Integrin-binding Peptide for Ocular Neovascularization and Macular Edema: Molecular Mechanism of Action

Johns Hopkins University, Baltimore MD

Investigators

Linked publications & trials

Abstract

There is mounting evidence that integrins avl33 and a5131 play an important role in the stimulation of retinal/choroidal neovascularization (NV) and vascular leakage, but there are gaps in our knowledge of the mechanisms by which they act that this proposal seeks to clarify. A collagen IV-derived peptide mimetic that blocks avl33 and a5131 and exerts strong antiangiogenic and anti-permeability activity, AXT107, and newly developed analogs that have different but overlapping activities, will be used as tools to facilitate those mechanistic studies. In addition, suprachoroidal injection of AXT107 microparticles will be tested for sustained delivery and prolonged suppression of NV and vascular leakage to take advantage of the therapeutic potential of AXT107.