"Researchers are making progress toward understanding how some cases of glaucoma begin. A new study from the National Eye Institute reveals that myocilin—a protein linked to a significant fraction of glaucoma—is needed to insulate peri"...
Levobunolol HCl is a noncardioselective beta-adrenoceptor blocking agent, equipotent at both beta 1 and beta 2 receptors. Levobunolol HCl is greater than 60 times more potent than its dextro isomer in its beta-blocking activity, yet equipotent in its potential for direct myocardial depression. Accordingly, the levo isomer, levobunolol HCl, is used. Levobunolol HCl does not have significant local anesthetic (membrane-stabilizing) or intrinsic sympathomimetic activity.
Beta-adrenergic receptor blockade reduces cardiac output in both healthy subjects and patients with heart disease. In patients with severe impairment of myocardial function, beta-adrenergic receptor blockade may inhibit the stimulatory effect of the sympathetic nervous system necessary to maintain adequate cardiac function.
Beta-adrenergic receptor blockade in the bronchi and bronchioles results in increased airway resistance from unopposed para-sympathetic activity. Such an effect in patients with asthma or other bronchospastic conditions is potentially dangerous.
BETAGAN® (levobunolol HCl ophthalmic solution USP) has been shown to be an active agent in lowering elevated as well as normal intraocular pressure (IOP) whether or not accompanied by glaucoma. 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.
The onset of action with one drop of BETAGAN® (levobunolol) can be detected within one hour after treatment, with maximum effect seen between 2 and 6 hours.
A significant decrease in IOP can be maintained for up to 24 hours following a single dose.
In two separate, controlled studies (one three month and one up to 12 months duration) BETAGAN® (levobunolol) ophthalmic solution 0.25% b.i.d. controlled the IOP of approximately 64% and 70% of the subjects.
The overall mean decrease from baseline was 5.4 mm Hg and 5.1 mm Hg respectively. In an open-label study, BETAGAN® (levobunolol) ophthalmic solution 0.25% q.d. controlled the IOP of 72% of the subjects while achieving an overall mean decrease of 5.9 mm Hg.
In controlled clinical studies of approximately two years duration, intraocular pressure was well-controlled in approximately 80% of subjects treated with BETAGAN® (levobunolol) Ophthalmic Solution 0.5% b.i.d. The mean IOP decrease from baseline was between 6.87 mm Hg and 7.81 mm Hg. No significant effects on pupil size, tear production or corneal sensitivity were observed. BETAGAN® (levobunolol) ophthalmic solution at the concentrations tested, when applied topically, decreased heart rate and blood pressure in some patients. The IOP-lowering effect of BETAGAN® (levobunolol) was well maintained over the course of these studies.
In a three month clinical study, a single daily application of 0.5% BETAGAN® (levobunolol) ophthalmic solution controlled the IOP of 72% of subjects achieving an overall mean decrease in IOP of 7.0 mm Hg.
The primary mechanism of the ocular hypotensive action of levobunolol HCl in reducing IOP is most likely a decrease in aqueous humor production. BETAGAN® (levobunolol) reduces IOP with little or no effect on pupil size or accommodation in contrast to the miosis which cholinergic agents are known to produce. The blurred vision and night blindness often associated with miotics would not be expected and have not been reported with the use of BETAGAN® (levobunolol) . This is particularly important in cataract patients with central lens opacities who would experience decreased visual acuity with pupillary constriction.
Last reviewed on RxList: 10/20/2008
This monograph has been modified to include the generic and brand name in many instances.
Additional Betagan Information
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