Timolol (Ophthalmic): Dosage, Mechanism/Onset of Action, Half-Life - Medicine.com (2024)

Dosage Forms

Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product

Gel Forming Solution, Ophthalmic, as maleate [strength expressed as base]:

Timoptic-XE: 0.25% (5 mL [DSC])

Timoptic-XE: 0.25% (5 mL) [contains tromethamine]

Timoptic-XE: 0.5% (5 mL)

Generic: 0.25% (5 mL); 0.5% (5 mL)

Solution, Ophthalmic, as hemihydrate [strength expressed as base]:

Betimol: 0.25% (5 mL); 0.5% (5 mL, 10 mL, 15 mL) [contains benzalkonium chloride]

Solution, Ophthalmic, as maleate [strength expressed as base]:

Istalol: 0.5% (2.5 mL, 5 mL) [contains benzalkonium chloride]

Timoptic: 0.25% (5 mL); 0.5% (5 mL, 10 mL) [contains benzalkonium chloride]

Generic: 0.25% (5 mL, 10 mL, 15 mL); 0.5% (2.5 mL, 5 mL, 10 mL, 15 mL)

Solution, Ophthalmic, as maleate [strength expressed as base, preservative free]:

Timoptic Ocudose: 0.25% (60 ea); 0.5% (60 ea)

Pharmacology

Mechanism of Action

Blocks both beta1- and beta2-adrenergic receptors and reduces intraocular pressure by reducing aqueous humor production or possibly increases the outflow of aqueous humor

Pharmacokinetics/Pharmacodynamics

Absorption

Solution: Timolol is measurable in the serum following ophthalmic use

Onset of Action

Solution: Intraocular pressure reduction: 30 minutes; Peak effect: 1 to 2 hours

Duration of Action

Solution: 24 hours

Half-Life Elimination

4 hours

Use: Labeled Indications

Elevated intraocular pressure: Treatment of elevated intraocular pressure (IOP) in patients with ocular hypertension or open-angle glaucoma (manufacturer's labeling) or as part of a 4-drug medical management regimen in acute angle-closure glaucoma when the patient cannot be seen by an ophthalmologist for ≥1 hour (off-label use) (Pokhrel 2007; Weizer 2019).

Contraindications

Hypersensitivity to timolol or any component of the formulation; bronchial asthma or history of bronchial asthma; severe chronic obstructive pulmonary disease (COPD); sinus bradycardia; second- or third-degree atrioventricular block; overt heart failure; cardiogenic shock

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

Dosage and Administration

Dosing: Adult

Elevated intraocular pressure: Ophthalmic:

Open-angle glaucoma:

Gel-forming solution: Instill 1 drop (either 0.25% or 0.5% solution) once daily

Solution:

Istalol: Instill 1 drop (0.5% solution) once daily in the morning

All other timolol solutions: Initial: Instill 1 drop (0.25% solution) into affected eye(s) twice daily; if response is not adequate, increase to 1 drop (0.5% solution) twice daily. May decrease dose to 1 drop once daily if intraocular pressure is well controlled

Angle-closure glaucoma, acute (off-label use): Instill 1 drop (0.5%) into the affected eye as part of a 4-drug regimen; may repeat in 30 to 60 minutes if intraocular pressure remains elevated (eg, >40 mm Hg). Note: Reserve medical management for emergency situations when an assessment by an ophthalmologist will be delayed by ≥1 hour (Pokhrel 2007; Weizer 2019).

Dosing: Geriatric

Refer to adult dosing.

