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细胞生物学 囊泡 肿瘤
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自噬 TEAD Antiparasitic 细胞凋亡诱导剂 凋亡
/ Verteporfin/维替泊芬

Verteporfin/维替泊芬 {[allProObj[0].p_purity_real_show]}

货号：A138297 同义名： CL 318952; BPD-MA

Verteporfin（维替泊芬)是一种YAP抑制剂，有效地破坏YAP-TEAD相互作用并诱导细胞凋亡，同时作为自噬抑制剂，通过阻止自噬体的形成来特异性阻断自噬的早期阶段。Verteporfin作为一种光敏剂，能够在光照下生成活性氧物质，IC50 值为 0.6 nM。Verteporfin 具有抗肿瘤和抗血管生成作用，可用于光动力疗法和年龄相关性黄斑变性的研究。

Verteporfin/维替泊芬 化学结构 CAS号：129497-78-5
Verteporfin/维替泊芬 化学结构
CAS号：129497-78-5
Verteporfin/维替泊芬 3D分子结构
CAS号：129497-78-5
Verteporfin/维替泊芬 化学结构 CAS号：129497-78-5
Verteporfin/维替泊芬 3D分子结构 CAS号：129497-78-5
规格 价格 会员价 库存 数量
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Verteporfin/维替泊芬 纯度/质量文件 产品仅供科研

货号：A138297 标准纯度： {[allProObj[0].p_purity_real_show]}
批次查询： 批次纯度:

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产品名称 Autophagy ↓ 其他靶点 纯度
SBI-0206965 +++

ULK1, IC50: 108 nM

ULK2, IC50: 711 nM

 		95%
Hydroxychloroquine sulfate ✔ 99%
Valproic acid sodium ✔ HDAC 97%
PFK-015 ++

PFKFB3, IC50: 207 nM

 		99%+
MRT68921 HCl ++++

ULK1, IC50: 2.9 nM

ULK2, IC50: 1.1 nM

 		99%+
ROC-325 ✔ 99%+
Autophinib +++

Autophagy, IC50: 40 nM

 		99%
Lys05 ✔ 99%+
1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多，抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用，但抑制强度暂时没有相关数据。

Verteporfin/维替泊芬 生物活性

靶点

  • VDA
描述 Verteporfin (CL 318952) is utilized as a photosensitizer in photodynamic therapy aimed at eradicating abnormal blood vessels in the eye, particularly in conditions like age-related macular degeneration. It also functions as a YAP inhibitor, effectively disrupting YAP-TEAD interactions and inducing apoptosis in cells[1]. Additionally, Verteporfin acts as an autophagy inhibitor, specifically blocking the early stages of autophagy by preventing autophagosome formation[3].
体内研究

In vivo studies have demonstrated that Verteporfin, administered at 10 mg/kg through c.s.c., significantly reduces the leukemia cell ratio in combination with BMS-354825. This combined therapy further decreases the number of leukemia cells found in the spleen[1].
体外研究

In a specific PDX-cell screening, Verteporfin demonstrated varying levels of efficacy. The concentrations required to achieve 50% growth inhibition (GI50) in PhLO, PhLH, and PhLK cells were 228 nM, 395 nM, and 538 nM, respectively. For other cell types such as ALL-1, TCC-Y/sr, and NPhA1, the GI50 values were significantly higher, at 3.93 μM, 2.11 μM, and 5.61 μM, respectively. The presence of glutathione (GSH) notably decreased the sensitivity of two out of three PDX cell models to Verteporfin. Furthermore, Verteporfin has been shown to lower the mitochondrial membrane potential in PDX cells[1].

Verteporfin also plays a role in reducing PTX-resistance in HCT-8/T cells by downregulating YAP expression. The combined use of Verteporfin with NSC 125973 exhibits synergistic effects in inhibiting YAP and enhancing cytotoxicity against HCT-8/T cells[2].
作用机制 Verteporfin is transported in the plasma primarily by lipoproteins and once been activated by light in the presence of oxygen, highly reactive, short-lived singlet oxygen and reactive oxygen radicals are generated. Light activation of verteporfin can locally damage neovascular endothelium, resulting in vessel occlusion. Damaged endothelium is known to release procoagulant and vasoactive factors through the lipo-oxygenase (leukotriene) and cyclo-oxygenase (eicosanoids such as thromboxane) pathways, resulting in platelet aggregation, fibrin clot formation and vasoconstriction. Verteporfin appears to somewhat preferentially accumulate in neovasculature, including choroidal neovasculature. However, animal models indicate that the drug is also present in the retina. As singlet oxygen and reactive oxygen radicals are cytotoxic, Verteporfin can also be used to destroy tumor cells. https://www.drugbank.ca/drugs/DB00460

