Verteporfin
YAP inhibitor / Verteporfin inhibits transcription by YAP/TAZ, IC50 = 2.5 µM, (via disruption of YAP-TEAD interaction) inhibiting autophagy and halting proliferation of cancer and cancer stem cell lines.1,2 Inhibits autophagosome formation.3 Reverses differentiation of Src-overexpressing embryonic stem cells.4 May be used to ablate unwanted neovasculature in the eye, esophageal mucosa, and elsewhere using light to create damaging free radicals.5
Biochemicals & reagents
129497-78-5
CL 318,952; BPD-MA
1) Saini et al. (2021), Verteporfin disrupts multiple steps of autophagy and regulates p53 to sensitize osteosarcoma cells; Cancer Cell Int., 21 52 2) Vigneswaran et al. (2021), YAP/TAZ Transcription Coactivators Create Therapeutic Vulnerability to Verteporfin in EGFR-mutant Glioblastoma; Clin. Cancer Res., 27 1553 3) Donohue et al. (2014), Induction of Covalently Crosslinked p62 Oligomers with Reduced Binding to Polyubiquitinated Proteins by the Autophagy Inhibitor Verteporfin; PLoS One, 9 e114964 4) Luo et al. (2021), Src-Yap1 signaling axis controls the trophectoderm and epiblast lineage differentiation in mouse embryonic stem cells; Stem Cell Res., 54 102413 5) Bressler et al. (2000), Photodynamic therapy with verteporfin (Visudyne): impact on ophthalmology and visual sciences; Ophthalmol. Vis. Sci., 41 624
-20°C
TARGET: Transcription factor -- PATHWAY: Transcription; Cell migration; Proliferation; Autophagy; p53 -- RESEARCH AREA: Oxidative stress; Angiogenesis; Cell death; Stem Cells -- DISEASE AREA: Cancer