New considerations for the clinical efficacy of old and new topical glaucoma medications

Abstract

Glaucoma is the most common form of irreversible blindness in the world. Lowering intraocular pressure (IOP) remains the only clinically established method of treatment to slow the progression of glaucoma. Primary open angle glaucoma is a disease of the optic nerve head and often is associated with changes to the trabecular meshwork that cause a reduction to aqueous humour outflow and an increase in intraocular pressure. Until recently, topical IOP lowering medication has been limited to the mechanisms of action of decreasing aqueous production and/or redirecting outflow to the unconventional uveoscleral outflow pathway. Both of these mechanisms neglect to treat or act on tissue that becomes altered from glaucoma. Latanoprostene-bunod 0.024%, a nitric-oxide donating prostanoid, netarsudil 0.02%, a potent Rho-associated protein kinase (ROCK) inhibitor and norepinephrine transporter inhibitor, and a once daily dosed fixed combination medication with netarsudil 0.02% and latanoprost 0.005% have recently come on the market. This paper will discuss and review the limitations to traditional IOP lowering glaucoma medications as well as the mechanism of actions and clinical efficacy of the new glaucoma medications. It will also discuss how the new class of glaucoma medications might help to overcome some known limitations in treatment and barriers to patient adherence.

Latanoprostene Bunod 0.024% in the Treatment of Open-Angle Glaucoma and Ocular Hypertension: A Meta-Analysis

“…LBN breaks down into two active components, latanoprost and a NO-donating agent, on the ocular surface which can increase aqueous humor outflow through the uveoscleral and trabecular routes, respectively [ 18 , 19 ]. LBN has an additional NO-donating property, thus explaining why LBN reduces IOP more than latanoprost and timolol.…”

Stable Gastric Pentadecapeptide BPC 157—Possible Novel Therapy of Glaucoma and Other Ocular Conditions

“…This was to directly prevent epithelial necrosis that may arise in the stomach from the direct injurious effect of various agents’ applications, and thereby in other tissues as well [ 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 ]. Of note, in initial [ 51 , 52 , 53 , 54 , 55 ] and later [ 56 , 57 , 58 , 59 ] eye studies, these points (i.e., pleiotropic cytoprotective beneficial effects of prostaglandins in glaucoma therapy) were not combined. The medical treatment following the approved formulation of latanoprost [ 60 ] resulted in annual global sales of more than 1 billion U.S. dollars [ 34 ].…”

“…The medical treatment following the approved formulation of latanoprost [ 60 ] resulted in annual global sales of more than 1 billion U.S. dollars [ 34 ]. Naturally, these implied resolutions (lower doses) [ 54 , 55 , 56 , 57 , 58 , 59 ] of severe ocular inflammation, resulted in ocular hypertension, pupillary miosis, and breakdown of the blood–aqueous barrier by prostaglandins (high doses) [ 51 , 52 , 53 ]. In addition, conceptual pitfalls regularly appeared in anti-glaucoma therapy courses and development.…”

Ocular Distribution of Brimonidine and Brinzolamide after Topical Instillation of a 0.1% Brimonidine Tartrate and 1% Brinzolamide Fixed-Combination Ophthalmic Suspension: An Interventional Study

“…Although medical treatments consist of eye drops and oral medications, eye drops are the major medical treatment for glaucoma patients because of their efficiency and tolerance. Currently, various types of IOP-lowering antiglaucoma ophthalmic solutions are available [ 4 , 5 ]. These IOP-lowering antiglaucoma ophthalmic solutions were classified into eight categories: prostanoid receptor-related drugs [ 6 ], ß-blockers [ 7 ], carbonic anhydrase inhibitors [ 8 ], α2 adrenergic agonists [ 9 ], rho-kinase inhibitors [ 10 ], parasympathomimetic drugs [ 11 ], α1 blockers [ 12 ], and ion channel openers [ 13 , 14 ].…”