녹내장의 최신 치료 안약 = New classes of glaucoma medical treatment

다국어 초록 (Multilingual 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 researchderived 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.

참고문헌 (Reference)

1 Friedman DS, "Using pharmacy claims data to study adherence to glaucoma medications : methodology and findings of the Glaucoma Adherence and Persistency Study(GAPS)" 48 : 5052-5057, 2007

2 Nilsson SF, "The prostanoid EP2 receptor agonist butaprost increases uveo-scleral outflow in the cynomolgus monkey" 47 : 4042-4049, 2006

3 Furchgott RF, "The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcho-line" 288 : 373-376, 1980

4 Stamer WD, "The many faces of the trabecular meshwork cell" 158 : 112-123, 2017

5 Kameda T, "The effect of Rho-associated protein kinase inhibitor on monkey Schle-mmʼs canal endothelial cells" 53 : 3092-3103, 2012

6 Kass MA, "The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma" 120 : 701-713, 2002

7 Okumura N, "Rho-associated kinase inhibitor eye drop(Ripasudil)transiently alters the morphology of corneal endothelial cells" 56 : 7560-7567, 2015

8 Tanna AP, "Rho kinase inhibitors as a novel treat-ment for glaucoma and ocular hypertension" 125 : 1741-1756, 2018

9 Heijl A, "Reduction of intraocular pressure and glaucoma progression : results from the Early Manifest Glaucoma Trial" 120 : 1268-1279, 2002

10 Kim CS, "Prevalence of primary open-angle glaucoma in central South Korea the Namil study" 118 : 1024-1030, 2011

11 Boimer C, "Preservative exposure and surgical outcomes in glaucoma patients : the PESO study" 22 : 730-735, 2013

12 Tanihara H, "Phase 2 randomized clinical study of a Rho kinase inhibitor, K-115, in primary open-angle glaucoma and ocular hypertension" 156 : 731-736, 2013

13 Tanihara H, "One-year clinical evaluation of 0.4% ripasudil (K-115) in patients with open-angle glaucoma and ocular hyperten-sion" 94 : e26-e34, 2016

14 Khouri AS, "Once-daily netarsudil vs twice-daily timolol in patients with elevated intraocular pressure, the randomized phase 3 ROCKET-4 study" 204 : 97-104, 2019

15 Olthoff CM, "Noncompliance with ocular hypotensive treatment in patients with glaucoma or ocular hypertension an evidence-based review" 112 : 953-961, 2005

16 Palmer RM, "Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor" 327 : 524-526, 1987

17 Asrani S, "Netarsudil/latanoprost fixed-dose combination for elevated intraocular pressure : 3-month data from a randomized phase 3 trial" 207 : 248-257, 2019

18 Jonas JB, "Glaucoma" 390 : 2183-2193, 2017

19 Cramer JA, "Effect of partial compliance on cardiovascular medication effectiveness" 88 : 203-206, 2002

20 Bacharach J, "Double-masked, ran-domized, dose-response study of AR-13324 versus latanoprost in patients with elevated intraocular pressure" 122 : 302-307, 2015

21 Wang JW, "Differential effects of prostaglandin E2-sensitive receptors on contractility of human ocular cells that regulate conventional outflow" 54 : 4782-4790, 2013

22 Medeiros FA, "Comparison of latanoprostene bunod 0.024% and timolol maleate 0.5% in open-angle glaucoma or ocular hypertension: the LUNAR study" 168 : 250-259, 2016

23 Collaborative Normal-Tension Glaucoma Study Group, "Comparison of glaucomatous progression between untreated patients with normal-tension glaucoma and patients with therapeutically reduced intraocular pressures" 126 : 487-497, 1998

24 Gabelt BT, "Adler’s physiology of the eye" Mosby Elsevier 274-307, 2011

25 Schwartz GF, "Adherence and persistence with glaucoma therapy" 53 (53): S57-S68, 2008

26 Tanihara H, "Addi-tive intraocular pressure-lowering effects of the rho kinase inhibitor ripasudil(K-115)combined with timolol or latan-oprost : a report of 2 randomized clinical trials" 133 : 755-761, 2015

27 Kalouda P, "Achieve-ments and limits of current medical therapy of glaucoma" 59 : 1-14, 2017

28 Weinreb RN, "A randomised, controlled comparison of latanoprostene bunod and latan-oprost 0.005% in the treatment of ocular hypertension and open angle glaucoma: the VOYAGER study" 99 : 738-745, 2015

29 Santen Inc, "A phase IIb safety and efficacy study of DE-126 ophthalmic solution in primary open-angle glaucoma or ocular hypertension: Angel Study"

30 Lu FH, "A phase 3 trial comparing omidenepag isopropyl 0.002% with latanoprost 0.005% in primary open-angle glaucoma and ocular hypertension: the AYAME study" 59 : 1235-, 2018

31 Myers JS, "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" 32 : 555-562, 2016