Atenolol: Adverse Reaction: Fatigue

Drug (Atenolol)

Conventional Therapy

Placebo

Indication

Number of Patients (Atenolol)

Number of Patients (Conventional Therapy)

Number of Patients (Placebo)

Comments

3%

N/A

1%

Hypertension

164

N/A

206

N/A

0.6%

N/A

0.5%

Hypertension

164

N/A

206

Described as "tiredness"

Respiratory: Bronchospasm (acute myocardial infarction: 1%) (table 5)

Atenolol: Adverse Reaction: Bronchospasm

Drug (Atenolol)

Conventional Therapy

Placebo

Indication

Number of Patients (Atenolol)

Number of Patients (Conventional Therapy)

Number of Patients (Placebo)

Comments

1%

0.9%

N/A

Acute myocardial infarction

244

233

N/A

Conventional therapy plus atenolol

<1%:

Cardiovascular: Cardiogenic shock

Nervous system: Drowsiness

Renal: Renal failure syndrome

Frequency not defined:

Cardiovascular: Raynaud disease (Marshall 1976)

Immunologic: Antibody development

Neuromuscular & skeletal: Lupus-like syndrome (Gouet 1986)

Postmarketing:

Cardiovascular: Sick sinus syndrome (Neto 2022)

Dermatologic: Exacerbation of psoriasis (Yilmaz 2022), psoriasiform eruption (Wakefield 1990), transient alopecia

Gastrointestinal: Xerostomia

Genitourinary: Impotence, Peyronie disease

Hematologic & oncologic: Purpuric disease, thrombocytopenia

Hepatic: Increased liver enzymes, increased serum bilirubin

Nervous system: Hallucination, headache, psychosis (Viadero 1983)

Ophthalmic: Visual disturbance

Contraindications

Hypersensitivity to atenolol or any component of the formulation; sinus bradycardia; heart block greater than first-degree (except in patients with a functioning artificial pacemaker); cardiogenic shock; uncompensated cardiac failure

Documentation of allergenic cross-reactivity for beta-blockers is limited. However, because of similarities in chemical structure and/or pharmacologic actions, the possibility of cross-sensitivity cannot be ruled out with certainty.

Canadian labeling: Additional contraindications (not in US labeling): Bradycardia (regardless of origin); cor pulmonale; hypotension; severe peripheral arterial disorders; anesthesia with agents that produce myocardial depression; Pheochromocytoma (in the absence of alpha-blockade); metabolic acidosis

Warnings/Precautions

Disease-related concerns:

• Anaphylaxis: Beta-blockers are unlikely to cause anaphylaxis; however, in susceptible patients, beta-blockers have been associated with an increase in the severity of anaphylaxis. Anaphylaxis in the presence of a beta-blocker may be severe, protracted, and resistant to conventional treatment (Lang 2008; Toogood 1987).

• Heart failure: Stabilize patients on heart failure regimen prior to initiation or titration of beta-blocker. Beta-blocker therapy should be initiated at very low doses with gradual and very careful titration. Adjustment of other medications (angiotensin-converting enzyme inhibitors and/or diuretics) may be required. Efficacy of atenolol in heart failure has not been demonstrated as with other beta-blockers.

• Myasthenia gravis: Use with caution in patients with myasthenia gravis.

• Peripheral vascular disease (PVD) and Raynaud disease: May precipitate or aggravate symptoms of arterial insufficiency in patients with PVD and Raynaud disease. Use with caution and monitor for progression of arterial obstruction.

• Pheochromocytoma (untreated): Adequate alpha-blockade is required prior to use of any beta-blocker.

• Psoriasis: Beta-blocker use has been associated with induction or exacerbation of psoriasis, but cause and effect have not been firmly established.

• Renal impairment: Use with caution in patients with renal impairment; dosage adjustment required.

• Thyroid disease: May mask signs of hyperthyroidism (eg, tachycardia). If hyperthyroidism is suspected, carefully manage and monitor; abrupt withdrawal may precipitate thyroid storm. Alterations in thyroid function tests may be observed.

