The Future of Glaucoma Medication

In glaucoma treatment, the sheer number of different compounds, variations, and brands on the market can become a little bit confusing. However, the future of glaucoma medication promises to be brighter, with safer and more effective treatments already on the horizon.

“Don’t despair. I am sure that meds are going to make glaucoma great again,” Gauti Jóhannesson MD, PhD commented in a recent presentation.

Dr Jóhannesson noted the only proven treatments for glaucoma are the IOP-lowering compounds, aiming at three main targets: the trabecular meshwork, uveoscleral outflow, and aqueous production. Their primary outcome is to correct the physiological defect involving the aqueous outflow.

One class of new compounds already on the market is the rho-kinase inhibitors, particularly netarsudil, usually in combination with prostaglandins.

Another interesting actor is nitric oxide-donating drugs. Nitric oxide (NO) is a strong vasodilator and regulator of vascular tone, which can increase outflow facility and reduce IOP by reducing trabecular meshwork cell volume, as well as relaxing the Schlemm’s canal. However, nitric oxide alone is a gaseous transmitter with an extremely short half-life, so it needs a donating drug to be released at the level of the target tissue. The first NO-donating drug approved by the FDA is latanoprostene bunod, which delivers nitric oxide to the trabecular meshwork while also providing the benefit of being a prostaglandin analogue.

“Normally, the prostaglandin analogues target the prostaglandin F (FP) receptors, but what if you also target the prostaglandin E (EP) receptors?” Dr Jóhannesson asked. The EP receptors are found in the trabecular meshwork and ciliary muscle. Targeting both FP and EP receptors causes muscle relaxation and dilatation, affecting uveoscleral as well as trabecular outflow. A novel compound with dual agonistic activity acting on both receptors is in an early stage of development, but the initial data is promising, he added.

Another long-sought option for glaucoma treatment is neuroprotection. First, citicoline, a nerve-protecting molecule studied in neurodegenerative diseases such as Alzheimer’s and Parkinson’s, has a multifactorial mechanism of action including homeostasis, mitochondrial dynamics, and neurotransmission. Several studies investigating citicoline have shown inconclusive results, urging further investigation into the compound. Hopefully, in the coming years, an upcoming large trial will shed light on the efficacy of citicoline, he said.

Glucagon-like peptide-1 (GLP-1) receptor agonists are also an interesting option. Already used in many different degenerative and metabolic diseases, GLP-1s are now being considered as a potential medication for glaucoma, with semaglutide tablets emerging as the most promising candidate, he said.

Another agent, nicotinamide, has shown a strong neuroprotective effect in animal models. The preclinical findings are robust, and two pilot studies on humans have indicated positive effects on visual function in glaucoma patients. Ongoing large randomised controlled trials will provide further evidence of nicotinamide’s efficacy as a neuroprotective drug for glaucoma.

The most exciting future possibility, Dr Jóhannesson said, is advanced therapy medicinal products (ATMPs). This umbrella term includes approaches such as gene therapy and tissue engineering.

“This is the true game changer for the future of glaucoma, a subject that is already exponentially increasing in interest year after year,” he said.

Dr Jóhannesson spoke at the 2025 ESCRS Annual Congress in Copenhagen.

Gauti Jóhannesson MD, PhD is Chief Physician at St Erik Eye Hospital in Stockholm and Associate Professor at the Department of Clinical Sciences, Ophthalmology, Umeå University, Umeå, Sweden. gauti.johannesson@umu.se