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Verteporfin

Catalog No. T3112 CAS 129497-78-5

Synonyms: BPD-MA, CL 318952

Verteporfin (BPD-MA) is a YAP inhibitor that inhibits YAP-TEAD interactions. Verteporfin is also a photosensitizer used in photodynamic therapy. Verteporfin also induces apoptosis and inhibits autophagy.

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Verteporfin, CAS 129497-78-5

Pack Size	Availability	Price/USD
1 mg	In stock	$ 34.00
2 mg	In stock	$ 47.00
5 mg	In stock	$ 77.00
10 mg	In stock	$ 117.00
25 mg	In stock	$ 237.00
50 mg	In stock	$ 385.00
100 mg	In stock	$ 486.00
1 mL * 10 mM (in DMSO)	In stock	$ 123.00

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Purity: 99.82%

Purity: 98.27%

Purity: 98.03%

Purity: 98%

Purity: 96.75%

Purity: 95.37%

Biological Description

Chemical Properties

Storage & Solubility Information

Description	Verteporfin (BPD-MA) is a YAP inhibitor that inhibits YAP-TEAD interactions. Verteporfin is also a photosensitizer used in photodynamic therapy. Verteporfin also induces apoptosis and inhibits autophagy.
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.
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.
Kinase Assay	Cells (5 × 103) are plated in 96 well plates. Cells are treated the next day for 24 to 48 hours and then assessed for caspase-3 activity by Caspase-Glo-3/7 Assay, as per manufacturer's instructions and a luminescence plate reader.
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.

Synonyms	BPD-MA, CL 318952
Molecular Weight	718.79
Formula	C41H42N4O8
CAS No.	129497-78-5

Storage

keep away from direct sunlight

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

Ethanol: < 1 mg/mL (insoluble or slightly soluble)

DMSO: 93 mg/mL (129.4 mM)

H2O: < 1 mg/mL (insoluble or slightly soluble)

References and Literature

1. Ma YW, et al. Verteporfin induces apoptosis and eliminates cancer stem-like cells in uveal melanoma in the absence of light activation. Am J Cancer Res. 2016 Dec 1;6(12):2816-2830. 2. Wei H, et al. Verteporfin suppresses cell survival, angiogenesis and vasculogenic mimicry of pancreatic ductal adenocarcinoma via disrupting the YAP-TEAD complex. Cancer Sci. 2017 Mar;108(3):478-487. 3. Zhang H, et al. Tumor-selective proteotoxicity of verteporfin inhibits colon cancer progression independently of YAP1. Sci Signal. 2015 Oct 6;8(397):ra98. 4. Isfort I, Elges S, Cyra M, et al. Prevalence of the Hippo Effectors YAP1/TAZ in Tumors of Soft Tissue and Bone[J]. Scientific Reports. 2019, 9(1): 1-9. 5. Zhuang Q, Li F, Liu J, et al. Nuclear exclusion of YAP exacerbates podocyte apoptosis and disease progression in Adriamycin-induced focal segmental glomerulosclerosis[J]. Laboratory Investigation. 2021, 101(2): 258-270. 6. Ilka Isfort, Magdalene Cyra, Sandra Elges, Sareetha Kailayangiri, Bianca Altvater, Claudia Rossig, Konrad Steinestel et al. SS18-SSX-dependent YAP/TAZ Signaling in Synovial Sarcoma [J]. Clinical Cancer Research. 2019 Feb 27: clincanres-3553. 7. Marcel Trautmann, Ya-Yun Cheng, Patrizia Jensen, Ninel Azoitei, Ines Brunner, Jennifer Hüllein, Mikolaj Slabicki et al. Requirement for YAP1 signaling in myxoid liposarcoma [J]. EMBO molecular medicine. 2019 May;11(5): e9889. 8. Tang Y, Fang G, Guo F, et al. Selective Inhibition of STRN3-Containing PP2A Phosphatase Restores Hippo Tumor-Suppressor Activity in Gastric Cancer[J]. Cancer Cell. 2020, 38(1): 115-128. e9. 9. Peng G, Suo S, Cui G, et al. Molecular architecture of lineage allocation and tissue organization in early mouse embryo[J]. Nature. 2019, 572(7770): 528-532.

Citations

1. Peng G, Suo S, Cui G, et al. Molecular architecture of lineage allocation and tissue organization in early mouse embryo. Nature. 2019, 572(7770): 528-532. 2. Tang Y, Fang G, Guo F, et al. Selective Inhibition of STRN3-Containing PP2A Phosphatase Restores Hippo Tumor-Suppressor Activity in Gastric Cancer. Cancer Cell. 2020, 38(1): 115-128. e9. 3. Isfort I, Cyra M, Elges S, et al. SS18-SSX-dependent YAP/TAZ Signaling in Synovial Sarcoma. Clinical Cancer Research. 2019, 25(12): 3718-3731 4. Trautmann M, Cheng Y Y, Jensen P, et al. Requirement for YAP1 signaling in myxoid liposarcoma. EMBO Molecular Medicine. 2019, 11(5): e9889 5. Zhuang Q, Li F, Liu J, et al. Nuclear exclusion of YAP exacerbates podocyte apoptosis and disease progression in Adriamycin-induced focal segmental glomerulosclerosis. Laboratory Investigation. 2021, 101(2): 258-270. 6. Isfort I, Elges S, Cyra M, et al. Prevalence of the Hippo Effectors YAP1/TAZ in Tumors of Soft Tissue and Bone. Scientific Reports. 2019, 9(1): 1-9

Related compound libraries

This product is contained In the following compound libraries：

Anti-Cancer Clinical Compound Library Anti-Cancer Drug Library Drug Repurposing Compound Library Inhibitor Library EMA Approved Drug Library Anti-Cancer Approved Drug Library Pediatric Drug Library Anti-Cancer Compound Library Angiogenesis related Compound Library Clinical Compound Library

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Keywords

Verteporfin 129497-78-5 Angiogenesis Apoptosis Autophagy Stem Cells YAP VDA CL318952 inhibit BPD-MA Yes-associated protein CL-318952 Inhibitor CL 318952 inhibitor

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