• Vasospastic angina: Beta-blockers without alpha1-adrenergic receptor blocking activity should be avoided in patients with Prinzmetal variant angina since unopposed alpha1-adrenergic receptors mediate coronary vasoconstriction and can worsen anginal symptoms (Mayer 1998).

Other warnings/precautions:

• Major surgery: Chronic beta-blocker therapy should not be routinely withdrawn prior to major surgery.

Metabolism/Transport Effects

Substrate of OCT1, OCT2

Drug Interactions

Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.

Acetylcholinesterase Inhibitors: May enhance the bradycardic effect of Beta-Blockers. Risk C: Monitor therapy

Alfuzosin: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Alpha1-Blockers: Beta-Blockers may enhance the orthostatic hypotensive effect of Alpha1-Blockers. The risk associated with ophthalmic products is probably less than systemic products. Risk C: Monitor therapy

Alpha2-Agonists: May enhance the AV-blocking effect of Beta-Blockers. Sinus node dysfunction may also be enhanced. Beta-Blockers may enhance the rebound hypertensive effect of Alpha2-Agonists. This effect can occur when the Alpha2-Agonist is abruptly withdrawn. Management: Closely monitor heart rate during treatment with a beta blocker and clonidine. Withdraw beta blockers several days before clonidine withdrawal when possible, and monitor blood pressure closely. Recommendations for other alpha2-agonists are unavailable. Risk D: Consider therapy modification

Amifostine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Amifostine. Management: When used at chemotherapy doses, hold blood pressure lowering medications for 24 hours before amifostine administration. If blood pressure lowering therapy cannot be held, do not administer amifostine. Use caution with radiotherapy doses of amifostine. Risk D: Consider therapy modification

Amiodarone: May enhance the bradycardic effect of Beta-Blockers. Possibly to the point of cardiac arrest. Amiodarone may increase the serum concentration of Beta-Blockers. Risk C: Monitor therapy

Amphetamines: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy

Ampicillin: May decrease the bioavailability of Atenolol. Risk C: Monitor therapy

Antidiabetic Agents: Beta-Blockers (Beta1 Selective) may enhance the hypoglycemic effect of Antidiabetic Agents. Risk C: Monitor therapy

Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may enhance the hypotensive effect of Antipsychotic Agents (Second Generation [Atypical]). Risk C: Monitor therapy

Bacampicillin: May decrease the bioavailability of Atenolol. Risk C: Monitor therapy

Barbiturates: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Benperidol: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Beta2-Agonists: Beta-Blockers (Beta1 Selective) may diminish the bronchodilatory effect of Beta2-Agonists. Of particular concern with nonselective beta-blockers or higher doses of the beta1 selective beta-blockers. Risk C: Monitor therapy

Bradycardia-Causing Agents: May enhance the bradycardic effect of other Bradycardia-Causing Agents. Risk C: Monitor therapy

Brigatinib: May diminish the antihypertensive effect of Antihypertensive Agents. Brigatinib may enhance the bradycardic effect of Antihypertensive Agents. Risk C: Monitor therapy

Brimonidine (Topical): May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Bromperidol: May diminish the hypotensive effect of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may enhance the hypotensive effect of Bromperidol. Risk X: Avoid combination

Bupivacaine: Beta-Blockers may increase the serum concentration of Bupivacaine. Risk C: Monitor therapy

Cannabis: Beta-Blockers may enhance the adverse/toxic effect of Cannabis. Specifically, the risk of hypoglycemia may be increased. Risk C: Monitor therapy

Ceritinib: Bradycardia-Causing Agents may enhance the bradycardic effect of Ceritinib. Management: If this combination cannot be avoided, monitor patients for evidence of symptomatic bradycardia, and closely monitor blood pressure and heart rate during therapy. Risk D: Consider therapy modification

Cholinergic Agonists: Beta-Blockers may enhance the adverse/toxic effect of Cholinergic Agonists. Of particular concern are the potential for cardiac conduction abnormalities and bronchoconstriction. Risk C: Monitor therapy

