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Complement depletion with humanized cobra venom factor in a mouse model of age-related macular degeneration

: Fritzinger, D.C.; Dean, R.; Meschter, C.; Wong, K.; Halter, R.; Borlak, J.; John, W.D.; Vogel, C.-W.


Lambris, J.D.:
Inflammation and retinal disease: Complement biology and pathology : First Aegean Conferences Conference on Inflammation and Retinal Disease: Complement Biology and Pathology; June 10-17, 2007 in Crete, Greece
Berlin: Springer, 2010 (Advances in experimental medicine and biology 703)
ISBN: 978-1-4419-5634-7
ISBN: 978-1-4419-5635-4
Conference on Inflammation and Retinal Disease - Complement Biology and Pathology <1, 2007, Crete>
Conference Paper
Fraunhofer ITEM ()
complement depletion; cobra venom factor; mouse model; age-related macular degeneration

The effect of complement depletion with humanized cobra venom factor (CVF) on retinal lesion development/neovascularization was determined in a mouse model of wet age-related macular degeneration (AMD). Mice were treated with the humanized CVF protein HC3-1496 prior to, and once daily for 28 days after laser coagulation surgery of the retina. CVF transgenic mice exhibiting permanently low levels of serum complement activity and PBS-treated mice served as positive and negative controls, respectively. Fluorescein isothiocyanate (FITC)-dextran funduscopy after laser surgery indicated the presence of lesions in all mice that underwent laser surgery. In HC3-1496-treated mice as well as CVF transgenic mice smaller lesions were seen after 8 days. Measurement of lesion sizes by histopathological examination of eyes after 28 days revealed a significant reduction of lesion area and volume in both HC3-1496-treated animals and CVF transgenic animals compared to PBS-treated control animals. Systemic complement depletion with a complement depletor, such as the humanized CVF protein HC3-1496, represents a promising therapeutic concept for patients with wet AMD.