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betaxolol hcl 0.5% eye drop

Out of Stock Manufacturer AKORN INC. 17478070511
Out of Stock

Uses

Ocular Hypertension and Glaucoma

In ophthalmology, topical betaxolol hydrochloride is used to reduce elevated IOP in various conditions, including chronic open-angle glaucoma and ocular hypertension. Elevated IOP presents a major risk factor in glaucomatous field loss; the higher the level of IOP, the greater the likelihood of optic nerve damage and visual field loss. Controlled studies of betaxolol 0.25% resin-formulated suspension versus the 0.5% solution in patients with primary open-angle glaucoma or ocular hypertension have demonstrated that the resin-formulated suspension is therapeutically equivalent (i.e., in terms of the magnitude and duration of the hypotensive effect) to the solution.

Betaxolol may be used alone or in conjunction with a topical miotic (e.g., pilocarpine), topical dipivefrin, topical epinephrine, and/or a carbonic anhydrase inhibitor. When used in conjunction with these agents, betaxolol may have an additive IOP-lowering effect. Because betaxolol has little or no effect on pupil size, a miotic should be used concomitantly in patients with angle-closure glaucoma.

Like timolol, betaxolol reduces elevated IOP in patients with chronic open-angle glaucoma without producing the miosis and/or ciliary spasm that are associated with miotic agents. In addition, use of betaxolol in patients with central lenticular opacities can avoid the visual impairment caused by a constricted pupil. Usual dosages of betaxolol appear to be as effective as usual dosages of timolol in reducing IOP in patients with chronic open-angle glaucoma; however, unlike timolol, betaxolol has been associated with minimal adverse pulmonary or cardiovascular effects. Several studies involving small numbers of patients indicate that topical betaxolol may be used safely in some patients with chronic open-angle glaucoma who have coexisting reactive airway disease (e.g., asthma, chronic bronchitis, chronic obstructive pulmonary disease), including some who cannot tolerate nonselective β-blocking agents (e.g., timolol) or in whom these nonselective agents are contraindicated; however, increased airway resistance and pulmonary distress have been reported following topical application of betaxolol to the eye and the drug should be used with caution in patients with evidence of reactive airway disease on pulmonary function testing or excessive restriction of pulmonary function.(See Cautions: Systemic Effects.)

During prolonged therapy with topical betaxolol, the effect in reducing IOP is generally well maintained, but tolerance has been reported in some patients. The reduction in mean IOP has been maintained for up to 4 years after initial stabilization with the drug in some patients. Betaxolol has been used effectively and has been well tolerated in some patients with glaucoma who have undergone laser trabeculoplasty and have needed additional long-term ocular hypotensive therapy; in some aphakic patients; and in patients with glaucoma who wear hard or soft contact lenses.

For systemic uses of betaxolol hydrochloride, see 24:24.

Dosage and Administration

Administration

Betaxolol hydrochloride is applied topically to the eye as an ophthalmic solution or resin-formulated suspension. Care should be taken to avoid contamination of the solution containers. The resin-formulated suspension should be shaken well prior to use. Betaxolol hydrochloride resin-formulated ophthalmic suspension should not be administered while wearing contact lenses.

Dosage

Although USP currently states that potency of betaxolol hydrochloride preparations should be expressed both in terms of the salt and the base (''active moiety''), dosage currently is expressed in terms of the base.(See Chemistry and Stability: Chemistry.)

For the treatment of open-angle glaucoma or ocular hypertension, the therapeutic regimen must be adjusted to the individual requirements and response of the patient as determined by tonometric readings before and during therapy.

For the initial treatment of open-angle glaucoma or ocular hypertension, the usual dosage of betaxolol is 1 or 2 drops of the 0.5% solution or 0.25% resin-formulated suspension in the affected eye(s) twice daily. Because of diurnal variations, it has been suggested that IOP be measured at different times during the day to determine if an adequate hypotensive effect is maintained in patients receiving twice-daily therapy. Since IOP may not stabilize for a few weeks after initiating betaxolol therapy in some patients, IOP should also be determined after about 4 weeks of therapy; thereafter, IOP should be determined as necessary. If further reduction of IOP is required in patients receiving 1 or 2 drops of betaxolol 0.5% ophthalmic solution or betaxolol 0.25% ophthalmic resin-formulated suspension twice daily, a topical miotic, topical dipivefrin, topical epinephrine, and/or a carbonic anhydrase inhibitor may be added to the betaxolol regimen.

