Method of using CCR3 binding agents to detect choroidal neovascularization
US8778616B2 · kind B2 · utility
Assignee
Inventors
Key dates
| Filing date | May 26, 2010 |
| Grant date | Jul 15, 2014 |
| Priority date | — |
| Expiry date | Jul 1, 2030 |
Classification
- Technology area (CPC G)Physics
- CPC primaryG01N2800/50
- WIPO fieldPharmaceuticals
- WIPO sectorChemistry
Abstract
The results presented herein demonstrate the specific expression of CCR3 in CNV endothelial cells in humans with AMD, and despite the expression of its ligands, eotaxin-1, -2, and -3, neither eosinophils nor mast cells are present in human CNV. The genetic or pharmacological targeting of CCR3 or eotaxins as disclosed herein inhibited injury-induced CNV in mice. CNV suppression by CCR3 blockade was due to direct inhibition of endothelial cell proliferation, and was uncoupled from inflammation as it occurred in mice lacking eosinophils or mast cells and was independent of macrophage and neutrophil recruitment. CCR3 blockade was more effective at reducing CNV than vascular endothelial growth factor-A (VEGF-A) neutralization, which is currently in clinical use, and, unlike VEGF-A blockade, not toxic to the mouse retina. In vivo imaging with CCR3-targeting quantum dots located spontaneous CNV invisible to standard fluorescein angiography in mice before retinal invasion. CCR3 targeting is useful in reducing vision loss due to AMD through early detection and therapeutic angioinhibition.
Source: USPTO / EPO open patent data. Objective bibliographic and citation counts.