Verteporfin/维替泊芬 细胞实验

Cell Line
Concentration Treated Time Description References
hiPSC-CMs 0.1, 1, 10, 50, 100 μM 24 h To pharmacologically inhibit YAP activity and assess its impact on hiPSC-CMs proliferation. Results showed that verteporfin treatment did not significantly reduce hiPSC-CMs proliferation. Cell Stem Cell. 2020 Jul 2;27(1):50-63.e5.
Huh-7 1μM To validate the sensitivity of ARID1A-silenced cells to Verteporfin. Nat Commun. 2022 Dec 14;13(1):7748.
HLE 1μM To validate the sensitivity of ARID1A-silenced cells to Verteporfin. Nat Commun. 2022 Dec 14;13(1):7748.
Hepa1-6 cells 0.25 to 1 μM 48 h Inhibition of YAP/TEAD complex, reduction of PAI-1 expression and secretion Cell Commun Signal. 2020 Oct 23;18(1):166.
Sk-Hep1 cells 0.25 to 1 μM 48 h Inhibition of YAP/TEAD complex, reduction of PAI-1 expression and secretion Cell Commun Signal. 2020 Oct 23;18(1):166.
HEK293A cells 6.45 µM 18 h Inhibition of the YAP-TEAD interaction reduces expression of CAV1 and CAVIN1 Curr Biol. 2019 Jan 21;29(2):242-255.e6.
Panc-1 cells 100 nM 48 h To evaluate the effect of Verteporfin on YAP1-TEAD interaction, results showed that Verteporfin significantly reduced the expression of YAP1 target genes. J Transl Med. 2020 Feb 13;18(1):77.
4T1 TNBC cells 0.25 μM 90 min The combination of PDT with 5-ADC exerted a synergistic cytotoxic effect on 4T1 cells in vitro, significantly reducing cell proliferation and viability. Front Immunol. 2023 Nov 7;14:1188087.
4T1 TNBC cells 0.15 μM 90 min The combination of PDT with 5-ADC exerted a synergistic cytotoxic effect on 4T1 cells in vitro, significantly reducing cell proliferation and viability. Front Immunol. 2023 Nov 7;14:1188087.
Huh-7 cells 1 μM To validate the sensitivity of Huh-7 cells to Verteporfin after ARID1A silencing, results showed that ARID1A-silenced Huh-7 cells were more sensitive to Verteporfin. Nat Commun. 2022 Dec 14;13(1):7748.
HLE cells 1 μM To validate the sensitivity of HLE cells to Verteporfin after ARID1A silencing, results showed that ARID1A-silenced HLE cells were more sensitive to Verteporfin. Nat Commun. 2022 Dec 14;13(1):7748.

Verteporfin/维替泊芬 动物实验

Species
Animal Model
Administration Dosage Frequency Description References
Balb/c mice 4T1 breast cancer model Intravenous injection 15mg/kg Single dose, lasting 5 days The combination of PDT with 5-ADC significantly increased the expression of splenic CD4+ and CD8+ T cells in vivo, suppressing tumor metastasis. Front Immunol. 2023 Nov 7;14:1188087.
Mice B16 melanoma model Intraperitoneal injection 2 mg/mouse Every two days Verteporfin combined with anti-PD-1 antibody or GM-Vac significantly suppressed tumor growth and enhanced the proportion of IFNγ-producing CD8+ and CD4+ T cells in the tumor microenvironment. Cancer Discov. 2018 Aug;8(8):1026-1043
Mice PVR mouse model Intraperitoneal injection 100 mg/kg Every other day for 4 weeks Verteporfin attenuated the upregulation of Cyclin D1, C-Myc, and Bcl-xl proteins in the PVR mouse model by inhibiting the YAP signaling pathway, indicating its therapeutic potential for PVR. Invest Ophthalmol Vis Sci. 2022 Jul 8;63(8):24

