Verteporfin (CL 318952) is a photosensitizer for photodynamic therapy to eliminate the abnormal blood vessels in the eye associated with conditions such as age-related macular degeneration. Verteporfin is a YAP inhibitor which disrupts YAP-TEAD interactions. Verteporfin induces cell apoptosis^[1]. Verteporfinis an autophagy inhibitor that blocks autophagy at an early stage by inhibiting autophagosome formation^[3].

IC50: YAP-TEAD interaction

Verteporfin is specifically selected by PDX-cell screening. The concentrations to cause 50% growth inhibition (GI₅₀) for PhLO, PhLH, and PhLK are 228 nM, 395 nM, and 538 nM, respectively, whereas GI₅₀ for ALL-1, TCC-Y/sr, and NPhA1 are 3.93 µM, 2.11 µM, and 5.61 µM, respectively. GSH significantly reduces the sensitivity of 2 out of 3 PDX cells to verteporfin. Verteporfin reduces the mitochondrial membrane potential in PDX cells^[1]. Verteporfin reduces the PTX-resistance on HCT-8/T cells by inhibiting YAP expression and combination therapy with verteporfin and NSC 125973 shows synergism on inhibition of YAP and cytotoxicity to HCT-8/T^[2].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Verteporfin (10 mg/kg, c.s.c.) and BMS-354825 significantly reduces the leukemia cell ratio, and combined therapy further reduced the number of leukemia cells in the spleen^[1].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

718.79

C₈₂H₈₄N₈O₁₆

129497-78-5

维替泊芬

Room temperature in continental US; may vary elsewhere.

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

DMSO : 75 mg/mL (104.34 mM; Need ultrasonic)

DMF : 25 mg/mL (34.78 mM; Need ultrasonic)

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (protect from light)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 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，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制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

• 1.

  请依序添加每种溶剂： 0.5% CMC-Na/saline water

  Solubility: 10 mg/mL (13.91 mM); Suspended solution; Need ultrasonic
• 2.

  请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

  Solubility: ≥ 7.5 mg/mL (10.43 mM); Clear solution

  此方案可获得 ≥ 7.5 mg/mL (10.43 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 75.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

• 3.

  请依序添加每种溶剂： 10% DMSO    90% (20% SBE-β-CD in saline)

  Solubility: ≥ 7.5 mg/mL (10.43 mM); Clear solution

  此方案可获得 ≥ 7.5 mg/mL (10.43 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 75.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

  将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
• 4.

  请依序添加每种溶剂： 10% DMSO    90% corn oil

  Solubility: ≥ 7.5 mg/mL (10.43 mM); Clear solution

  此方案可获得 ≥ 7.5 mg/mL (10.43 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 75.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

• 5.

  请依序添加每种溶剂： 10% DMF    40% PEG300    5% Tween-80    45% saline

  Solubility: ≥ 2.5 mg/mL (3.48 mM); Clear solution
• 6.

  请依序添加每种溶剂： 10% DMF    90% (20% SBE-β-CD in saline)

  Solubility: 2.5 mg/mL (3.48 mM); Suspended solution; Need ultrasonic
• 7.

  请依序添加每种溶剂： 10% DMF    90% corn oil

  Solubility: 2.5 mg/mL (3.48 mM); Clear solution; Need ultrasonic

• [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.

PDX cells co-cultured with S17 cells are treated with 16 combinations of verteporfin (60 nM, 120 nM, 180 nM, and 240 nM) and BMS-354825 (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 BMS-354825, 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.

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

Mice: PhLO cells (1.0×10⁷/mouse) are injected intravenously into 6-week-old male NOG mice, which are then treated with vehicle, verteporfin (140 mg/kg/day), BMS-354825 (20 mg/kg/day), and a combination of these drugs from days 22 to 28. Verteporfin is administered by continuous subcutaneous infusion (c.s.c.) using Alzet osmotic pumps. An intraperitoneal injection (i.p.) is performed for BMS-354825. All mice are sacrificed on day 28 and the chimerism of leukemia cells is investigated by flow cytometer using an anti-human CD19 antibody and antimouse CD45 antibody. Blood concentrations of verteporfin are calculated by LCMS-2020.

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

• [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.