Cautions

Betaxolol hydrochloride ophthalmic solution and resin-formulated suspension are generally well tolerated following topical application to the eye.

Ocular Effects

The most frequent adverse effect following instillation of either topical betaxolol 0.5% solution or 0.25% resin-formulated suspension is mild ocular stinging and discomfort, which occurs in about 25% of patients receiving the solution and in about 11% of patients receiving the resin-formulated suspension; it is usually transient and well tolerated. Tearing occurs in less than 5% of patients receiving the solution or the resin-formulated suspension. Blurred vision, corneal punctate keratitis, itching and/or foreign body sensation, erythema, inflammation, photophobia, ocular pain and/or discharge, ocular dryness, and an increase in manifestations of myasthenia gravis have been reported rarely in patients receiving either the solution or resin-formulated suspension. Decreased corneal sensitivity, corneal punctate staining, edema, and anisocoria, have been reported rarely in patients receiving the solution only. Decreased visual acuity and crusting of the eyelashes have been reported rarely in patients receiving the resin-formulated suspension only. Additional adverse ocular effects associated with other formulations of betaxolol include edema and allergic reactions.

Systemic Effects

Use of betaxolol hydrochloride ophthalmic solution or resin-formulated suspension to date has been associated with a low potential for causing systemic effects. Generally, there has not been evidence of substantial adverse pulmonary or cardiovascular effects following topical application of the drug to the eye. Ophthalmic betaxolol has had little, if any, effect on blood pressure or heart rate, although slight decreases in mean systolic (about 6 mm Hg) and diastolic (about 7 mm Hg) blood pressures have been observed in some patients. However, one patient with a history of well-compensated congestive heart failure secondary to atrial fibrillation experienced bradycardia and worsening of the heart failure following initiation of therapy with betaxolol ophthalmic solution. Ophthalmic betaxolol has been used safely in some patients with chronic open-angle glaucoma and coexisting reactive airway disease (e.g., asthma, chronic bronchitis, chronic obstructive pulmonary disease); however, increased airway resistance and pulmonary distress (characterized by dyspnea, bronchospasm, thickened bronchial secretions, asthma, and respiratory failure) have been reported in patients receiving ophthalmic betaxolol, although to a lesser degree than with timolol, and betaxolol should be used with caution in patients with evidence of reactive airway disease on pulmonary function testing or excessive restriction of pulmonary function.

Other adverse effects reported rarely in patients receiving ophthalmic betaxolol include bradycardia, heart block, congestive heart failure, hives, toxic epidermal necrolysis, hair loss, glossitis, taste or smell perversion, insomnia, dizziness, vertigo, headache, lethargy, and depressive neurosis.

Precautions and Contraindications

Clinical studies to date have shown that topical betaxolol has a low potential for systemic effects; however, the usual precautions associated with systemic use of β-adrenergic blocking agents should be considered when using topical betaxolol, especially in patients with excessive restriction of pulmonary function. Severe respiratory and cardiac reactions, including death resulting from bronchospasm in patients with asthma and, rarely, death associated with cardiac failure, have been reported in patients receiving topical (ocular) β-adrenergic blocking agents. In addition, patients receiving topical betaxolol and a systemic β-adrenergic blocking agent concomitantly should be observed carefully for potential additive effects on IOP and/or systemic effects of β-adrenergic blockade.

Betaxolol hydrochloride ophthalmic preparations have been used successfully in patients with glaucoma or ocular hypertension and coexisting reactive airway disease; however, asthmatic attacks and pulmonary distress have been reported in these patients during betaxolol therapy. Although pulmonary function test results in these patients have not been adversely affected on rechallenge, the possibility of adverse pulmonary effects in patients unusually sensitive to β-adrenergic blocking agents cannot be ruled out.

Betaxolol hydrochloride ophthalmic solution and resin-formulated suspension should be used with caution in patients with a history of cardiac failure or heart block, and the drug should be discontinued at the first sign or symptom of impending cardiac failure. Ophthalmic betaxolol should also be used with caution in patients subject to spontaneous hypoglycemia or with diabetes mellitus, especially those with labile disease who are receiving insulin or oral hypoglycemic agents or those prone to hypoglycemia, since β-blocking agents may mask the signs and symptoms of hypoglycemia (e.g., tachycardia and blood pressure changes but not sweating). Patients having or suspected of developing thyrotoxicosis should be monitored closely during ophthalmic betaxolol therapy, since β-blocking agents may mask certain clinical signs and symptoms of hyperthyroidism (e.g., tachycardia) and abrupt withdrawal of these agents can precipitate thyroid storm.