Verteporfin/维替泊芬 动物研究

Dose Mice: 2 mg/kg - 6 mg/kg[1] (i.p.), 10 mg/kg[2] (i.p.), 100 mg/kg[3] (i.p.)
Rat: 0.25 mg/kg - 1 mg/kg[4] (i.v.)
Cynomolgus monkey: 0.25 mg/kg - 1 mg/kg[5] (i.v.)
Administration i.p., i.v.
Pharmacokinetics
Animal Rats[6]
Dose 2 mg/kg
Administration i.v.
AUC0-inf 13.653 μg·h/ml (male)
12.628 μg·h/ml (female)
T1/2 7.12 h (male)
2.94 h (female)
Tmax 0.017 h (male)
0.017 h (female)
CL 2.44 ml/min/kg (male)
2.64 ml/min/kg (female)
Cmax 20.360 μg/ml (male)
25.203 μg/ml (female)
Vss 0.57 L/kg (male)
0.35 L/kg (female)
AUC0→t 9.297 μg·h/ml (male)
11.323 μg·h/ml (female)

Verteporfin/维替泊芬 临床研究

NCT号 适应症或疾病 临床期 招募状态 预计完成时间 地点
NCT00211484 Age-Related Macular Degenerati... 展开 >>ons. Subfoveal Neovascularization. 收起 << Phase 2 Completed - United States, New York ... 展开 >> Manhattan Eye, Ear & Throat Hospital New York, New York, United States, 10021 收起 <<
NCT02587767 Acute Central Serous Chorioret... 展开 >>inopathy 收起 << Not Applicable Active, not recruiting December 2018 China, Guangdong ... 展开 >> Zhongshan Ophthalmic Center, Sun Yat-sen University Guangzhou, Guangdong, China, 510060 收起 <<
NCT02072408 Polypoidal Choroidal Vasculopa... 展开 >>thy Without Active Polyp 收起 << Phase 4 Completed - Korea, Republic of ... 展开 >> Seoul National University Bundang Hospital Seongnam, Gyunggi-do, Korea, Republic of Konyang University Kim's Eye Hospital Seoul, Korea, Republic of Samsung Medical Center Seoul, Korea, Republic of 收起 <<

Verteporfin/维替泊芬 参考文献

[1]Morishita T, et al. The photosensitizer verteporfin has light-independent anti-leukemic activity for Ph-positive acute lymphoblastic leukemia and synergistically works with BMS-354825. Oncotarget. 2016 Aug 2.

[2]Pan W, et al. Verteporfin can Reverse the NSC 125973 Resistance Induced by YAP Over-Expression in HCT-8/T Cells without Photoactivation through Inhibiting YAP Expression. Cell Physiol Biochem. 2016;39(2):481-90.

[3]Donohue E, et al. The autophagy inhibitor verteporfin moderately enhances the antitumor activity of gemcitabine in a pancreatic ductal adenocarcinoma model.J Cancer. 2013 Aug 28;4(7):585-96.

Verteporfin/维替泊芬 实验方案

计算器
存储液制备 1mg 5mg 10mg

1 mM

5 mM

10 mM

1.39mL

0.28mL

0.14mL

6.96mL

1.39mL

0.70mL

13.91mL

2.78mL

1.39mL

Verteporfin/维替泊芬 技术信息

CAS号129497-78-5
分子式C41H42N4O8
分子量 718.79
SMILES Code NONE
MDL No. MFCD28098202
别名 CL 318952; BPD-MA; DB00460, CL 318952, BPD-MA, BpdMA, Benzoporphyrin D, Benzoporphyrin derivative monoacid ring A, Verteporfin, Visudyne.
运输蓝冰
存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Keep in dark place, inert atmosphere, store in freezer, under -20°C
溶解方案

DMSO: 50 mg/mL，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO

DMF: 10 mg/mL，配合低频超声，并水浴加热至45℃助溶

请根据您的动物给药指南选择适当的溶解方案。
以下溶解方案都请先按照体外实验的方式配制澄清的储备液，再依次添加助溶剂：
——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议现用现配，当天使用； 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶
方案 一
方案 二
配制的工作液建议现用现配，短期内尽快用完。 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶。
方案 一
方案 二

Tags: Verteporfin | 129497-78-5 | CL 318952 | CL318952 | CL-318952 | YAP Inhibitor | Stem Cell/Wnt | Apoptosis | Autophagy | YAP | Apoptosis | Autophagy | 仅供科研使用 | AmBeed-信号通路专用抑制剂 | Verteporfin/维替泊芬 纯度/质量文件 | Verteporfin/维替泊芬 亚型比较 | Verteporfin/维替泊芬 生物活性 | Verteporfin/维替泊芬 动物研究 | Verteporfin/维替泊芬 临床数据 | Verteporfin/维替泊芬 参考文献 | Verteporfin/维替泊芬 实验方案 | Verteporfin/维替泊芬 技术信息

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