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Verteporfin

CAS号

129497-78-5

分子式

C41H42N4O8

主要靶点

Apoptosis|YAP|VDA|Autophagy

仅限科研使用

Cat No : CM00566

Print datasheet

Synonyms

Inhibitor|VDA|YAP|Yes-associated protein|Verteporfin|维替泊芬|Apoptosis|CL 318952|CL318952|CL-318952|Autophagy|BPD-MA|inhibit

验证数据展示

  • CAS No.: 129497-78-5

    Verteporfin
    CAS#: 129497-78-5

产品信息

CAS号 129497-78-5
分子式 C41H42N4O8
主要靶点 Apoptosis|YAP|VDA|Autophagy
主要通路 凋亡|血管生成|干细胞|自噬
分子量 718.79
纯度 99.82%， 此纯度可做参考，具体纯度与批次有关系，可咨询客服
储存条件 keep away from direct sunlight,keep away from moisture | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice.
别名 Inhibitor|VDA|YAP|Yes-associated protein|Verteporfin|维替泊芬|Apoptosis|CL 318952|CL318952|CL-318952|Autophagy|BPD-MA|inhibit

体内活性

方法：为检测体内抗肿瘤活性，将 Verteporfin (100 mg/kg) 腹腔注射给携带人胰腺癌肿瘤 PANC‐1 或 SW1990 的 BALB/c nude 小鼠，每两天一次，持续三周。 结果：Verteporfin 抑制 PDAC 异种移植物模型中的肿瘤生长。[2] 方法：为检测体内抗肿瘤活性，将 Verteporfin (100 mg/kg) 腹腔注射给 DSS 诱导结肠癌的 C57BL/6 小鼠，每三天一次，给药六次。 结果：Verteporfin 治疗显著且快速地降低了肿瘤的多重性和肿瘤大小。[3]

体外活性

方法：葡萄膜黑色素瘤细胞 92.1、Mel 270、Omm 1 和 Omm 2.3 用 Verteporfin (0-10 μM) 处理 72 h，使用 MTS 方法检测细胞活力。 结果：Verteporfin 剂量依赖性显著抑制 92.1、Mel 270、Omm 1 和 Omm 2.3 细胞的细胞活力，IC50 分别为 4.67 μM、6.43 μM、5.89 μM 和 7.27 μM。[1] 方法：人胰腺癌细胞 PANC-1 和 SW1990 用 Verteporfin (1-8 μM) 处理 24 h，使用 Western Blot 方法检测靶点蛋白表达水平。 结果：Verteporfin 以剂量依赖的方式抑制了总 YAP、p-YAP 和 TEAD 的表达。Verteporfin 还增加了 Bax 的表达，降低了 Bcl-2 的表达，并激活了 PARP。Verteporfin 以剂量依赖的方式抑制 cyclinD1 或 cyclinE1 的表达。[2]

溶解度

H2O:< 1 mg/mL (insoluble or slightly soluble);Ethanol:< 1 mg/mL (insoluble or slightly soluble);DMSO:100 mg/mL (139.12 mM)

细胞实验

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.

参考文献

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.

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