Dosing: Pediatric

Glaucoma: Infants, Children, and Adolescents: Use lowest effective dose; the gel formulation may be preferable due to decreased systemic absorption (Coppens 2009): Ophthalmic:

Gel-forming solution (Timolol GFS, Timoptic-XE): Instill 1 drop (either 0.25% or 0.5%) once daily into affected eye(s) (Coppens 2009; Moore 2007)

Solution: Limited data available: Initial: 0.25% solution, instill 1 drop twice daily into affected eye(s); increase to 0.5% solution if response not adequate; decrease to 1 drop once daily into affected eye(s) if controlled; maximum dose: 1 drop (0.5% solution)/dose (Hoskins 1985; Moore 2007)

Infantile hemangioma, superficial: Limited data available: Infants and Children: Topical: Gel-forming solution: Apply 1 drop of the 0.5% gel-forming solution twice daily to the site (Chakkittakandiyil 2012; Chan 2013; Chen 2013; Lee 2013; Pope 2010). The largest experience is a multicenter retrospective report describing use in over 60 patients which showed improvement in all but one patient with a mean duration of treatment of 3.4 ± 2.7 months (Chakkittakandiyil 2012). A smaller, randomized trial compared timolol 0.5% gel (n=15) to placebo (n=17) on superficial infantile lesions covering various areas of the body; initial lesion improvements were observed after 12 to 16 weeks, and significant color changes reported at week 24 (Chan 2013). A smaller (n=13) retrospective, open-label trial also showed success with two drops of 0.25% timolol gel-forming solution twice daily on periocular infantile hemangiomas (Chambers 2012). Timolol was reported as being well tolerated in the trials.

Administration

Ophthalmic: For topical ophthalmic use only. Wash hands before use; invert closed bottle and shake gel-forming solutions once before use. Remove contact lenses prior to administration; wait 15 minutes before reinserting if using products containing benzalkonium chloride. In most cases, separate administration of other ophthalmic agents by at least 5 to 10 minutes. When treating acute angle-closure glaucoma, separate administration of other ophthalmic agents by ≥1 minute (Pokhrel 2007; Weizer 2019).

Storage

Store at 15°C to 30°C (59°F to 86°F); do not freeze. Protect from light.

Timoptic in OcuDose: Store in the protective foil wrap and use within 1 month after opening foil package.

Drug Interactions

Abiraterone Acetate: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Management: Avoid concurrent use of abiraterone with CYP2D6 substrates that have a narrow therapeutic index whenever possible. When concurrent use is not avoidable, monitor patients closely for signs/symptoms of toxicity. Consider therapy modification

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

Ajmaline: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). 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. 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

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

Asunaprevir: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Consider therapy modification

Barbiturates: May decrease the serum concentration of Beta-Blockers. Monitor therapy

Beta2-Agonists: Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Beta2-Agonists. Avoid combination

Bradycardia-Causing Agents: May enhance the bradycardic effect of other Bradycardia-Causing Agents. 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

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. Exceptions are discussed in separate monographs. 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. Monitor therapy

CloBAZam: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

Cobicistat: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

CYP2D6 Inhibitors (Moderate): May decrease the metabolism of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

CYP2D6 Inhibitors (Strong): May increase the serum concentration of Timolol (Ophthalmic). Monitor therapy

Dacomitinib: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Management: Avoid concurrent use of dacomitinib with CYP2D6 subtrates that have a narrow therapeutic index. Consider therapy modification

Darunavir: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). 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

EPINEPHrine (Nasal): Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Nasal). Monitor therapy

EPINEPHrine (Oral Inhalation): Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Oral Inhalation). Monitor therapy

Epinephrine (Racemic): Beta-Blockers (Nonselective) may enhance the hypertensive effect of Epinephrine (Racemic). Monitor therapy

EPINEPHrine (Systemic): Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Systemic). Monitor therapy

Ergot Derivatives: Beta-Blockers may enhance the vasoconstricting effect of Ergot Derivatives. Exceptions: Nicergoline. Consider therapy modification

Fexinidazole [INT]: Bradycardia-Causing Agents may enhance the arrhythmogenic effect of Fexinidazole [INT]. Avoid combination

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

Imatinib: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

Insulins: Beta-Blockers may enhance the hypoglycemic effect of Insulins. Monitor therapy

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

Lacosamide: Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. 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

Lumefantrine: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). 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. Monitor therapy

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

Midodrine: May enhance the bradycardic effect of Bradycardia-Causing Agents. 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

Opioids (Anilidopiperidine): May enhance the bradycardic effect of Beta-Blockers. Opioids (Anilidopiperidine) may enhance the hypotensive effect of Beta-Blockers. Monitor therapy