Dexmethylphenidate: May diminish the therapeutic effect of Antihypertensive Agents. Risk C: Monitor therapy

Diazoxide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Dipyridamole: May enhance the bradycardic effect of Beta-Blockers. Risk C: Monitor therapy

Disopyramide: May enhance the bradycardic effect of Beta-Blockers. Beta-Blockers may enhance the negative inotropic effect of Disopyramide. Risk C: Monitor therapy

DOBUTamine: Beta-Blockers may diminish the therapeutic effect of DOBUTamine. Risk C: Monitor therapy

Dronedarone: May enhance the bradycardic effect of Beta-Blockers. Dronedarone may increase the serum concentration of Beta-Blockers. This likely applies only to those agents that are metabolized by CYP2D6. Management: Use lower initial beta-blocker doses; adequate tolerance of the combination, based on ECG findings, should be confirmed prior to any increase in beta-blocker dose. Increase monitoring for clinical response and adverse effects. Risk D: Consider therapy modification

DULoxetine: Blood Pressure Lowering Agents may enhance the hypotensive effect of DULoxetine. Risk C: Monitor therapy

EPHEDrine (Systemic): Beta-Blockers may diminish the therapeutic effect of EPHEDrine (Systemic). Risk C: Monitor therapy

EPINEPHrine (Nasal): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of EPINEPHrine (Nasal). Risk C: Monitor therapy

EPINEPHrine (Oral Inhalation): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of EPINEPHrine (Oral Inhalation). Risk C: Monitor therapy

Epinephrine (Racemic): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of Epinephrine (Racemic). Risk C: Monitor therapy

EPINEPHrine (Systemic): Beta-Blockers (Beta1 Selective) may diminish the therapeutic effect of EPINEPHrine (Systemic). Risk C: Monitor therapy

Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates): Beta-Blockers may enhance the vasoconstricting effect of Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates). Risk C: Monitor therapy

Etilefrine: May enhance the bradycardic effect of Beta-Blockers. Beta-Blockers may diminish the therapeutic effect of Etilefrine. Risk C: Monitor therapy

Etofylline: Beta-Blockers may diminish the therapeutic effect of Etofylline. Risk X: Avoid combination

Fexinidazole: Bradycardia-Causing Agents may enhance the arrhythmogenic effect of Fexinidazole. Risk X: Avoid combination

Fingolimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Fingolimod. Management: Consult with the prescriber of any bradycardia-causing agent to see if the agent could be switched to an agent that does not cause bradycardia prior to initiating fingolimod. If combined, perform continuous ECG monitoring after the first fingolimod dose. Risk D: Consider therapy modification

Flunarizine: May enhance the therapeutic effect of Antihypertensive Agents. Risk C: Monitor therapy

Glycopyrrolate (Systemic): May increase the serum concentration of Atenolol. Risk C: Monitor therapy

Grass Pollen Allergen Extract (5 Grass Extract): Beta-Blockers may enhance the adverse/toxic effect of Grass Pollen Allergen Extract (5 Grass Extract). More specifically, Beta-Blockers may inhibit the ability to effectively treat severe allergic reactions to Grass Pollen Allergen Extract (5 Grass Extract) with epinephrine. Some other effects of epinephrine may be unaffected or even enhanced (e.g., vasoconstriction) during treatment with Beta-Blockers. Management: Consider alternatives to either grass pollen allergen extract (5 grass extract) or beta-blockers in patients with indications for both agents. Canadian product labeling specifically lists this combination as contraindicated. Risk D: Consider therapy modification

Herbal Products with Blood Pressure Increasing Effects: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy

Herbal Products with Blood Pressure Lowering Effects: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Hypotension-Associated Agents: Blood Pressure Lowering Agents may enhance the hypotensive effect of Hypotension-Associated Agents. Risk C: Monitor therapy

Isoproterenol: Beta-Blockers may diminish the therapeutic effect of Isoproterenol. Risk C: Monitor therapy

