Digital Insert | Editorially independent content supported by advertising from Santen
Glaucoma Pipeline
A View Into Ongoing Innovation
Digital Insert | Editorially independent content supported by advertising from Santen
A View Into Ongoing Innovation
Iqbal Ike K. Ahmed, MD, FRCSC
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Drainage to Ocular Surface
AQUEOUS OUTFLOW AT MESHWORK
Schlemm Canal
Aqueous Production
Supraciliary Drainage
Subconjunctival
Filtering Bleb Procedures
John R. Samples, MD
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Uveoscleral Outflow
Aqueous Outflow: The Canal and Beyond
Aqueous Production
Aqueous Outflow at Meshwork
Commercially Available in US; Predominant Mode(s) of Action
Pipeline Candidate
Prostaglandins
Nitric Oxide-Donating Compounds
Rho Kinase Inhibitors
Omidenepag Isopropyl (DE-117, Santen)
NCX 470 (Nicox)
Muscarinic Agonists (Miotics)
Beta-Blockers
Alpha-Agonists
Carbonic Anhydrase Inhibitors
ATP Potassium Channel Modulators
Autotaxin-Lysophosphatidic Acid
AKB-9778 (Aerpio) (Presumed mode of action)
(Advantages ↑compliance, adherence ↓preservative, copay)
Rocklatan
Cosopt / Cosopt PF (Dorzolomide HCI & Timolol Maleate; Akorn)
Combigan (Brimonidine Tartrate & Timolol Maleate; Allergan)
Simbrinza (Brinzolamide & Brimonidine tartrate; Novartis)
* The quality of the literature supporting neuroprotective benefits of the following is widely variable; these agents and molecules may or may not have neuroregenerative properties, which would be associated with beneficial effect on retinal ganglion cells
† Pressure-lowering drug classes with alleged neuroprotection effect; no human studies have been conducted to date
‡ Nutrient-overlap
¶ Indirect neuroprotective mechanism
R. Rand Allingham MD, Sayoko E. Moroi MD, PhD, M. Bruce Shields MD, Karim F. Damji MD, MBA. Shields’ Textbook of Glaucoma. Wolters Kluwer Health, Inc. 2020.
The concept of disease modification has garnered a lot of attention in glaucoma research. The future of pharmaceutical management may well belong to small and large molecules and antibodies capable of addressing the cause(s) of elevated pressure. Based on current evidence, there is potential for such therapeutic targeting in at least three zones:
1. TM – Reverse structural/functional damage to facilitate outflow; Rho Kinase Inhibitors likely exhibit this effect, evidence is emerging that prostaglandins have a similar effect, and newer drugs may stimulate macrophage-like activity by trabecular cells
2. SC / JXT – Reversing SC stiffening in high-pressure glaucoma; ATP Potassium Channel Modulators and Autotaxin-lysophosphatidic acid may work here, either reversing stiffening or increasing function of the extracellular matrix
3. Ostia / collector channels / veins – Several lines of research are exploring targeting potential beyond the canal