New classes of glaucoma medical treatment

Jin A Choi

doi:10.5124/jkma.2019.62.9.497

J Korean Med Assoc > Volume 62(9); 2019 > Article

Choi: New classes of glaucoma medical treatment

Pharmacotherapeutics

J Korean Med Assoc 2019; 62(9): 497-504.

Published online: July 17, 2019

DOI: http://dx.doi.org/10.5124/jkma.2019.62.9.497

New classes of glaucoma medical treatment

Jin A Choi, MD

Department of Ophthalmology and Visual Science, St. Vincent's Hospital, The Catholic University of Korea College of Medicine, Seoul, Korea

Corresponding author: Jin A Choi E-mail: jinah616@catholic.ac.kr

Received June 26, 2019 Accepted July 29, 2019

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Glaucoma is a progressive degenerative disease of the optic nerve head, characterized by a specific pattern of axonal loss and visual field deterioration. This review aims at introducing the different novel pharmacologic agents for its treatment, as well as their mechanisms. Most glaucoma patients require lifelong care and individualized treatment. Intraocular pressure (IOP), which is regulated by aqueous humor production, outflow via the trabecular meshwork (parasympathomimetics only) and uveoscleral outflow pathways, is currently the only treatable target for glaucoma treatment. Conventional glaucoma medications are categorized as β blockers, α agonists, carbonic anhydrase inhibitors, parasympathomimetics, and prostaglandin analogues. The development of basic research-derived novel classes of pharmacologic agents features novel action mechanisms, which are different from those of conventional medications. New classes of recently approved or clinical trial-tested medications include Rho-kinase inhibitors, nitric oxide donors, adenosine agonists, and prostaglandin analogs targeting E-type prostanoid receptors, etc. Their integration and future development will facilitate the expansion and customization of therapeutic options.

Key words: Glaucoma; Ocular hypertension; Intraocular pressure; Drug development

REFERENCES

1. Kass MA, Heuer DK, Higginbotham EJ, Johnson CA, Keltner JL, Miller JP, Parrish RK II, Wilson MR, Gordon MO. the Ocular Hypertension Treatment Study Group. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol 2002;120:701-713.

2. Kim CS, Seong GJ, Lee NH, Song KC. Namil Study Group, Korean Glaucoma Society. Prevalence of primary open-angle glaucoma in central South Korea the Namil study. Ophthalmology 2011;118:1024-1030.

3. Collaborative Normal-Tension Glaucoma Study Group. Comparison of glaucomatous progression between untreated patients with normal-tension glaucoma and patients with therapeutically reduced intraocular pressures. Am J Ophthalmol 1998;126:487-497.

4. 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;120:1268-1279.

5. Jonas JB, Aung T, Bourne RR, Bron AM, Ritch R, Panda-Jonas S. Glaucoma. Lancet 2017;390:2183-2193.

6. Kalouda P, Keskini C, Anastasopoulos E, Topouzis F. Achievements and limits of current medical therapy of glaucoma. Dev Ophthalmol 2017;59:1-14.

7. Cramer JA. Effect of partial compliance on cardiovascular medication effectiveness. Heart 2002;88:203-206.

8. Olthoff CM, Schouten JS, van de Borne BW, Webers CA. Noncompliance with ocular hypotensive treatment in patients with glaucoma or ocular hypertension an evidence-based review. Ophthalmology 2005;112:953-961.

9. Schwartz GF, Quigley HA. Adherence and persistence with glaucoma therapy. Surv Ophthalmol 2008;53((6 Suppl1):S57-S68.

10. Friedman DS, Quigley HA, Gelb L, Tan J, Margolis J, Shah SN, Kim EE, Zimmerman T, Hahn SR. Using pharmacy claims data to study adherence to glaucoma medications: methodology and findings of the Glaucoma Adherence and Persistency Study (GAPS). Invest Ophthalmol Vis Sci 2007;48:5052-5057.

11. Boimer C, Birt CM. Preservative exposure and surgical outcomes in glaucoma patients: the PESO study. J Glaucoma 2013;22:730-735.

12. Tanna AP, Johnson M. Rho kinase inhibitors as a novel treatment for glaucoma and ocular hypertension. Ophthalmology 2018;125:1741-1756.

13. Stamer WD, Clark AF. The many faces of the trabecular meshwork cell. Exp Eye Res 2017;158:112-123.

14. Kameda T, Inoue T, Inatani M, Fujimoto T, Honjo M, Kasaoka N, Inoue-Mochita M, Yoshimura N, Tanihara H. The effect of Rho-associated protein kinase inhibitor on monkey Schle-mmʼs canal endothelial cells. Invest Ophthalmol Vis Sci 2012;53:3092-3103.

