Drugs & Aging

, Volume 12, Issue 3, pp 225–241 | Cite as


A Review of its Pharmacological Properties and Clinical Potential in the Management of Open-Angle Glaucoma and Ocular Hypertension
  • Julie C. AdkinsEmail author
  • Julia A. Balfour
Adis Drug Evaluation



Brimonidine is a highly selective α2- adrenoceptor agonist which reduces intraocular pressure (IOP) by reducing aqueous humour production and increasing aqueous humour outflow via the uveoscleral pathway. Brimonidine is indicated for the topical management of open- angle glaucoma or ocular hypertension.

In 3 large comparative studies in patients with open- angle glaucoma or ocular hypertension, the ocular hypotensive efficacy of brimonidine was maintained during treatment periods of up to 1 year. Mean reductions in peak (measured 2 hours after the morning dose) and trough (measured 12 hours after the evening dose) IOP were 5.6 to 5.9 and 3.3 to 3.7mm Hg, respectively, after 3 or 12 months of treatment with brimonidine 0.2% twice daily. The efficacy of brimonidine in this setting was similar to that of timolol 0.5% twice daily at peak only (−6.0mm Hg), and superior to that of betaxolol 0.25% twice daily at both peak (−3.5mm Hg) and trough (−2.7mm Hg). When added to topical β-adrenoceptor antagonist therapy, initial results showed brimonidine 0.2% twice daily to have additive ocular hypotensive efficacy similar to that of pilocarpine 2% 3 times daily. Thus, brimonidine 0.2% may be a useful adjunct in this setting.

According to combined data from 2 large comparative studies, the most frequent adverse events associated with brimonidine therapy were oral dryness (30.0% of patients), ocular hyperaemia (26.3%) and ocular burning and/or stinging (24.0%). Ocular allergic reactions including allergic blepharitis, blepharoconjunctivitis and follicular conjunctivitis occurred with an incidence of 9.6% in 1 study. In a third comparative study, the incidence of adverse events associated with brimonidine therapy was lower, with conjunctival hyperaemia (11.4%) the most frequently reported event. Changes in systolic and diastolic blood pressure and, to a lesser extent, heart rate have been reported in patients treated with therapeutic doses of topical brimonidine for up to 12 months, but these changes were not clinically significant. Unlike β-adrenoceptor antagonists, brimonidine is not contraindicated in patients with cardiopulmonary disease, although it should be used with caution in individuals with severe cardiovascular disease.

Thus, further studies are warranted to determine the efficacy of brimonidine when used in combination with other glaucoma medications and its efficacy relative to newer drugs such as dorzolamide and latanoprost. However, available data suggest that brimonidine is a promising alternative option for the lowering of IOP in the management of open- angle glaucoma and ocular hypertension, particularly in patients with cardiopulmonary disease in whom topical β -adrenoceptor antagonist therapy is contraindicated.

Pharmacodynamic Properties

Brimonidine is a highly selective α2-adrenoceptor agonist which has markedly greater affinity for α2-adrenoceptors than apraclonidine (23- to 32-fold) and clonidine (6- to 12-fold).

Brimonidine lowers intraocular pressure (IOP) by a dual mechanism of action, involving a reduction in aqueous humour production and an increase in aqueous humour outflow via the uveoscleral pathway. In patients with ocular hypertension, unilateral treatment with brimonidine 0.2% twice daily for 1 week significantly reduced aqueous humour flow (20%) and increased uveoscleral outflow (approximately 5-fold) in the treated eye. Aqueous humour flow was also reduced by 12% in the contralateral eye.

Brimonidine lowers IOP in animals and humans with normotensive or hypertensive eyes. In humans, single ocular doses of brimonidine 0.08, 0.2 and 0.5% reduced IOP for up to 12 hours, with a peak hypotensive effect occurring at 2 hours. Initial pharmacodynamic studies also suggest that, as with other α2-adrenoceptor agonists, the drug may have a neuroprotective effect; however, further research is required to confirm this.

Although topical brimonidine (50 to 500μg) produced miosis in some animal studies, clinically significant changes in pupil size did not occur in humans. Data from animal and human studies suggest that brimonidine does not significantly alter ocular blood flow.

Changes in systolic and diastolic blood pressure and, to a lesser extent, heart rate have been reported in patients and healthy volunteers treated with therapeutic doses of topical brimonidine; however, these changes were not associated with adverse clinical effects. In 3 large comparative studies, brimonidine 0.2% twice daily for up to 12 months had a minimal effect on systolic (mean change −3.52 to +0.64mm Hg) and diastolic blood pressure (−1.7 to +1.04mm Hg) and heart rate (−0.1 to −3.1 beats/min).

Pharmacokinetic Properties

Studies in rabbits suggest that the intraocular absorption of brimonidine occurs primarily via the cornea and, to a lesser extent, via the conjunctival and scierai pathways. In this species, the ocular absorption and retention of brimonidine are increased by drug binding to ocular melanin. Peak drug concentration and terminal elimination half-life values in the iris-ciliary body were, respectively, approximately 4- and 580-fold greater in pigmented than albino rabbits’ eyes after a single dose of brimonidine 0.5% (20.1 vs 5.0 mg/L and 580 vs 1 hours).

