(be TAKS oh lol)
- Betaxolol HCl
- Betaxolol Hydrochloride
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Generic: 0.5% (5 mL, 10 mL, 15 mL)
Betoptic-S: 0.25% (10 mL, 15 mL)
Brand Names: U.S.
- Ophthalmic Agent, Antiglaucoma
Competitively blocks beta1-receptors, with little or no effect on beta2-receptors; with ophthalmic use, reduces intraocular pressure by reducing the production of aqueous humor
Rapidly absorbed into the systemic circulation (concentrations ~1/10 to 1/20 of oral dosing) (Vainio-Jylhä, 2001)
Urine (>80%, as unchanged drug [15%] and inactive metabolites)
Onset of Action
Within 30 minutes; Peak effect: Intraocular pressure reduction: ~2 hours
Duration of Action
Use: Labeled Indications
Treatment of chronic open-angle glaucoma or ocular hypertension
Hypersensitivity to betaxolol 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
Solution: Instill 1-2 drops into affected eye(s) twice daily.
Suspension (Betoptic® S): Instill 1 drop into affected eye(s) twice daily.
Refer to adult dosing.
Elevated intraocular pressure: Ophthalmic suspension (Betoptic® S): Instill 1 drop into affected eye(s) twice daily.
Shake suspension well before using. Tilt head back and instill in eye. Keep eye open and do not blink for 30 seconds. Apply gentle pressure to lacrimal sac for 1 minute. Wipe away excess from skin. Do not touch applicator to eye and do not contaminate tip of applicator.
Store ophthalmic suspension upright at 2°C to 25°C (36°F to 77°F). Store ophthalmic solution at 20°C to 25°C (68°F to 77°F).
Abiraterone Acetate: May increase the serum concentration of CYP1A2 Substrates. Monitor therapy
Acetylcholinesterase Inhibitors: May enhance the bradycardic effect of Beta-Blockers. Monitor therapy
Alpha-/Beta-Agonists (Direct-Acting): Beta-Blockers may enhance the vasopressor effect of Alpha-/Beta-Agonists (Direct-Acting). Epinephrine used as a local anesthetic for dental procedures will not likely cause clinically relevant problems. Some beta-adrenoceptor mediated effects of Alpha-/Beta-Agonists (Direct-Acting), including anti-anaphylactic effects of epinephrine, may be diminished by Beta-Blockers. Management: Cardioselective beta-blockers and lower doses of epinephrine may confer a more limited risk. Patients who may require acute subcutaneous epinephrine (e.g., bee sting kits) should probably avoid beta blockers. Exceptions: Dipivefrin. Consider therapy modification
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. 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. Exceptions: Apraclonidine. Consider therapy modification
Aminoquinolines (Antimalarial): May decrease the metabolism of Beta-Blockers. Monitor therapy
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. Monitor therapy
Anilidopiperidine Opioids: May enhance the bradycardic effect of Beta-Blockers. Anilidopiperidine Opioids may enhance the hypotensive effect of Beta-Blockers. Monitor therapy
Antipsychotic Agents (Phenothiazines): May enhance the hypotensive effect of Beta-Blockers. Beta-Blockers may decrease the metabolism of Antipsychotic Agents (Phenothiazines). Antipsychotic Agents (Phenothiazines) may decrease the metabolism of Beta-Blockers. Monitor therapy
Barbiturates: May decrease the serum concentration of Beta-Blockers. 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. Monitor therapy
Bupivacaine: Beta-Blockers may increase the serum concentration of Bupivacaine. Monitor therapy
Calcium Channel Blockers (Nondihydropyridine): May enhance the hypotensive effect of Beta-Blockers. Bradycardia and signs of heart failure have also been reported. Calcium Channel Blockers (Nondihydropyridine) may increase the serum concentration of Beta-Blockers. Exceptions: Bepridil. Monitor therapy
Cardiac Glycosides: Beta-Blockers may enhance the bradycardic effect of Cardiac Glycosides. Monitor therapy
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. Management: Administer these agents in combination with caution, and monitor for conduction disturbances. Avoid methacholine with any beta blocker due to the potential for additive bronchoconstriction. Monitor therapy
CYP1A2 Inhibitors (Moderate): May decrease the metabolism of CYP1A2 Substrates. Monitor therapy
CYP1A2 Inhibitors (Strong): May decrease the metabolism of CYP1A2 Substrates. Consider therapy modification
Deferasirox: May increase the serum concentration of CYP1A2 Substrates. Monitor therapy
Dipyridamole: May enhance the bradycardic effect of Beta-Blockers. Monitor therapy
