Figure 1. Redaporfin-induced cellular stress and compartmental alteration.

(A) Redaporfin accumulates in the endoplasmic reticulum (ER) and Golgi apparatus (GA). Photoactivation of redaporfin triggers the generation of reactive oxygen species (ROS), which in turn leads to local damage, dysfunction of the ER/GA network and impairment of global protein secretion. In addition, redaporfin-induced ER/GA damage operates upstream of mitochondria to induce apoptosis. In vivo the photodynamic therapy with redaporfin triggers cell death of the primary tumor and elicits antitumor immunity that is able to control distant leasions.