Ivabradine: Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine. Risk C: Monitor therapy

Lacosamide: Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. Risk C: Monitor therapy

Levodopa-Containing Products: Blood Pressure Lowering Agents may enhance the hypotensive effect of Levodopa-Containing Products. Risk C: Monitor therapy

Lidocaine (Systemic): Beta-Blockers may increase the serum concentration of Lidocaine (Systemic). Risk C: Monitor therapy

Loop Diuretics: May enhance the hypotensive effect of Antihypertensive Agents. Risk C: Monitor therapy

Lormetazepam: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Mavacamten: Beta-Blockers may enhance the adverse/toxic effect of Mavacamten. Specifically, negative inotropic effects may be increased. Risk C: Monitor therapy

Mepivacaine: Beta-Blockers may increase the serum concentration of Mepivacaine. Risk C: Monitor therapy

Methacholine: Beta-Blockers may enhance the adverse/toxic effect of Methacholine. Risk C: Monitor therapy

Methoxyflurane: May enhance the hypotensive effect of Beta-Blockers. Risk C: Monitor therapy

Methylphenidate: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy

Midodrine: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy

Mivacurium: Beta-Blockers may enhance the therapeutic effect of Mivacurium. Risk C: Monitor therapy

Molsidomine: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Naftopidil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Nicergoline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Nicorandil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

NIFEdipine: May enhance the hypotensive effect of Beta-Blockers. NIFEdipine may enhance the negative inotropic effect of Beta-Blockers. Risk C: Monitor therapy

Nitroprusside: Blood Pressure Lowering Agents may enhance the hypotensive effect of Nitroprusside. Risk C: Monitor therapy

Nonsteroidal Anti-Inflammatory Agents: May diminish the antihypertensive effect of Beta-Blockers. Risk C: Monitor therapy

Nonsteroidal Anti-Inflammatory Agents (Topical): May diminish the therapeutic effect of Beta-Blockers. Risk C: Monitor therapy

Obinutuzumab: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Management: Consider temporarily withholding blood pressure lowering medications beginning 12 hours prior to obinutuzumab infusion and continuing until 1 hour after the end of the infusion. Risk D: Consider therapy modification

Ozanimod: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy

Pentoxifylline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Pholcodine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Pholcodine. Risk C: Monitor therapy

Phosphodiesterase 5 Inhibitors: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Ponesimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Ponesimod. Management: Avoid coadministration of ponesimod with drugs that may cause bradycardia when possible. If combined, monitor heart rate closely and consider obtaining a cardiology consult. Do not initiate ponesimod in patients on beta-blockers if HR is less than 55 bpm. Risk D: Consider therapy modification

Prostacyclin Analogues: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Quinagolide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Reserpine: May enhance the hypotensive effect of Beta-Blockers. Risk C: Monitor therapy

Rivastigmine: May enhance the bradycardic effect of Beta-Blockers. Risk X: Avoid combination

Siponimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. If combined, consider obtaining a cardiology consult regarding patient monitoring. Risk D: Consider therapy modification

Succinylcholine: Beta-Blockers may enhance the neuromuscular-blocking effect of Succinylcholine. Risk C: Monitor therapy

Sulfonylureas: Beta-Blockers may enhance the hypoglycemic effect of Sulfonylureas. Cardioselective beta-blockers (eg, acebutolol, atenolol, metoprolol, and penbutolol) may be safer than nonselective beta-blockers. All beta-blockers appear to mask tachycardia as an initial symptom of hypoglycemia. Ophthalmic beta-blockers are probably associated with lower risk than systemic agents. Risk C: Monitor therapy

Tasimelteon: Beta-Blockers may diminish the therapeutic effect of Tasimelteon. Management: Consider avoiding nighttime administration of beta-blockers during tasimelteon therapy due to the potential for reduced tasimelteon efficacy. Risk D: Consider therapy modification

Theophylline Derivatives: Beta-Blockers (Beta1 Selective) may diminish the bronchodilatory effect of Theophylline Derivatives. Risk C: Monitor therapy

Tofacitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Risk C: Monitor therapy

White Birch Allergen Extract: Beta-Blockers may enhance the adverse/toxic effect of White Birch Allergen Extract. Specifically, beta-blockers may reduce the effectiveness of beta-agonists that may be required to treat systemic reactions to white birch allergen extract. Risk X: Avoid combination

Food Interactions

Atenolol serum concentrations may be decreased if taken with food. Management: Administer without regard to meals.

