Fritzinger, D.C.D.C.FritzingerDean, R.R.DeanMeschter, C.C.MeschterWong, K.K.WongHalter, R.R.HalterBorlak, J.J.BorlakJohn, W.D.W.D.JohnVogel, C.-W.C.-W.Vogel2022-03-112022-03-112010https://publica.fraunhofer.de/handle/publica/36780010.1007/978-1-4419-5635-4_11The 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.encomplement depletioncobra venom factormouse modelage-related macular degeneration610620conference paper