Verteporfin

SKU: orb1304525

Description

Verteporfin is a clinically used photosensitizer and a small molecule inhibitor of the YAP-TEAD protein interaction, a key pathway in the Hippo signaling cascade. It has been widely utilized in research to study oncogenesis, fibrosis, and regenerative processes, demonstrating effects on apoptosis and autophagy in both cellular and animal models.

Research Area

Cardiovascular Research, Cell Biology, Stem Cell & Developmental Biology

Key Properties

• CAS Number: 129497-78-5
• MW: 718.79
• Purity: 98.24%
• Formula: C₄₁H₄₂N₄O₈
• SMILES: COC(=O)CCc1c(C)c2cc3[nH]c(cc4nc(cc5[nH]c(cc1n2)c(CCC(O)=O)c5C)[C@]1(C)[C@H](C(=O)OC)C(=CC=C41)C(=O)OC)c(C)c3C=C
• Target: YAP,Photosensitizer,Apoptosis,Autophagy,VDA
• Solubility: H2O:< 1 mg/mL (insoluble or slightly soluble);DMSO:130 mg/mL (180.86 mM);Ethanol:< 1 mg/mL (insoluble or slightly soluble);10% DMSO+40% PEG300+5% Tween 80+45% Saline:5 mg/mL (6.96 mM)

Bioactivity

• Target IC50:
  OMM1 cells:5.89 μM|Mel 270 cells:6.43 μM|Omm 2.3 cells:7.27 μM
• In Vivo:
  Verteporfin forms a complex with LDL, which may be taken up by proliferating cells (e.g., neovascular endothelial cells) through LDL receptors or endocytosis. The therapy with Verteporfin achieves complete vascular occlusion through thrombosis in the vascular channels following selective endothelial damage. As shown by optical and electron microscopy, Verteporfin therapy selectively induces occlusion in regenerating and detached choroidal capillaries, without altering the overlying photoreceptors or ganglion cells. Verteporfin rapidly exhibits apoptotic changes in conjunction with light, as demonstrated by the activation of caspase-3 and caspase-9 and the cleavage of PARP in HL-60 cells, changes that are inhibited by the broad-spectrum caspase inhibitor ZVAD.fmk.
• In Vitro:
  Verteporfin metabolizes into a less active form within the body and is rapidly cleared, primarily excreted via feces and to a lesser extent through urine. Its therapy is effective and selectively prevents fluorescein dye leakage from choroidal neovascularization (CNV) induced in experimental monkeys. Verteporfin quickly accumulates in the choroidal vasculature, retinal pigment epithelium (RPE), and photoreceptors of established rabbit eyes. Upon intravenous injection in mice, peak tissue levels of Verteporfin are reached within 3 hours, followed by a rapid decline within 24 hours.
• Cell Research:
  Verteporfin is dissolved in DMSO. PDX cells co-cultured with S17 cells are treated with 16 combinations of verteporfin (60 nM, 120 nM, 180 nM, and 240 nM) and dasatinib (12 nM, 24 nM, 36 nM, and 48 nM). The viabilities of cells treated with each combination are measured after 48 h using FACS Aria flow cytometer. In order to estimate drug interaction between verteporfin and dasatinib, a normalized isobologram and fraction affectedcombination index (CI) plot are made using CompuSyn software. CI values greater than 1.0 indicated antagonistic effects, equal to 1.0 additive effects, and below 1.0 synergistic effects.

Storage & Handling

• Storage: keep away from direct sunlight,keep away from moisture,store at low temperature | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

CL318952, CL-318952, CL 318952, Apoptosis, Autophagy, BPD-MA, Inhibitor, inhibit, Yes-associated protein, YAP, Verteporfin, VDA

Compound Identifiers

PubChem CID

91181808