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

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.