• β blockers
• monotherapy
• chronic open angle glaucoma

βBlockers lower intraocular pressure (IOP) by reducing the rate of aqueous inflow.¹ Shortly after the commercial release of topical timolol maleate in 1978 it became the most widely used ocular hypotensive agent. Its potency, combined with its twice daily frequency of instillation and lack of induction of miosis or accommodative spasm, was seen as a major advantage.² Timolol was considered a revolutionary advance in the medical management of glaucoma.

In Australia, only laevobunolol later provided an alternative to timolol as a non-selective β blocker, and in 1995 betaxolol hydrochloride offered the choice of a relatively selective β₁ blocker. Betaxolol has been demonstrated to have a wider safety margin than the non-selective agents, particularly for the cardiovascular and respiratory systems.³ It is less likely than timolol to provoke bradyarrhythmias, heart block, and bronchoconstriction. It is also somewhat less effective as an ocular hypotensive agent.⁴ In the laboratory, betaxolol has been found to have calcium channel blocking effects independent of its β blocking properties,⁵ and this has led to speculation that it may be useful not only in IOP reduction, but also as an inhibitor of episodic vasoconstriction in the optic nerve head region (one of the postulated mechanisms of glaucomatous damage),⁶ and as an agent that may offer a modicum of neuroprotection by inhibiting the calcium influx that is an inherent part of apoptosis.⁷ To date, optic nerve head concentrations of topically applied betaxolol necessary to produce these additional benefits have not been demonstrated, and there has been no clear, adequately controlled, and robust clinical evidence to support these speculations.

Particularly in Europe, other β blockers, such as carteolol, have been available. Possible advantages for some of these molecules include differences in membrane stabilisation properties and partial agonist activity. In Germany, for example, …