Stable for 2 years from date of purchase as supplied. Solutions in DMSO may be stored at -20°C for up to 3 months.
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Verteporfin (129497-78-5) 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
References/Citations:
Saini et al. (2021), Verteporfin disrupts multiple steps of autophagy and regulates p53 to sensitize osteosarcoma cells; Cancer Cell Int., 21 52
Vigneswaran et al. (2021), YAP/TAZ Transcription Coactivators Create Therapeutic Vulnerability to Verteporfin in EGFR-mutant Glioblastoma; Clin. Cancer Res., 27 1553
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
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
Bressler et al. (2000), Photodynamic therapy with verteporfin (Visudyne): impact on ophthalmology and visual sciences; Invest. Ophthamol. Vis. Sci., 41 624
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a restocking/refund fee
Verteporfin (129497-78-5) 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
References/Citations:
Saini et al. (2021), Verteporfin disrupts multiple steps of autophagy and regulates p53 to sensitize osteosarcoma cells; Cancer Cell Int., 21 52
Vigneswaran et al. (2021), YAP/TAZ Transcription Coactivators Create Therapeutic Vulnerability to Verteporfin in EGFR-mutant Glioblastoma; Clin. Cancer Res., 27 1553
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
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
Bressler et al. (2000), Photodynamic therapy with verteporfin (Visudyne): impact on ophthalmology and visual sciences; Invest. Ophthamol. Vis. Sci., 41 624
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