scholarly journals Additive Intraocular Pressure-Lowering Effects of Ripasudil with Glaucoma Therapeutic Agents in Rabbits and Monkeys

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Yoshio Kaneko ◽  
Masayuki Ohta ◽  
Tomoyuki Isobe ◽  
Yuto Nakamura ◽  
Ken Mizuno

Ripasudil hydrochloride hydrate (K-115), a specific Rho-associated coiled-coil containing protein kinase (ROCK) inhibitor, is developed for the treatment of glaucoma and ocular hypertension. Topical administration of ripasudil decreases intraocular pressure (IOP) by increasing conventional outflow through the trabeculae to Schlemm’s canal, which is different from existing agents that suppress aqueous humor production or promote uveoscleral outflow. In this study, we demonstrated that ripasudil significantly lowered IOP in combined regimens with other glaucoma therapeutic agents in rabbits and monkeys. Ripasudil showed additional effects on maximum IOP lowering or prolonged the duration of IOP-lowering effects with combined administration of timolol, nipradilol, brimonidine, brinzolamide, latanoprost, latanoprost/timolol fixed combination, and dorzolamide/timolol fixed combination. These results indicate that facilitation of conventional outflow by ripasudil provides additive IOP-lowering effect with other classes of antiglaucoma agents. Ripasudil is expected to have substantial utility in combined regimens with existing agents for glaucoma treatment.

2014 ◽  
Vol 23 (5) ◽  
pp. 329-332 ◽  
Author(s):  
Tae-Woo Kim ◽  
Martha Kim ◽  
Eun Ji Lee ◽  
Jin Wook Jeoung ◽  
Ki Ho Park

2012 ◽  
Vol 90 ◽  
pp. 0-0
Author(s):  
K HOLLANDERS ◽  
D SIJNAVE ◽  
T VAN BERGEN ◽  
S VAN DE VELDE ◽  
L MOONS ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
A. Rocha-Sousa ◽  
J. Rodrigues-Araújo ◽  
Petra Gouveia ◽  
João Barbosa-Breda ◽  
S. Azevedo-Pinto ◽  
...  

Primary open-angle glaucoma (POAG) is a leading cause of irreversible and preventable blindness and ocular hypertension is the strongest known risk factor. With current classes of drugs, management of the disease focuses on lowering intraocular pressure (IOP). Despite of their use to modify the course of the disease, none of the current medications for POAG is able to reduce the IOP by more than 25%–30%. Also, some glaucoma patients show disease progression despite of the therapeutics. This paper examines the new described physiological targets for reducing the IOP. The main cause of elevated IOP in POAG is thought to be an increased outflow resistance via the pressure-dependent trabecular outflow system, so there is a crescent interest in increasing trabecular meshwork outflow by extracellular matrix remodeling and/or by modulation of contractility/TM cytoskeleton disruption. Modulation of new agents that act mainly on trabecular meshwork outflow may be the future hypotensive treatment for glaucoma patients. There are also other agents in which modulation may decrease aqueous humour production or increase uveoscleral outflow by different mechanisms from those drugs available for glaucoma treatment. Recently, a role for the ghrelin-GHSR system in the pathophysiology modulation of the anterior segment, particularly regarding glaucoma, has been proposed.


Ophthalmology ◽  
2008 ◽  
Vol 115 (10) ◽  
pp. 1728-1734.e2 ◽  
Author(s):  
Martin Kaback ◽  
Stephen V. Scoper ◽  
George Arzeno ◽  
John E. James ◽  
Steven Y. Hua ◽  
...  

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