Betaxolol, a cardioselective (beta-1-adrenergic) receptor blocking agent, does not have significant membrane-stabilizing (local anesthetic) activity and is devoid of intrinsic sympathomimetic action. Orally administered beta-adrenergic blocking agents reduce cardiac output in healthy subjects and patients with heart disease. In patients with severe impairment of myocardial function, beta-adrenergic receptor antagonists may inhibit the sympathetic stimulatory effect necessary to maintain adequate cardiac function. 

When instilled in the eye, Betaxolol has the action of reducing elevated as well as normal intraocular pressure, whether or not accompanied by glaucoma. Ophthalmic betaxolol has minimal effect on pulmonary and cardiovascular parameters. 

Ophthalmic betaxolol (one drop in each eye) was compared to timolol and placebo in a three-way crossover study challenging nine patients with reactive airway disease who were selected on the basis of having at least a 15% reduction in the forced expiratory volume in one second (FEV1) after administration of ophthalmic timolol. Betaxolol had no significant effect on pulmonary function as measured by FEV1, Forced Vital Capacity (FVC) and FEV1/VC. Additionally, the action of Isoproterenol, a beta stimulant administered at the end of the study was not inhibited by ophthalmic betaxolol. In contrast, ophthalmic timolol significantly decreased these pulmonary functions. 

No evidence of cardiovascular beta-adrenergic blockade during exercise was observed with betaxolol in a double-masked, three-way crossover study in 24 normal subjects comparing ophthalmic betaxolol, timolol and placebo for effect on blood pressure and heart rate. Mean arterial blood pressure was not affected by any treatment; however, ophthalmic timolol produced a significant decrease in the mean heart rate. 

Clinical Studies: Optic nerve head damage and visual field loss are the result of a sustained elevated intraocular pressure and poor ocular perfusion. Betaxolol has the action of reducing elevated as well as normal intraocular pressure, and the mechanism of ocular hypotensive action appears to be a reduction of aqueous production as demonstrated by tonography and aqueous fluorophotometry. The onset of action with Betaxolol Hydrochloride Ophthalmic Solution can generally be noted within 30 minutes and the maximal effect can usually be detected 2 hours after topical administration. A single dose provides a 12-hour reduction in intraocular pressure. Clinical observation of glaucoma patients treated with betaxolol ophthalmic solution for up to three years shows that the intraocular pressure lowering effect is well maintained. 

Clinical studies show that topical betaxolol ophthalmic solution reduces mean intraocular pressure 25% from baseline. In trials using 22 mmHg as a generally accepted index of intraocular pressure control, betaxolol ophthalmic solution was effective in more than 94% of the population studied, of which 73% were treated with the beta blocker alone. In controlled, double-masked studies, the magnitude and duration of the ocular hypotensive effect of ophthalmic betaxolol solution and ophthalmic timolol solution were clinically equivalent. 

Betaxolol Ophthalmic Solution has also been used successfully in glaucoma patients who have undergone a laser trabeculoplasty and have needed additional long-term ocular hypotensive therapy. 

Betaxolol Ophthalmic Solution has been well tolerated in glaucoma patients wearing hard or soft contact lenses and in aphakic patients. 

Betaxolol Ophthalmic Solution does not produce miosis or accommodative spasm which are frequently seen with miotic agents. The blurred vision and night blindness often associated with standard miotic therapy are not associated with Betaxolol Ophthalmic Solution. Thus, patients with central lenticular opacities avoid the visual impairment caused by a constricted pupil.