Retinal pigment epithelium (RPE) has an important role for maintenance of visual function by phagocytosis of photoreceptor outer segment. Recent studies have elucidated that this phagocytosis shares a non-canonical form of autophagic degradation. Also, patients with non-exudative age-related macular degeneration show dysregulation of autophagic degradation in RPE. To find effective therapeutic agent, we used in vitro photoreceptor outer segment phagocytosis assay by RPE cells. We found that an Nrf2 activating triterpenoid, RS9, accelerated photoreceptor outer segment phagocytosis. Notably, RS9 activated both AMPK/mTOR and Nrf2/SQSTM1 signaling pathway. These signals are known to facilitate autophagic degradation by different mechanism. In the early phase, RS9 phosphorylated AMPK, then dephosphorylated mTOR. In the late phase, RS9 activated Nrf2, then induced SQSTM1. A canonical Nrf2 activator diethyl maleate showed same effects; however, it has a much weaker potential compared with RS9. In conclusion, these findings indicate that RS9 is a prominent autophagy inducer and promising therapeutic agent against non-exudative age-related macular degeneration.