Pregnancy Considerations

Atenolol crosses the placenta and is found in cord blood.

Maternal use of atenolol may cause harm to the fetus. Adverse events, such as bradycardia, hypoglycemia and reduced birth weight, have been observed following in utero exposure to atenolol. If maternal use of a beta-blocker is needed, fetal growth should be monitored during pregnancy and the newborn should be monitored for 48 hours after delivery for bradycardia, hypoglycemia, and respiratory depression (ESC [Regitz-Zagrosek 2018]).

Chronic maternal hypertension is also associated with adverse events in the fetus/infant. Chronic maternal hypertension may increase the risk of birth defects, low birth weight, premature delivery, stillbirth, and neonatal death. Actual fetal/neonatal risks may be related to duration and severity of maternal hypertension. Untreated chronic hypertension may also increase the risks of adverse maternal outcomes, including gestational diabetes, preeclampsia, delivery complications, stroke, and myocardial infarction (ACOG 203 2019).

The maternal pharmacokinetic parameters of atenolol during the second and third trimesters are within the ranges reported in nonpregnant patients (Hebert 2005). When treatment of chronic hypertension in pregnancy is indicated, atenolol is not recommended due to adverse fetal/neonatal events (ACOG 203 2019; ESC [Regitz-Zagrosek 2018]; Magee 2014). If atenolol is used in patients with preexisting hypertension, it should be discontinued as soon as pregnancy is diagnosed (Magee 2014). Atenolol is also not recommended for the treatment of atrial fibrillation or supraventricular tachycardia during pregnancy; consult current guidelines for specific recommendations (ESC [Regitz-Zagrosek 2018]).

Breastfeeding Considerations

Atenolol is present in breast milk.

Bradycardia has been observed in some breastfeeding infants and neonates may also be at risk for hypoglycemia. Adverse events may be more likely in premature infants or infants with impaired renal function.

Atenolol can be detected in the plasma of breastfeeding infants not previously exposed during pregnancy (Lwin 2018). Per the manufacturer, the milk/plasma ratio of atenolol is 1.5 to 6.8; however, larger ranges have been reported and ratios have been shown to vary within the same patient (Holt 1982; Lwin 2018). Beta-blockers with higher M/P ratios, such as atenolol, should be avoided while breastfeeding (Beardmore 2002). The relative infant dose (RID) of atenolol has also been calculated by authors of various studies, providing a large variability in ranges (~3% to ~35%) which may also reflect postpartum age and maternal dose (Atkinson 1988; Eyal 2010; Lwin 2018). In general, breastfeeding is considered acceptable when the RID of a medication is <10%; when the RID is >25% breastfeeding should generally be avoided (Anderson 2016; Ito 2000).

The manufacturer recommends that caution be exercised when administering atenolol to breastfeeding women. Use of a beta-blocker other than atenolol may be preferred in a breastfeeding female (Anderson 2017; Ito 2000).

Monitoring Parameters

Signs of bronchospasm (in patients with preexisting bronchospastic disease).

Acute cardiac treatment: Monitor ECG and BP.

Hypertension: BP, heart rate, serum glucose regularly (in patients with diabetes).

The 2017 Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults (ACC/AHA [Whelton 2018]):

Confirmed hypertension and known CVD or 10-year ASCVD risk ≥10%: Target blood pressure <130/80 mm Hg is recommended.

Confirmed hypertension without markers of increased ASCVD risk: Target blood pressure <130/80 mm Hg may be reasonable.

