Background and Purpose. Retina plays a pivotal role in sensory perception, and degenerative diseases lead to visual deficits. The therapeutic approach includes anti-inflammatory drugs and new therapeutic protocols, including Anti-VEGF medicines and monoclonal antibodies. TnP is a drug candidate in preclinical development indicated for inflammatory diseases, with the ability to interfere with the dynamic of immune cells. Zebrafish offer several advantages as a research model, including genetic similarity with humans. Therefore, we aim to evaluate the therapeutic effect of TnP on zebrafish retinopathy. Experimental Approach. We used cobalt chloride-induced (CoCl2) retinopathy and intense light-induced retinal damage (LIRD) and TnP prophylactic treatment. Visual motor response and histology were conducted. Key Results. Swimming pattern of CoCl2-exposed larvae demonstrated inertia compared to negative-control, and exposure to LIRD induced a shorter distance covered. Histology revealed that CoCl2-induced damage or LIRD provoked changes in the retina morphology. Treatment with TnP did not reverse the reduced distance covered by CoCl2-damaged or LIRD larvae. TnP failed to reverse all retinal layers thinned by injury by both protocols, except for the IPL, which seemed to be restored. We found that TnP acts on INL, probably promoting cell proliferation and increasing synaptic connections among retinal neurons. This cell modulating activity could represent neuronal plasticity activity of TnP. Conclusion and Implications. Our findings support further exploration of TnP as a therapeutic agent for retinal and neurodegenerative diseases, given its role in neuronal protection and immune modulation. Alternatively, TnP might require combination with other therapeutic agents to enhance its efficacy.