[Skip to Content]
[Skip to Content Landing]
December 1992

Intraocular Pressure Reduction With PhXA34, a New Prostaglandin Analogue, in Patients With Ocular Hypertension

Author Affiliations

From the Departments of Ophthalmology, Mt Sinai School of Medicine (Drs Camras, Schumer, Lustgarten, Serle, and Podos) and Columbia University College of Physicians and Surgeons, New York, NY (Dr Bito), and Kabi Pharmacia Ophthalmics, Uppsala, Sweden (Mr Marsk and Dr Stjernschantz). Dr Camras is currently in the Department of Ophthalmology, University of Nebraska Medical Center, Omaha. Drs Camras and Bito are consultants for Kabi Pharmacia Ophthalmics, and Dr Podos is a consultant for Alcon Research Laboratories, Fort Worth, Tex, and Allergan Pharmaceuticals, Irvine, Calif. Mr Marsk and Dr Stjernschantz are employees of Kabi Pharmacia Ophthalmics. Dr Bito has a proprietary interest in the development of prostaglandins and their derivatives for the treatment of ocular hypertension and glaucoma through relevant patents and patent applications that were developed, in part, under research grant EY00333 from the National Eye Institute, and were assigned, according to the National Institutes of Health directives, to the Trustees of Columbia University.

Arch Ophthalmol. 1992;110(12):1733-1738. doi:10.1001/archopht.1992.01080240073034

• In a randomized, double-masked, parallel study, one drop of 0.003% (1 μg; n=9) or 0.01% (3 μg; n=10) PhXA34, a new phenyl-substituted prostaglandin F analogue (13,14-dihydro-15[R,S]-17-phenyl18,19,20-trinor-prostaglandin F-1-isopropyl ester), or its vehicle (n=10) was applied topically twice daily for 6 days to one eye in each of 29 patients with ocular hypertension. Compared with either baseline, contralateral, or vehicle control values, PhXA34 caused a significant (P<.001) dose-dependent reduction of intraocular pressure. The reduction lasted at least 12 hours after each drop and 24 to 48 hours after the last drop, with a significant (P<.0001) mean±SEM reduction of as much as 10±1 mm Hg (40%). Conjunctival hyperemia was not produced by 0.003% PhXA34, but was noted in some eyes treated with 0.01% PhXA34, and after repeated tonometry with either concentration. The prostaglandin analogue did not produce clinically obvious miosis, anterior chamber flare or cellular response, or any subjective adverse effects. PhXA34 is a potent, effective, and welltolerated ocular hypotensive agent based on our results in this small, short-term study. Its potential as a new drug for glaucoma therapy warrants further investigation in long-term, larger studies.