Panobinostat: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

Peginterferon Alfa-2b: May decrease the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Peginterferon Alfa-2b may increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

Perhexiline: CYP2D6 Substrates (High risk with Inhibitors) may increase the serum concentration of Perhexiline. Perhexiline may increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Monitor therapy

Propafenone: May increase the serum concentration of Beta-Blockers. Propafenone possesses some independent beta blocking activity. Monitor therapy

QuiNINE: May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). 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

Ruxolitinib: May enhance the bradycardic effect of Bradycardia-Causing Agents. Management: Ruxolitinib Canadian product labeling recommends avoiding use with bradycardia-causing agents to the extent possible. Monitor therapy

Selective Serotonin Reuptake Inhibitors: May increase the serum concentration of Beta-Blockers. Exceptions: Citalopram; Escitalopram; FluvoxaMINE. Monitor therapy

Siponimod: Bradycardia-Causing Agents may enhance the bradycardic effect of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. Consider therapy modification

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

Terlipressin: May enhance the bradycardic effect of Bradycardia-Causing Agents. Monitor therapy

Theophylline Derivatives: Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Theophylline Derivatives. Monitor therapy

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

Adverse Reactions

>10%: Ophthalmic: Burning sensation of eyes, stinging of eyes

Frequency not defined:

Cardiovascular: Angina pectoris, bradycardia, cardiac arrhythmia, cardiac failure, cerebral ischemia, cerebrovascular accident, claudication, cold extremities, edema, heart block, hypertension, hypotension, palpitations, Raynaud's phenomenon

Central nervous system: Amnesia, anxiety, confusion, depression, disorientation, dizziness, drowsiness, exacerbation of myasthenia gravis, hallucination, headache, insomnia, nervousness, nightmares, paresthesia

Dermatologic: Alopecia, exacerbation of psoriasis, pemphigoid-like lesion, psoriasiform eruption, skin rash, urticaria

Endocrine & metabolic: Hypoglycemia (masked), decreased libido

Gastrointestinal: Anorexia, diarrhea, dyspepsia, nausea, xerostomia

Genitourinary: Impotence, Peyronie's disease, retroperitoneal fibrosis

Hypersensitivity: Angioedema, hypersensitivity reaction

Neuromuscular & skeletal: Systemic lupus erythematosus

Ophthalmic: Blepharitis, blepharoptosis, blurred vision, cataract, choroidal detachment (following filtration surgery), conjunctival injection, conjunctivitis, cystoid macular edema, decreased corneal sensitivity, decreased visual acuity, diplopia, eye discharge, eye pain, eye pruritus, foreign body sensation of eye, hyperemia, keratitis, lacrimation, visual disturbance (including refractive changes), xerophthalmia

Otic: Tinnitus

Respiratory: Bronchospasm, cough, dyspnea, nasal congestion, pulmonary edema, respiratory failure

Warnings/Precautions

Concerns related to adverse events:

  • Anaphylactic reactions: Use with caution in patients with history of atopy or a history of severe anaphylaxis to a variety of 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.
  • Choroidal detachment: Beta-blockade and/or other aqueous suppressive therapy have been associated with choroidal detachment following filtration procedures.

Disease-related concerns:

  • Cerebrovascular disease: Use with caution in cerebrovascular insufficiency; consider alternative therapy for patients with signs/symptoms of decreased cerebral blood flow after therapy initiation.
  • Diabetes: Use with caution in patients with diabetes mellitus (especially labile diabetes); may potentiate hypoglycemia and/or mask signs and symptoms.
  • Heart failure: Use with caution in patients with compensated heart failure and monitor for a worsening of the condition; may lead to heart failure in patients without a history of heart failure. Use is contraindicated in overt heart failure. In a scientific statement from the American Heart Association, timolol 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 or other myasthenic symptoms (eg, diplopia, ptosis, and generalized weakness).
  • Peripheral vascular disease (PVD) and Raynaud disease: Can precipitate or aggravate symptoms of arterial insufficiency in patients with PVD and Raynaud disease. Use with caution and monitor for progression of arterial obstruction.
  • Respiratory disease: In general, patients with bronchospastic disease should not receive beta-blockers; if used at all, should be used cautiously with close monitoring. Severe respiratory reactions, including fatalities due to bronchospasm in patients with asthma, have been reported with ophthalmic use. Use is contraindicated in bronchial asthma or history of bronchial asthma and severe COPD.
  • 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.

