Background: Intraocular ranibizumab (Lucentis®, Novartis, Basel Switzerland) is the primary choice in the treatment of neovascular age-related macular degeneration (AMD). VEGF is known to be a survival factor for neuronal cells. Therefore, blockage of all VEGF isoforms by ranibizumab could induce retinal dysfunction.
Methods: Using isolated bovine retinas the electroretinogram (ERG) was recorded as a transretinal potential using Ag/AgCl electrodes while the retinas were perfused with an oxygen pre-incubated nutrient solution. For 45 min ranibizumab was applied at a concentration of 0.2mg/mL and alternatively the solvent carrier without the active agent. The ERG was monitored before, during and after exposure.
Results: The concentration of 0.2mg/mL ranibizumab induced a not significant b-wave reduction of 22.32 % after exposure (p = 0.13). For the a-wave amplitude only a reduction of 4 % was detected (p = 0.18). The solvent carrier induced no significant reduction of the a- and b-wave amplitudes (p = 0.30 and p = 0.979, respectively).
Conclusion: In our ex vivo model, the isolated perfused vertebrate retina, ranibizumab has been proven to be a safe compound at the concentrations applied. The stability of the ERG-amplitudes rules out a considerable retinal dysfunction after an injection of up to 1mg ranibizumab.
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