Statement of Need

Primary open-angle glaucoma (POAG) is a complex and typically slowly progressive disease for which intraocular pressure (IOP) is the only known modifiable risk factor. While many aspects of glaucoma pathophysiology and progression remain to be uncovered, it is known that over time, every mm Hg of pressure reduction has an impact.1,2

Research into the mechanisms underlying aqueous humor dynamics, and thus, IOP regulation, points to the trabecular meshwork pathway (the “conventional” pathway) as the primary route of aqueous outflow, and, in POAG, the site of resistance that results in elevated IOP. Research has found that nitric oxide (NO), an endogenous signaling molecule involved in processes throughout the body, also plays a key role in IOP regulation via this outflow pathway.3

NO-donating drugs and other compounds aimed at the NO signaling cascade have been developed for use in cardiovascular and pulmonary diseases, and also represent an important new area of drug development in glaucoma.3 This is particularly the case because most currently available glaucoma treatments bypass the trabecular meshwork altogether, targeting either aqueous humor production or outflow through the uveoscleral (“nonconventional”) pathway.4,5

As at least one drug with an NO-donating moiety (latanoprostene bunod) is poised to enter the glaucoma marketplace, there is a need for ophthalmologists to understand the role of NO in the trabecular meshwork and glaucoma, and the place of NO-donating drugs in practice.6,7

As a leading cause of irreversible vision loss and blindness worldwide, glaucoma is an important part of comprehensive ophthalmology practice; and ophthalmologists, especially those who are not glaucoma specialists, need up-to-date and clearly presented information about new research into the disease and its treatment.8

A Closer Look at Nitric Oxide in Glaucoma will translate the available preclinical and clinical evidence about how NO works in the eye, addressing the mechanism of NO-donating drugs in glaucoma and how the availability of medical glaucoma therapy that targets the trabecular meshwork could factor into treatment decisions.


  1. The AGIS Investigators. The Advanced Glaucoma Intervention Study (AGIS): 7. The relationship between control of intraocular pressure and visual field deterioration. Am J Ophthalmol. 2000;130(4):429-40.

  2. Heijl A, Leske MC, Bengtsson B, Hyman L, Bengtsson B, Hussein M; Early Manifest Glaucoma Trial Group. Reduction of intraocular pressure and glaucoma progression: results from the Early Manifest Glaucoma Trial. Arch Ophthalmol. 2002;120(10):1268-79.

  3. Stamer WD, Lei Y, Boussommier-Calleja A, Overby DR, Ethier CR. eNOS, a pressure-dependent regulator of intraocular pressure. Invest Ophthalmol Vis Sci. 2011;52(13):9438-44.

  4. Stamer WD, Acott TS. Current understanding of conventional outflow dysfunction in glaucoma. Curr Opin Ophthalmol. 2012;23:135-43.

  5. Weinreb RN, Aung T, Medeiros FA. The pathophysiology and treatment of glaucoma: a review. JAMA. 2014;311(18):1901-11.

  6. Weinreb RN, Ong T, Scassellati Sforzolini B, et al, for the VOYAGER study group. A randomised, controlled comparison of latanoprostene bunod and latanoprost 0.005% in the treatment of ocular hypertension and open angle glaucoma: the VOYAGER study British Journal of Ophthalmology. 2015;99:738-45.

  7. Cavet ME, Vollmer TR, Harrington KL, et al. Regulation of endothelin-1-induced trabecular meshwork cell contractility by latanoprostene bunod. Invest Ophthalmol Vis Sci. 2015;56(6):4108-16. 

  8. Kapetanakis VV, Chan MPY, Foster PJ, Cook DG, Owen CG, Rudnicka AJ. Global variations and time trends in the prevalence of primary open angle glaucoma (POAG): a systematic review and analysis. Br J Ophthalmol. 2016;100:86-93.

Off-label Use Statement: This work may discuss off-label uses of medications.

General Information: This CME activity is sponsored by the University of Florida College of Medicine and is supported by an unrestricted educational grant from Bausch + Lomb, Inc.

Accreditation Statement: This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of the University of Florida College of Medicine and Candeo Clinical/Science Communications, LLC. The University of Florida College of Medicine is accredited by the ACCME to provide continuing medical education for physicians.

Credit Designation Statement: The University of Florida College of Medicine designates this enduring material for a maximum of 0.25 AMA PRA Category 1 CreditTM. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Date of Original Release: November 2018. Approved for a period of 12 months.