Concurrent drug therapy issues:

  • Drug-drug interactions: Potentially significant interactions may exist, requiring dose or frequency adjustment, additional monitoring, and/or selection of alternative therapy. Consult drug interactions database for more detailed information

Special populations:

  • Contact lens wearers: Some products may contain benzalkonium chloride, which may be absorbed by soft contact lenses; remove lens prior to administration and wait 15 minutes before reinserting.

Other warnings/precautions:

  • Absorption: Systemic absorption of timolol and adverse effects may occur with ophthalmic use, including respiratory and cardiovascular effects (eg, bradycardia and/or hypotension). Beta-blocker therapy should not be withdrawn abruptly in order to avoid acute tachycardia, hypertension, and/or ischemia.
  • Appropriate use: Should not be used alone in angle-closure glaucoma (has no effect on pupillary constriction). Concomitant use of 2 topical beta-blockers is not recommended. Multidose vials have been associated with development of bacterial keratitis; avoid contamination.
  • Surgery: May block systemic effects of beta agonists (eg, epinephrine, norepinephrine); notify anesthesiologist if patient is receiving ophthalmic beta blocker therapy. Patients undergoing planned major surgery should be gradually tapered off therapy (if possible) prior to procedure. If necessary during surgery, effects of beta blocker therapy may be reversed by adrenergic agonists.

Monitoring Parameters

Intraocular pressure (after ~4 weeks of therapy for chronic use; 30 to 60 minutes after acute administration for acute use [Pokhrel 2007; Weizer 2019]); monitor for systemic effect of beta-blockade with ophthalmic administration; blood pressure.

Pregnancy

Pregnancy Considerations

Decreased fetal heart rate has been observed following maternal use of ophthalmic timolol during pregnancy (Wagenvoort 1998). Timolol is absorbed systemically following ophthalmic use; additional adverse effects observed with systemic administration may occur.

If ophthalmic agents are needed to treat glaucoma in pregnancy, the minimum effective dose should be used in combination with punctal occlusion to decrease exposure to the fetus (Johnson 2001; Salim 2014; Wagenvoort 1998).

Patient Education

What is this drug used for?

  • It is used to treat glaucoma.
  • It is used to lower high eye pressure.

Frequently reported side effects of this drug

  • Burning
  • Common cold symptoms
  • Stinging

Other side effects of this drug: Talk with your doctor right away if you have any of these signs of:

  • Severe cerebrovascular disease like change in strength on one side is greater than the other, difficulty speaking or thinking, change in balance, or vision changes
  • Vision changes
  • Eye pain
  • Severe eye irritation
  • Shortness of breath
  • Excessive weight gain
  • Swelling of arms or legs
  • Severe dizziness
  • Passing out
  • Severe headache
  • Slow heartbeat
  • Muscle weakness
  • Signs of a significant reaction like 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. Talk to your doctor if you have questions.

Consumer Information Use and Disclaimer: This information should not be used to decide whether or not to take this medicine or any other medicine. Only the healthcare provider has the knowledge and training to decide which medicines are right for a specific patient. This information does not endorse any medicine as safe, effective, or approved for treating any patient or health condition. This is only a brief summary of general information about this medicine. It does NOT include all information about the possible uses, directions, warnings, precautions, interactions, adverse effects, or risks that may apply to this medicine. This information is not specific medical advice and does not replace information you receive from the healthcare provider. You must talk with the healthcare provider for complete information about the risks and benefits of using this medicine.

Source: Wolters Kluwer Health. Last updated January 20, 2020.

Timolol (Ophthalmic): Dosage, Mechanism/Onset of Action, Half-Life - Medicine.com (2024)
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