Prostaglandin E2 binding site distribution and subtype classification in the rabbit iris-ciliary body

Targeted Delivery of Antiglaucoma Drugs to the Supraciliary Space Using Microneedles

“…We carried out this assessment by delivering antiglaucoma drugs to the supraciliary space and measuring reduction in intraocular pressure (IOP) over time and comparing IOP to that with topical delivery of the same drugs. Both of the drugs used in this study, sulprostone and brimonidine, have sites of action in the ciliary body, [11][12][13] which suggested that supraciliary targeting should be beneficial.…”

“…[8][9][10] As with many antiglaucoma drugs, the site of therapeutic action is the ciliary body. [11][12][13] Also, the poorly targeted nature of eye drops leads to extensive systemic exposure, which causes 8% to 53% of glaucoma patients taking topical antiglaucoma drugs to experience side effects. 14, 15 Poor patient compliance and low bioavailability of glaucoma drugs create the need for a better delivery method.…”

“…12 Receptors for the prostaglandin E2 analogs (e.g., sulprostone) are found in the ciliary body and iris of the rabbit. 11 Although the mechanisms of action of prostaglandin E2 and F2a are different, 12,36 the targeting or binding sites for both drugs are in the ciliary body. 11,12 We therefore used sulprostone as a model analog with a targeting site similar to other prostaglandin F2a analogs.…”

“…11 Although the mechanisms of action of prostaglandin E2 and F2a are different, 12,36 the targeting or binding sites for both drugs are in the ciliary body. 11,12 We therefore used sulprostone as a model analog with a targeting site similar to other prostaglandin F2a analogs. 11,12 Our other drug, brimonidine, is a commonly used clinical agent for antiglaucoma therapy and is active in the rabbit eye too.…”

Studies on Prostanoid Receptors in Ocular Tissues

“…This suggests that 3H-PGE2 binding sites are highly specific. In the rabbit ciliary body, PGE2 and 11-deoxy PGE1 (IC50 of 4.7 and 5.7 nM respectively) are more potent that either 17-phenyl trinor PGE2 or sulprostone in inhibiting 3H-PGE2 binding sites (15) (Fig. 2).…”