Betaxolol Ophthalmic Solution USP, contains Betaxolol hydrochloride, a cardioselective beta-adrenergic receptor blocking agent, in a sterile isotonic solution. Betaxolol hydrochloride is a white, crystalline powder, soluble in water, with a molecular weight of 343.90. The structural formula is presented below:
Molecular Formula: C18H29NO3•HCl
Chemical Name: (±)-1[p-[2-(Cyclopropylmethoxy)ethyl]phenoxy]-3-
(isopropylamino)-2-propanol hydrochloride.
Each mL of Betaxolol Ophthalmic Solution for ophthalmic administration contains:
Active: 5.6 mg Betaxolol hydrochloride equivalent to Betaxolol base 5 mg;
Inactives: Edetate Disodium, Sodium Chloride, Hydrochloric Acid and/or Sodium
Hydroxide may be added to adjust pH and Purified Water;
Preservative: Benzalkonium Chloride 0.01%.


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.Read More