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. 2018 Aug;16(7):903–918. doi: 10.2174/1570159X15666170705101910

Table 2.

Update on the new strategies for glaucoma therapy based on the distinct pathogenic mechanisms.

Mechanisms Substance Effect
Renin-Angiotensin System
ACE inhibitors
Enalaprilat, Fosinopril, Perindopril, Ramiprilat, Ocular hypotensive effect
Calcium Channels Ion channel blockers/inhibitors Betaxolol, Diltiazem, flunarizine, Iganidipine, lomerizine, Nifedipine, Nimodipine, Nilvadipine Verapamil, Nimodipine, Improving ocular blood perfusion, neuroprotection and IOP lowering.
Cell kinases Cell cyclin-dependent kinase inhibitor Roscovitine Cell contraction-relaxation in trabecular meshwork
Cell kinases (Rho family) AMA0076
AR-13324
K-115
PG324
Y-39983
RKI-983
H-1152
Modulating signal transduction pathways and actin cytoskeleton function and cell motility of trabecular meshwork, canal of Schelmm and ciliary muscle cells
Aqueous humor homeostasis. PGAs EP2 receptor agonist SAR366234 EP2 receptor agonist. Lowering IOP
Aqueous humor homeostasis PGAs Dual receptor affinity for FP and EP3 receptors, ONO 9054 Lower and more sustained IOP reduction
Energy supplier Adenosine A2a receptor agonist OPA-6566 Increase aqueous outflow facility by shrinking TM cell volume
Aqueous humor homeosthasis TM cells contractility Actin modulator Latrunculin B (INS115644) marine macrolide Improves TM outflow facility by inhibiting the assembly of actin microfilaments in cell cytoplasm

Abbreviations: ACE: angiotensin converting enzyme; IOP: Intraocular pressure; PGAs: prostaglandin analogs; EP2: prostaglandin E2; EP3: prostaglandin E3; FP: prostaglandin F; TM: trabecular meshwork.