The Rho family GTPases regulates axon growth and regeneration. Inactivation of Rho with C3, a toxin from Clostridium botulinum, can stimulate regeneration and sprouting of injured axons. The present invention provides novel chimeric C3-like Rho antagonists. The invention further provides evidence that these compounds promote repair when applied to the injured mammalian central nervous system, such as the retina. The present invention provide agents which are able to diffuse readily and therefore can promote repair for neurodegenerative disease of the eye, such as macular degeneration. The present invention further provides methods of treating macular degeneration, methods of inhibiting or reducing the rate of subretinal neovascularization and proliferation of neovascular tissue and methods of protecting retinal photoreceptor cell death.