We are executing a multi-pronged approach to fully explore the potential of our owned assets as well as investigate new and interesting ophthalmic opportunities outside of our current domain.

Starting with Rhopressa® (netarsudil ophthalmic solution) 0.02% and Roclatan™ (netarsudil/latanoprost ophthalmic solution) 0.02%/0.005%, we are exploring the potential longer-term impact of these treatments on the trabecular meshwork. By increasing trabecular outflow, we believe these products may have the potential to stop the degeneration of outflow tissues. This may be possible because as the trabecular meshwork becomes relaxed and opens as a result of the action of our products, the increased throughput of eye fluid, or aqueous humor, helps deliver nutrients and antioxidants to regions of the trabecular outflow pathway that were otherwise blocked from passage. The flow of fluid through the trabecular meshwork is the only known mechanism for delivering such nutrients to the diseased tissue, as there are no blood vessels present. Work is underway to explore whether our products may be able to prevent, or possibly even reverse, damage to the trabecular meshwork pathway through this effect. We recently completed preclinical studies demonstrating that Rhopressa® ophthalmic solution may have the potential for disease modification, including stopping and reversing fibrosis and increasing perfusion in the trabecular meshwork, which would represent a breakthrough in glaucoma treatment. The illustrations below show the ability of netarsudil (AR-13324), the active ingredient in Rhopressa® ophthalmic solution, to block TGF-beta-induced expression of fibrosis proteins in human trabecular meshwork cells and expand the trabecular meshwork tissue, opening spaces for increased outflow.

We also have a library of Rho kinase (ROCK) inhibitors of over 3,000 compounds. All of these compounds are wholly owned by Aerie.

One of these compounds, AR-13503, inhibits both Rho kinase and protein kinase C, and has shown preclinically that it may be effective for diseases of the retina such as wet age-related macular degeneration (AMD) and diabetic macular edema (DME). Our pipeline also includes AR-1105, a dexamethasone steroid with potential in the treatment of DME. We are currently evaluating a bio-erodible polymer technology to provide sustained release of AR-13503 to the retina over a period of several months.

In addition, our expansive library of molecules is also being evaluated for potential benefit in the treatment of diseases beyond ophthalmology including pulmonary health, dermatology indications and cancer.


Rhopressa® Disease Modification Potential


Netarsudil* May Have Anti-Fibrotic Activity in Human Trabecular Meshwork Cells


Netarsudil* Causes Expansion of Trabecular Meshwork Tissue, Opening Spaces for Increased Outflow


Rhopressa® has shown preclinically the promotion of retinal ganglion cell survival and axon regeneration following optic nerve injury

ROCK Inhibitors for AMD


Early results of the research performed thus far on our preclinical molecule AR-13503 has shown lesion size decreases in a model of wet AMD at levels that are numerically higher than a current market-leading product. AR-13503 inhibits Rho kinase, PKC, JAK2 and PDGFR-β. If proven out, we may have the potential to provide new mechanisms and pathways to treat this disease. The graph below depicts the results of a recent preclinical study designed to show reduced neovascularization in an animal model. AR-13503 demonstrated greater lesion size reduction than Eylea® in this in vivo preclinical study involving laser-induced choroidal neovascularization. Additionally, in our preclinical studies and as depicted in the graph below, we have seen a promising effect of this molecule on reducing neovascularization in a model of proliferative diabetic retinopathy. We are also exploring if there is any benefit of our other compounds in DME (diabetic macular edema), as it is known that ROCK inhibitors reduce the weakening of vessel walls and microvascular damage in animal models of diabetes.


AR-13154 (precursor to AR-13503) vs. Eylea in Preclinical AMD Model

Posters and Research Information
Date Title View
Jan 10, 2018 840 KB
Aug 10, 2017 1 MB
May 10, 2017 386 KB
May 10, 2017 151 KB
May 10, 2017 556 KB
May 10, 2017 418 KB
May 10, 2017 330 KB
May 9, 2017 1024 KB
March 2, 2017 149 KB
March 2, 2017 65.5 KB
August 8, 2016 859 KB
May 2, 2016 790 KB
May 2, 2016 550 KB
May 2, 2016 110.75 KB
May 2, 2016 115 KB
May 2, 2016 2.0 MB
March 2, 2016 437.6 KB
March 2, 2016 429.4 KB
March 2, 2016 426.7 KB
March 2, 2016 716.5 KB
February 24, 2016 593 KB
May 7, 2015 300.6 KB
Mar 2, 2015 679.9 KB
Mar 2, 2015 1.5 MB
May 30, 2014 748.4 KB
Feb 14, 2014 547.5 KB
May 15, 2013 469.5 KB
May 21, 2012 530.8 KB
May 21, 2012 1.3 MB