Prolonged inhibition of semaphorine3a pathway via a bio-degradable implant towards a better therapy for visual sensory impairments

FP7-coo euflag Financing: European Union’s Seventh Framework Programme (FP7/2007-2013) under grant agreement nº HEALTH-F2-2012-304884
Duration: September 2012 – August 2015
Web of the project:

The consortium that will develop the VISION project consists of five partners made up of universities (Tel Aviv University, IL, (coordinator)), research centers (Institute for Advanced Chemistry of Catalonia (CSIC), ES) and companies (Nicast Ltd., IL; Synovo GmbH, DE; ANAXOMICS Biotech, ES)

Glaucoma is a term which covers different pathological conditions leading to neuropathy, degeneration of the vulnerable optic nerve axons and cell bodies (Retinal Ganglion Cells = RGC). The most common glaucoma is associated with high intraocular pressure. The treatment today is based on lowering the IOP but is inefficient in preventing RGC loss. Thus there is an urgent need for treatment that protects the RGCs.

The project goal is to develop a therapy for glaucoma and acute optic nerve neuropathy using the same therapeutic approach, i.e. inhibiting further death of vision related neural cells by prolonged inhibition of Sema3A apoptotic pathway. The therapy will be based on a minimally invasive implant for controlled release of novel therapeutic moieties. Thus, the project will develop two Sema3A inhibitors: a low MW compound and a Sema3A targeted antibody. These inhibitors will be loaded into a novel controlled and prolonged release minimal invasive, injectable implant. Sema3A is a cell secreted protein thus its putative interaction with inhibitors will occur outside the cells. This is a substantial advantage of the proposed therapeutic strategy, due to the fact that it eliminates the need for structural optimisation and delivery vehicles required to facilitate cell penetration. The clinical efficacy of this approach will be evaluated.