In common with other drugs applied topically to the eye, brimonidine can enter the systemic circulation; peak plasma concentrations were <0.3 μg/L after administration of a single ocular dose of brimonidine (0.08 to 0.5%) to both eyes of healthy volunteers. The plasma elimination half-life of brimonidine was approximately 2 to 5 hours.

In vitro and in vivo studies suggest that brimonidine undergoes extensive hepatic metabolism, mainly by liver aldehyde oxidase to produce oxo- and dioxo-brimonidine derivatives. In animal studies, urinary excretion was the major route of elimination, accounting for approximately 60 to 75% of an orally or intravenously administered dose.

Therapeutic Potential

In a dose-ranging study in 186 patients with glaucoma or ocular hypertension, topical administration of brimonidine 0.08, 0.2 and 0.5% twice daily produced significant reductions in mean morning IOP throughout a 1-month treatment period. After 28 days of treatment 16, 31 and 21% of patients, respectively, treated with brimonidine 0.08, 0.2 and 0.5% experienced a ≥20% reduction in IOP. A dose-frequency study showed similar efficacy with twice-daily and 3-times-daily administration of brimonidine 0.2%.

In 3 large double-masked comparative studies, the ocular hypotensive efficacy of brimonidine was maintained during treatment periods of up to 1 year. Brimonidine 0.2% administered twice daily was almost as effective as timolol 0.5% and more effective than betaxolol 0.25% both administered twice daily. After 3 or 12 months of treatment, mean reductions in peak (measured 2 hours after the morning dose) and trough (measured 12 hours after the evening dose) IOP ranged from 5.6 to 5.9 and from 3.3 to 3.7mm Hg, respectively, with brimonidine. Corresponding reductions were 6.0 and 5.9mm Hg with timolol and 3.5 and 2.7mm Hg with betaxolol. Timolol was significantly more effective than brimonidine at reducing trough IOP Clinically significant effects on cup-to-disc ratio and visual field were not demonstrated with any drug in these studies.

Initial results suggest that brimonidine 0.2% twice daily may be a useful adjunct in the management of patients with primary open-angle glaucoma or ocular hypertension inadequately controlled with topical β-adrenoceptor antagonist therapy.


According to combined tolerability data from 2 large comparative studies (n = 513), dry mouth (30.0%), ocular hyperaemia (26.3%), ocular burning and/or stinging (24.0%), headache (18.7%), blurred vision (17.5%), foreign body sensation (17.0%) and fatigue and/or drowsiness (15.8%) were the most frequent adverse events among patients treated with brimonidine 0.2% twice daily for 6 or 12 months. Other ocular adverse events including pruritus, allergy, corneal staining and erosion and conjunctival follicles occurred in <11% of patients. In these studies, brimonidine was associated with a significantly higher incidence of dry mouth (30 vs 15.5%), ocular allergy (9.6 vs 0.2%) and conjunctival follicles (7.8 vs 2.9%) than timolol (0.5% twice daily; n = 413), whereas ocular burning and stinging were significantly more common with timolol (40.7 vs 24.0%). All other reported adverse events occurred with a similar frequency in the 2 treatment groups.

In another comparative study, brimonidine 0.2% twice daily was associated with a significantly lower incidence of blurred vision than betaxolol 0.25% twice daily (0 vs 5.0%) but tended to cause more ocular allergy (4.8 vs 0%). Although ocular allergy may develop during brimonidine treatment, it appears to occur far less frequently than with the α2-adrenoceptor agonist apraclonidine.

Changes in systolic and diastolic blood pressure and heart rate have been reported in patients treated with therapeutic doses of topical brimonidine for up to 12 months, but these changes were not clinically significant.

Dosage and Administration

In the management of open-angle glaucoma and ocular hypertension, the recommended dose of brimonidine is 1 drop of a 0.2% solution instilled into the affected eye(s). The recommended dosage regimen is 3 times daily in the US and twice daily in all other countries where the drug is approved.

Brimonidine may impair the ability to drive or operate machinery. It should be used with caution in patients with severe cardiovascular disease, hepatic or renal impairment, depression, cerebral or coronary insufficiency, Raynaud’s phenomenon, orthostatic hypotension or thromboangiitis obliterans. Brimonidine should not be used in patients receiving monoamine oxidase inhibitors. Caution is also recommended in patients receiving concomitant β-adrenoceptor antagonists, antihypertensives, cardiac glycosides or tricyclic antidepressants.

Wearers of soft contact lenses should allow a period of at least 15 minutes to elapse between instillation of the drug and insertion of their lenses.


Glaucoma Adis International Limited Timolol Ocular Hypertension Betaxolol 
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Copyright information

© Adis International Limited 1998

Authors and Affiliations

  1. 1.Adis International LimitedMairangi Bay, Auckland 10New Zealand

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