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Statement of Need / Off-label Use / Accreditation

Glaucoma, a group of ocular diseases characterized by progressive damage to the optic nerve, is the second leading cause of blindness worldwide, affecting a significant and growing portion of the US population.1,2

Much remains to be understood about the pathophysiology of glaucoma, but intraocular pressure (IOP) has been identified as an important causative factor and modifiable risk factor.3 As demonstrated in several large clinical trials, IOP reduction can prevent progression of optic nerve damage and visual field loss in both early and late stages of the disease.4,5

Despite multiple drug choices, however, current data shows that a significant proportion of glaucoma patients do not reach target IOP with a single-agent regimen.6,7 Even if pressure is maintained within target levels, some patients may continue to develop progressive glaucoma damage and field loss. These treatment challenges highlight a continued need for more effective therapies.

The conventional trabecular meshwork pathway is the primary route of aqueous outflow in the human eye and the site of extra resistance that results in elevated pressure in primary open-angle glaucoma.8 Even so, therapies targeting trabecular outflow have largely been lacking: the medications that are currently used to treat glaucoma reduce IOP primarily by modulating aqueous production or uveoscleral outflow.

Latanoprostene bunod, a nitric oxide (NO)-donating prostaglandin F2α receptor agonist, is a novel glaucoma drug with a unique dual mechanism of action, achieved by chemically fusing two moieties— latanoprost and an NO donor—into one molecule.9 While latanoprost increases uveoscleral outflow like other PGAs do, the NO donor contributes to IOP lowering by increasing aqueous outflow through the trabecular meshwork.10

To give their glaucoma patients the full benefit of treatment advances, clinicians require clear, actionable insights from knowledgeable subspecialists and researchers. Nitric Oxide in Glaucoma: What Clinicians Need to Know will distill and organize findings about the role of NO in glaucoma and the role NO donation in glaucoma therapy in order to make them accessible to ophthalmologists and medical optometrists who want to optimize their decision-making in glaucoma.

OFF-LABEL USE STATEMENT:  This work may discuss off-label uses of medications.

CME GENERAL INFORMATION

(For ophthalmologists, including those in residency and fellowship training.) 

Accreditation Statement: This activity has been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship 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 educational activity for a maximum of 4.0 AMA PRA Category 1 Credit™. Physicians should only claim credit commensurate with the extent of their participation in the activity.

CE GENERAL INFORMATION

(For optometrists.)

Accreditation Statement: This activity has been planned and implemented through the joint sponsorship of the New England College of Optometry and Candeo Clinical/Science Communications, LLC. The New England College of Optometry is accredited by The Council on Optometric Practitioner Education® (COPE®), created by the Association of Regulatory Boards of Optometry (ARBO) to accredit continuing education on behalf of optometric licensing boards.

Credit Designation Statement: The New England College of Optometry designates this activity for a maximum of 4 hours of COPE-approved continuing education credit. Clinicians should only claim credit commensurate with the extent of their participation in the activity.

References

  1. Resnikoff S, Pascolini D, Etya’ale D, et al. Global data on visual impairment in the year 2002. Bull World Health Organ. 2004 November;82(11):844-51.
  2. Eye Diseases Prevalence Research Group. Prevalence of open-angle glaucoma among adults in the United States. Arch Ophthalmol. 2004;122:532-8.
  3. Kapetanakis VV, Chan MP, Foster PJ, et al. Global variations and time trends in the prevalence of primary open angle glaucoma (POAG): a systematic review and meta-analysis. Br J Ophthalmol. 2016;100(1):86-93.
  4. 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.
  5. Leske MC, Heijl A, Hussein M, et al; Early Manifest Glaucoma Trial Group. Factors for glaucoma progression and the effect of treatment: the early manifest glaucoma trial. Arch Ophthalmol. 2003;121(1):48-56.
  6. Schmier JK, Hulme-Lowe CK, Covert DW. Adjunctive therapy patterns in glaucoma patients using prostaglandin analogs. Clin Ophthalmol. 2014;8:1097-104.
  7. Aptel F, Chiquet C, Romanet JP. Intraocular pressure-lowering combination therapies with prostaglandin analogues. Drugs. 2012;72(10):1355-71.
  8. Stamer WD, Acott TS. Current understanding of conventional outflow dysfunction in glaucoma. Curr Opin Ophthalmol. 2012;23:135-43.
  9. Krauss AH, Impagnatiello F, Toris CB, et al. Ocular hypotensive activity of BOL-303259-X, a nitric oxide donating prostaglandin F2a agonist, in preclinical models. Exp Eye Res. 2011;93:250-5.
  10. 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.