Disopyramide: May enhance the bradycardic effect of Beta-Blockers. Beta-Blockers may enhance the negative inotropic effect of Disopyramide. 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. Consider therapy modification
Ergot Derivatives: Beta-Blockers may enhance the vasoconstricting effect of Ergot Derivatives. Exceptions: Nicergoline. Consider therapy modification
Fingolimod: Beta-Blockers may enhance the bradycardic effect of Fingolimod. Management: Avoid the concomitant use of fingolimod and beta-blockers if possible. If coadministration is necessary, patients should have overnight continuous ECG monitoring conducted after the first dose of fingolimod. Monitor patients for bradycardia. Consider therapy modification
Floctafenine: May enhance the adverse/toxic effect of Beta-Blockers. Avoid combination
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. Consider therapy modification
Insulin: Beta-Blockers may enhance the hypoglycemic effect of Insulin. Monitor therapy
Lidocaine (Systemic): Beta-Blockers may increase the serum concentration of Lidocaine (Systemic). Monitor therapy
Lidocaine (Topical): Beta-Blockers may increase the serum concentration of Lidocaine (Topical). Monitor therapy
Mepivacaine: Beta-Blockers may increase the serum concentration of Mepivacaine. Monitor therapy
Methacholine: Beta-Blockers may enhance the adverse/toxic effect of Methacholine. Avoid combination
Methoxyflurane: May enhance the hypotensive effect of Beta-Blockers. Monitor therapy
Midodrine: Beta-Blockers may enhance the bradycardic effect of Midodrine. Monitor therapy
NIFEdipine: May enhance the hypotensive effect of Beta-Blockers. NIFEdipine may enhance the negative inotropic effect of Beta-Blockers. Monitor therapy
Nonsteroidal Anti-Inflammatory Agents: May diminish the antihypertensive effect of Beta-Blockers. Monitor therapy
Obeticholic Acid: May increase the serum concentration of CYP1A2 Substrates. Monitor therapy
Peginterferon Alfa-2b: May increase the serum concentration of CYP1A2 Substrates. Monitor therapy
Propafenone: May increase the serum concentration of Beta-Blockers. Propafenone possesses some independent beta blocking activity. Monitor therapy
Regorafenib: May enhance the bradycardic effect of Beta-Blockers. Monitor therapy
Reserpine: May enhance the hypotensive effect of Beta-Blockers. Monitor therapy
Rifamycin Derivatives: May decrease the serum concentration of Beta-Blockers. Exceptions: Rifabutin. Monitor therapy
Rivastigmine: May enhance the bradycardic effect of Beta-Blockers. Avoid combination
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. Monitor therapy
Theophylline Derivatives: Beta-Blockers (Beta1 Selective) may diminish the bronchodilatory effect of Theophylline Derivatives. Management: Monitor for reduced theophylline efficacy during concomitant use with any beta-blocker. Beta-1 selective agents are less likely to antagonize theophylline than nonselective agents, but selectivity may be lost at higher doses. Monitor therapy
Vemurafenib: May increase the serum concentration of CYP1A2 Substrates. Management: Consider alternatives to such combinations whenever possible, particularly if the CYP1A2 substrate has a relatively narrow therapeutic index. Consider therapy modification
Frequency not always defined.
Ophthalmic: Eye discomfort (≤25%; short-term), anisocoria, blurred vision, choroidal detachment, corneal staining, crusting of eyelash, decreased corneal sensitivity, decreased visual acuity, eye discharge, eye pain, eye pruritus, eye redness, foreign body sensation of eye, hypersensitivity reaction (ophthalmic), keratitis, lacrimation, ocular edema, ophthalmic inflammation, photophobia, punctate corneal staining (with or without dendritic formations), superficial punctate keratitis, xerophthalmia
<1% (Limited to important or life-threatening): Alopecia, altered sense of smell, asthma, bradycardia, bronchospasm, cardiac failure, depression, dizziness, dysgeusia, dyspnea, exacerbation of myasthenia gravis, glossitis, heart block, headache, insomnia, lethargy, respiratory failure, thickening of bronchial secretions, toxic epidermal necrolysis, urticaria, vertigo
Concerns related to adverse events:
• Anaphylactic reactions: Use caution with history of severe anaphylaxis to allergens; patients taking beta-blockers may become more sensitive to repeated challenges. Treatment of anaphylaxis (eg, epinephrine) in patients taking beta-blockers may be ineffective or promote undesirable effects.