β-Adrenergic blockade has been reported to potentiate muscle weakness consistent with certain myasthenic symptoms (e.g., diplopia, ptosis, and generalized weakness); β-adrenergic blocking agents should be used with caution in patients with these symptoms.

The necessity of withdrawing β-blocking agents prior to major surgery is controversial. The manufacturer states that gradual withdrawal of betaxolol prior to administration of general anesthesia should be considered, since β-blocking agents may reduce the ability of the heart to respond to reflex β-adrenergic stimuli; however, some clinicians state that the risk of this effect is probably small following ophthalmic use of betaxolol since such use is associated with minimal systemic effects.

Patients who have a history of atopy or of a severe anaphylactic reaction to a variety of allergens reportedly may be more reactive to repeated accidental, diagnostic, or therapeutic challenges with such allergens while taking β-blocking agents and may be unresponsive to usual doses of epinephrine used to treat anaphylactic reactions.

Since topical betaxolol alone has little or no effect on the size of the pupil, a miotic should be used concomitantly for the treatment of increased IOP in patients with angle-closure glaucoma. The manufacturer states that betaxolol hydrochloride ophthalmic solution and the resin-formulated suspension are contraindicated in patients with sinus bradycardia, atrioventricular block greater than first-degree, cardiogenic shock, or overt cardiac failure that is not adequately compensated (e.g., with cardiac glycosides and/or diuretics). Ophthalmic betaxolol is also contraindicated in patients with known hypersensitivity to the drug or any ingredient in the formulations.

Pediatric Precautions

Safety and efficacy of betaxolol hydrochloride ophthalmic solution or resin-formulated suspension in children younger than 18 years of age have not been established.

Mutagenicity and Carcinogenicity

In vitro and in vivo microbial and mammalian test systems using betaxolol have not revealed evidence of mutagenicity.

Lifetime studies in mice using oral betaxolol dosages of 6, 20, or 60 mg/kg daily and in rats using oral dosages of 3, 12, or 48 mg/kg daily did not reveal evidence of carcinogenic potential. Higher dosages have not been studied.

Pregnancy, Fertility, and Lactation

Pregnancy

Reproduction studies in rats using oral betaxolol dosages of 4, 40, or 400 mg/kg daily (more than 300, 3000, or 30,000 times the recommended human daily ocular dose, respectively) and in rabbits using oral dosages of 1, 4, 12, and 36 mg/kg daily have not revealed evidence of teratogenicity. There are no adequate and controlled studies to date using betaxolol hydrochloride ophthalmic solution or resin-formulated suspension in pregnant women, and the drug should be used during pregnancy only when clearly needed.

Fertility

Reproduction studies in male and female rats using oral betaxolol dosages of 4, 32, or 256 mg/kg daily did not reveal evidence of impaired fertility; however, increased postimplantation loss in rats and rabbits occurred at dosages greater than 128 and 12 mg/kg daily, respectively.

Lactation

Since betaxolol is distributed into milk, the drug should be used with caution in nursing women. Although betaxolol concentrations in milk may be up to 3 times those in maternal blood, it is unlikely that clinically important doses of the drug would be ingested by breast-fed infants during ophthalmic use of usual betaxolol dosages in the woman.

Drug Interactions

Ocular Hypotensive Agents

When used in conjunction with topical miotics, topical dipivefrin, topical epinephrine, and/or systemically administered carbonic anhydrase inhibitors, the effect of betaxolol hydrochloride in lowering IOP may be additive. This effect may be used to therapeutic advantage in the treatment of glaucoma or ocular hypertension. Although topical betaxolol used alone has little or no effect on pupil size, mydriasis resulting from concomitant therapy with topical betaxolol solution and epinephrine has been reported occasionally.

Systemic β-Adrenergic Blocking Agents

The possibility of an additive effect on IOP and/or systemic β-adrenergic blockade should be considered in patients receiving a systemic β-blocking agent and topical betaxolol concomitantly.

Catecholamine-depleting Drugs

The manufacturer states that when topical betaxolol is administered concomitantly with a catecholamine-depleting drug (e.g., reserpine), the patient should be observed closely for possible additive effects and the production of hypotension and/or bradycardia.