Mechanism of Action

Competitively blocks response to beta-adrenergic stimulation, selectively blocks beta1-receptors with little or no effect on beta2-receptors except at high doses

Pharmacokinetics

Onset of action: Beta-blocking effect: Onset: Oral: ≤1 hour; Peak effect: Oral: 2 to 4 hours

Duration: Normal renal function: Beta-blocking effect: 12 to 24 hours; Antihypertensive effect: Oral: 24 hours

Absorption: Oral: Rapid, incomplete (~50%)

Distribution: Low lipophilicity; does not cross blood-brain barrier

Protein binding: 6% to 16%

Metabolism: Limited hepatic

Half-life elimination: Beta:

Newborns (<24 hours of age) born to mothers receiving atenolol: Mean: 16 hours; up to 35 hours (Rubin 1983)

Children and Adolescents 5 to 16 years of age: Mean: 4.6 hours; range: 3.5 to 7 hours; Patients >10 years of age may have longer half-life (>5 hours) compared to children 5 to 10 years of age (<5 hours) (Buck 1989)

Adults: Normal renal function: 6 to 7 hours, prolonged with renal impairment; End-stage renal disease (ESRD): 15 to 35 hours

Time to peak, plasma: Oral: 2 to 4 hours

Excretion: Feces (50%); urine (40% as unchanged drug)

Pharmacokinetics: Additional Considerations

Altered kidney function: Elimination is closely related to glomerular filtration rate. Significant accumulation occurs when CrCl falls below 35 mL/minute per 1.73 m2.

Older adult: Total clearance is about 50% lower than in younger subjects. Half-life is markedly longer in older adults.

Pricing: US

Tablets (Atenolol Oral)

25 mg (per each): $0.24 - $0.82

50 mg (per each): $0.79 - $0.85

100 mg (per each): $1.22 - $1.49

Tablets (Tenormin Oral)

25 mg (per each): $16.03

50 mg (per each): $16.03

100 mg (per each): $16.03

Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.