• Bronchospastic disease: In general, patients with bronchospastic disease should not receive beta-blockers; if used at all, should be used cautiously with close monitoring; asthma exacerbation and pulmonary distress has been reported during betaxolol use.
• Cardiovascular insufficiency: Use with caution in patients with cardiovascular insufficiency; if signs of decreased cerebral blood flow occur, consider alternative therapy.
• Diabetes: Use with caution in patients with diabetes mellitus; may potentiate hypoglycemia and/or mask signs and symptoms.
• Heart failure: Use with caution in patients with compensated heart failure (HF) and monitor for a worsening of the condition. Discontinue at the first signs of cardiac failure. In a scientific statement from the American Heart Association, betaxolol has been determined to be an agent that may exacerbate underlying myocardial dysfunction (magnitude: major) (AHA [Page 2016]).
• Myasthenia gravis: Use with caution in patients with myasthenia gravis; may worsen disease.
• Thyroid disease: May mask signs of hyperthyroidism (eg, tachycardia). If thyrotoxicosis is suspected, carefully manage and monitor; abrupt withdrawal may exacerbate symptoms of hyperthyroidism or precipitate thyroid storm.
• Vascular insufficiency: Use with caution in patients with vascular insufficiency due to potential effects on blood pressure and pulse; if signs/symptoms of reduced cerebral blood flow or Raynaud phenomenon (RP) develop during therapy, consider alternative therapy.
• Contact lens wearers: Ophthalmic solution/suspension contains benzalkonium chloride which may be absorbed by contact lenses; remove contact lens prior to administration and wait 15 minutes before reinserting.
Dosage form specific issues:
• Ophthalmic: Inadvertent contamination of multiple-dose ophthalmic solutions has caused bacterial keratitis. Should not be used alone in angle-closure glaucoma (has no effect on pupillary constriction). Choroidal detachment has been reported with aqueous suppressant therapy after filtration procedures.
• Absorption: Systemic absorption of betaxolol and adverse effects may occur with ophthalmic use, including severe respiratory and cardiac reactions.
Pregnancy Risk Factor
Animal reproduction studies have not been conducted with the ophthalmic drops. When administered orally, betaxolol crosses the placenta and can be detected in the amniotic fluid and umbilical cord blood (Morselli 1990). The amount of betaxolol available systemically following topical application of the ophthalmic drops is significantly less in comparison to oral doses (Vainio-Jylhä 2001). However, the same adverse effects observed with systemic administration may occur. If ophthalmic agents are needed during pregnancy, the minimum effective dose should be used in combination with punctual occlusion to decrease potential exposure to the fetus (Johnson 2001; Salim 2014; Samples 1988).
• Discuss specific use of drug and side effects with patient as it relates to treatment. (HCAHPS: During this hospital stay, were you given any medicine that you had not taken before? Before giving you any new medicine, how often did hospital staff tell you what the medicine was for? How often did hospital staff describe possible side effects in a way you could understand?)
• Patient may experience short-term pain. Have patient report immediately to prescriber vision changes, eye pain, severe eye irritation, shortness of breath, excessive weight gain, swelling of arms or legs, bradycardia, or muscle weakness (HCAHPS).
• Educate patient about signs of a significant reaction (eg, wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat). Note: This is not a comprehensive list of all side effects. Patient should consult prescriber for additional questions.
Intended Use and Disclaimer: Should not be printed and given to patients. This information is intended to serve as a concise initial reference for health care professionals to use when discussing medications with a patient. You must ultimately rely on your own discretion, experience, and judgment in diagnosing, treating, and advising patients.
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- Drug class: ophthalmic glaucoma agents