Other Drugs

The manufacturer states that since betaxolol is a β-adrenergic-blocking agent, caution should be exercised in patients receiving concomitant therapy with adrenergic psychotropic drugs.

Pharmacokinetics

In all studies described in the pharmacokinetics section, betaxolol was administered as the hydrochloride salt; dosages and concentrations of the drug are expressed in terms of betaxolol. Data from animal studies demonstrate that topically (i.e., to the eye) administered betaxolol 0.25% resin-formulated suspension and the 0.5% solution are bioequivalent.

Absorption

The extent of ocular and systemic absorption of betaxolol hydrochloride following topical application to the eye has not been elucidated.

Following topical application to the eye of a 0.5% solution or a 0.25% resin-formulated suspension of betaxolol, reduction in IOP is usually evident within 0.5-1 hour, reaches a maximum within about 2 hours, and persists for about 12 hours or longer. The effect of a single dose of betaxolol on IOP usually dissipates within 24 hours after instillation; however, as with other ophthalmic β-blocking agents, some reduction in IOP may persist for as long as 1 week after discontinuance of betaxolol. In patients with open-angle glaucoma, the maximal lowering of IOP occurs after approximately 1-2 weeks of twice-daily application of the drug.

Betaxolol is well absorbed following oral administration. Following oral administration of a single 20-mg dose of betaxolol in healthy adults, peak blood concentrations of about 46 ng/mL occur within approximately 3-4 hours. Following oral administration of betaxolol, β-adrenergic blocking activity (e.g., as measured by a decrease in exercise-induced heart rate) and/or reduction in systolic blood pressure begins within 3-6 hours and generally persists for 24 hours or longer.

Distribution

Distribution of betaxolol into human ocular tissues and fluids has not been characterized to date.

Following IV administration in animals, betaxolol hydrochloride is widely distributed, with highest concentrations attained in liver, kidneys, heart, and lungs; the drug is also rapidly distributed into the CNS. The apparent volume of distribution of betaxolol is reportedly about 4.9-9.8 L/kg in healthy adults.

In vitro, betaxolol is approximately 45-60% bound to plasma proteins, mainly to albumin and, to a lesser extent, to α1-acid glycoprotein (α1-AGP). Betaxolol crosses the placenta. In one study in several pregnant women, the median ratio of fetal cord to maternal plasma drug concentrations was 0.7. No accumulation of betaxolol was observed in the fetus or in amniotic fluid. Betaxolol is distributed into milk in humans.

Elimination

The metabolic fate and elimination characteristics of betaxolol hydrochloride following topical application to the eye have not been described to date.

Following oral or IV administration, the elimination half-life of betaxolol is about 15 hours (range: 11-21 hours) in healthy adults and about 20 hours (range: 10.5-29) in hypertensive patients. The half-life of betaxolol is prolonged in patients with renal or hepatic insufficiency, and in geriatric patients.

Systemically absorbed betaxolol is extensively metabolized to at least 5 metabolites. The principal metabolite is the carboxylic acid derivative formed by oxidative deamination. The drug also undergoes O-dealkylation, yielding an alcohol derivative, and subsequent oxidation to form another carboxylic acid derivative. Small amounts of hydroxybetaxolol are formed by hydroxylation at the α carbon of the benzene ring. Small amounts of a dihydroxy metabolite are also formed from hydroxybetaxolol and from the O-dealkylated derivative. Only hydroxybetaxolol has β-adrenergic blocking activity (approximately 50% that of betaxolol).

Following oral administration of a single dose of betaxolol in healthy adults, about 80-90% of the dose is excreted in urine and 1-3% in feces within 7 days; approximately 16% of the dose is excreted in urine unchanged, 35% as the deaminated carboxylic acid derivative, 24% as the carboxylic acid derivative formed by O-dealkylation and subsequent oxidation, 1% as hydroxybetaxolol, and less than 1% each as the alcohol and dihydroxy derivatives. It is not known whether the drug and metabolites excreted in feces represent unabsorbed drug or were excreted via biliary elimination. In animals, small amounts of the drug and/or its metabolites are excreted in feces via biliary elimination.

Renal clearance of betaxolol is reduced in patients with renal insufficiency; however, total body clearance of the drug in patients with renal or hepatic insufficiency is similar to that in healthy individuals.

Betaxolol is not appreciably removed by hemodialysis or peritoneal dialysis.

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