15. Tanihara H, Inoue T, Yamamoto T, Kuwayama Y, Abe H, Fukushima A, Suganami H, Araie M. K-115 Clinical Study Group. One-year clinical evaluation of 0.4% ripasudil (K-115) in patients with open-angle glaucoma and ocular hypertension. Acta Ophthalmol 2016;94:e26-e34.

16. Tanihara H, Inoue T, Yamamoto T, Kuwayama Y, Abe H, Araie M. K-115 Clinical Study Group. Phase 2 randomized clinical study of a Rho kinase inhibitor, K-115, in primary open-angle glaucoma and ocular hypertension. Am J Ophthalmol 2013;156:731-736.

17. Okumura N, Okazaki Y, Inoue R, Nakano S, Fullwood NJ, Kinoshita S, Koizumi N. Rho-associated kinase inhibitor eye drop (Ripasudil) transiently alters the morphology of corneal endothelial cells. Invest Ophthalmol Vis Sci 2015;56:7560-7567.

18. Tanihara H, Inoue T, Yamamoto T, Kuwayama Y, Abe H, Suganami H, Araie M. K-115 Clinical Study Group. Additive intraocular pressure-lowering effects of the rho kinase inhibitor ripasudil (K-115) combined with timolol or latanoprost: a report of 2 randomized clinical trials. JAMA Ophthalmol 2015;133:755-761.

19. Bacharach J, Dubiner HB, Levy B, Kopczynski CC, Novack GD. AR-13324-CS202 Study Group. Double-masked, randomized, dose-response study of AR-13324 versus latanoprost in patients with elevated intraocular pressure. Ophthalmology 2015;122:302-307.

20. Khouri AS, Serle JB, Bacharach J, Usner DW, Lewis RA, Braswell P, Kopczynski CC, Heah T. Once-daily netarsudil vs twice-daily timolol in patients with elevated intraocular pressure, the randomized phase 3 ROCKET-4 study. Am J Ophthalmol 2019;204:97-104.

21. Asrani S, Robin AL, Serle JB, Lewis RA, Usner DW, Kopczynski CC, Heah T. Netarsudil/latanoprost fixed-dose combination for elevated intraocular pressure: 3-month data from a randomized phase 3 trial. Am J Ophthalmol 2019;207:248-257.

22. Furchgott RF, Zawadzki JV. The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine. Nature 1980;288:373-376.

23. Palmer RM, Ferrige AG, Moncada S. Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor. Nature 1987;327:524-526.

24. Gabelt BT, Kaufman PL. Production and flow of aqueous humor. In: Levin LA, Nilsson SF, Ver Hoeve J, editor. editors.. Adler's physiology of the eye. 11th ed.. St. Louis: Mosby Elsevier; 2011. p. 274-307.

25. Medeiros FA, Martin KR, Peace J, Scassellati Sforzolini B, Vittitow JL, Weinreb RN. Comparison of latanoprostene bunod 0.024% and timolol maleate 0.5% in open-angle glaucoma or ocular hypertension: the LUNAR study. Am J Opthalmol 2016;168:250-259.

26. Weinreb RN, Ong T, Scassellati Sforzolini B, Vittitow JL, Singh K, Kaufman PL. 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. Br J Ophthalmol 2015;99:738-745.

27. Myers JS, Sall KN, DuBiner H, Slomowitz N, McVicar W, Rich CC, Baumgartner RA. A dose-escalation study to evaluate the safety, tolerability, pharmacokinetics, and efficacy of 2 and 4 weeks of twice-daily ocular trabodenoson in adults with ocular hypertension or primary open-angle glaucoma. J Ocul Pharmacol Ther 2016;32:555-562.

28. Wang JW, Woodward DF, Stamer WD. Differential effects of prostaglandin E2-sensitive receptors on contractility of human ocular cells that regulate conventional outflow. Invest Ophthalmol Vis Sci 2013;54:4782-4790.

29. Nilsson SF, Drecoll E, Lutjen-Drecoll E, Toris CB, Krauss AH, Kharlamb A, Nieves A, Guerra T, Woodward DF. The prostanoid EP2 receptor agonist butaprost increases uveoscleral outflow in the cynomolgus monkey. Invest Ophthalmol Vis Sci 2006;47:4042-4049.

30. Lu FH, Aihara M, Kawata H, Iwata A, Odani-Kawabata N, Shams NK. A phase 3 trial comparing omidenepag isopropyl 0.002% with latanoprost 0.005% in primary open-angle glaucoma and ocular hypertension: the AYAME study. Invest Ophthalmol Vis Sci 2018;59:1235.

31. Santen Inc. A phase IIb safety and efficacy study of DE-126 ophthalmic solution in primary open-angle glaucoma or ocular hypertension: Angel Study [Internet]. Bethesda: ClinicalTrials.gov; 2017. [cited 2019 Jul 15]. Available from:. https://clinicaltrials.gov/ct2/show/NCT03216902?term=ONO-9054&rank=3.