Verteporfin (CL 318952) is a photosensitizer for photodynamic therapy to eliminate the abnormal blood vessels in the eye associated with conditions such as age-related macular degeneration. Verteporfin is a YAP inhibitor which disrupts YAP-TEAD interactions. Verteporfin induces cell apoptosis^[1].Verteporfinis an autophagy inhibitor that blocks autophagy at an early stage by inhibiting autophagosome formation^[3]. IC50 & Target: IC50: YAP-TEAD interaction In Vitro: Verteporfin is specifically selected by PDX-cell screening. The concentrations to cause 50% growth inhibition (GI₅₀) for PhLO, PhLH, and PhLK are 228 nM, 395 nM, and 538 nM, respectively, whereas GI₅₀ for ALL-1, TCC-Y/sr, and NPhA1 are 3.93 µM, 2.11 µM, and 5.61 µM, respectively. GSH significantly reduces the sensitivity of 2 out of 3 PDX cells to verteporfin. Verteporfin reduces the mitochondrial membrane potential in PDX cells^[1]. Verteporfin reduces the PTX-resistance on HCT-8/T cells by inhibiting YAP expression and combination therapy with verteporfin and NSC 125973 shows synergism on inhibition of YAP and cytotoxicity to HCT-8/T^[2]. In Vivo: Verteporfin (10 mg/kg, c.s.c.) and BMS-354825 significantly reduces the leukemia cell ratio, and combined therapy further reduced the number of leukemia cells in the spleen^[1].