Brand Names: International
  • Ablok (BR);
  • Alonet (HK);
  • Angipress (BR);
  • Angiten (LK);
  • Antipressan (GB);
  • Apo-Atenol (HK);
  • Arandin (KR);
  • Atarox (PY);
  • Atcord (CR, DO, GT, HN, NI, PA, SV);
  • Atecard (IN);
  • Atecor (IE);
  • Atehexal (CZ, LU);
  • AteHexal (DE, NZ);
  • Atelol (BF, BJ, CI, EG, ET, GH, GM, GN, JO, KE, LR, MA, ML, MR, MU, MW, NE, NG, QA, SC, SD, SL, SN, TN, TZ, UG, ZM, ZW);
  • Atenal (KR);
  • Atenblock (FI);
  • Atendol (DE);
  • Atenex (LK);
  • Ateni (IE);
  • Atenil (CH);
  • Ateno (CY, IQ, IR, JO, KW, LB, LY, OM, SA, SY, YE);
  • Atenobene (HU, UA);
  • Atenocor (RO);
  • Atenodan (DK);
  • Atenodeks (LV);
  • Atenogamma (DE);
  • Atenol (EG, IT);
  • Atenolin (KR);
  • Atenolol Pharmavit (HU);
  • Atenolol von ct (LU);
  • Atenolol-B (HU);
  • Atenomel (HU);
  • Atestad (PH);
  • Atinol (TW);
  • Atoken (CR, DO, GT, HN, MX, NI, PA, SV);
  • Atomex (CL);
  • Atonium (LB);
  • Atormin (AE, BH, KW, QA, SA);
  • Aveten (MY);
  • Azectol (GR);
  • B-Vasc (ZA);
  • Betablok (ID);
  • Betacar (CL);
  • Betacard (BH, IN, RU);
  • Betaday (TH);
  • Betaten (QA);
  • Betatop (FR);
  • Beten (LK, MY);
  • Betenol (KR);
  • Biofilen (CR, DO, GT, HN, MX, NI, PA, SV);
  • Bloket (PY);
  • Blokium (BF, BJ, CI, CY, ES, ET, GH, GM, GN, HU, IQ, IR, JO, KE, KW, LB, LR, LY, MA, ML, MR, MU, MW, NE, NG, OM, PY, SA, SC, SD, SL, SN, SY, TN, TZ, UG, VE, YE, ZA, ZM, ZW);
  • Blotex (MX);
  • Cardioten (PH);
  • Catenol (BF, BJ, CI, ET, GH, GM, GN, KE, LR, MA, ML, MR, MU, MW, NE, NG, SC, SD, SL, SN, TH, TN, TZ, UG, ZM, ZW);
  • Colaptyn (AU);
  • Corotenol (CY, IQ, IR, JO, KW, LB, LY, OM, SA, SY, YE);
  • Durabeta (PH);
  • Enolol (TH);
  • Etnol (BD);
  • Eutensin (TH);
  • Felo-Bits (AR);
  • Hiblok (ID);
  • Hipros (ZW);
  • Hypernol (SG);
  • Hypoten (AE, CY, IQ, IR, JO, KW, LB, LY, OM, QA, SA, SY, YE);
  • Internolol (ID);
  • Lorten (BD);
  • Lotenac (ID);
  • Lotenal (KR);
  • Myocord (AR);
  • Neocardon (GR);
  • Normalol (IL);
  • Normaten (HK, MY);
  • Normiten (IL);
  • Normocard (PL);
  • Normoten (AE);
  • Nortelol (HK);
  • Noten (AU);
  • Oraday (TH);
  • Ormidol (HR, SI);
  • Paesumex (CY, IQ, IR, JO, KW, LB, LY, OM, SA, SY, YE);
  • Plenacor (BR, CO, EC);
  • Prenolol (SG, TH);
  • Prenormine (AR);
  • Pretenol (MY);
  • Prinorm (HU);
  • Procor (LK);
  • Rotelol (PH);
  • Sotacor (CL);
  • Stermin (TW);
  • Temoret (ET);
  • Tenamed (LK);
  • Tendiol (EC);
  • Tenoblock (FI);
  • Tenocard (EG);
  • Tenocor (TH);
  • Tenol (BH, EG, ET, SA);
  • Tenoloc (BD);
  • Tenolol (BF, BJ, CI, ET, GH, GM, GN, KE, LR, LU, MA, ML, MR, MU, MW, NE, NG, NZ, SC, SD, SG, SL, SN, TH, TN, TZ, UG, ZA, ZM, ZW);
  • Tenopress (CY, IQ, IR, JO, KW, LB, LY, OM, SA, SY, YE);
  • Tenoprin (FI);
  • Tenoren (BD);
  • Tenormin (AE, AT, AU, BB, BD, BE, BF, BG, BJ, BM, BS, BZ, CH, CI, CO, CR, CU, CY, CZ, DE, DO, EE, EG, ES, ET, GB, GH, GM, GN, GR, GT, GY, HK, HN, HU, ID, IE, IN, IQ, IR, IT, JM, JO, JP, KE, KR, KW, LB, LK, LR, LU, LY, MA, ML, MR, MT, MU, MW, MX, MY, NE, NG, NI, NO, OM, PA, PE, PH, PK, PT, QA, RU, SA, SC, SD, SE, SI, SK, SL, SN, SR, SV, SY, TH, TN, TR, TT, TZ, UG, UY, VE, VN, YE, ZM, ZW);
  • Tenormin ICN (HU);
  • Tenormine (FR);
  • Tenorvas (PH);
  • Tensig (AU);
  • Tensinor (TR);
  • Tensotin (AE, QA);
  • Ternolol (MY);
  • Totamol (HK);
  • Tredol (CY, IQ, IR, JO, KW, LB, LY, OM, SA, SY, YE);
  • Urosin (ET, MY, TW);
  • Vascoten (BH, MY, SG);
  • Velorin (MT, MY);
  • Vericordin (AR);
  • Wesipin (TW)


For country code abbreviations (show table)
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