Cucurbitacin E is a natural compound which from the climbing stem of Cucumic melo L. Cucurbitacin E significantly suppresses the activity of the cyclin B1/CDC2 complex.

To explore the antitumor activity of Cucurbitacin E (CuE) against colorectal cancer (CRC) cells, an in vitro study is initiated in which each of the CRC cell lines is exposed to increasing doses of Cucurbitacin E (0, 2.5, 5, and 7.5 μM) over a period of 24 h. The proliferation of the Cucurbitacin E-treated cancer cells is then measured using the MTT method. Cucurbitacin E is shown to induce morphological changes in the primary colon cancer cells. Microscopic observation showed that following exposure to Cucurbitacin E (5 μM) between 6 and 24 h, the primary colon cancer cells underwent a remarkable change in morphology. Cucurbitacin E inhibits tumor growth by arresting the cell cycle in the G₂/M phase via GADD45γ gene expression and the blockage of cyclin B1/CDC2 complex in primary CRC cells^[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.

A high fat diet mice model of metabolic syndrome (HFD-MetS) is developed to assess the role of Cucurbitacin E (CuE) on body weight and fat tissue biology. Significant decrease in body weights of HFD-MetS mice treated with Cucurbitacin E (0.5mg/kg) are found as compared to HFD-MetS mice treated with vehicle alone. Cucurbitacin E treatment reduces all fat pads weights in HFD-MetS mice. 55% reduction is observed in total fat in mice, after treatment with Cucurbitacin E in comparison to HFD-MetS mice. Abdominal obesity is strongly associated with metabolic syndrome. Central obesity is reduced to 50% after Cucurbitacin E treatment as compared to HFD MetS mice, elucidating the effectiveness of Cucurbitacin E in targeting MetS^[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.

556.69

C₃₂H₄₄O₈

18444-66-1

葫芦素 E

Room temperature in continental US; may vary elsewhere.

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

In Vitro: 

DMSO : 50 mg/mL (89.82 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。-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。

In Vivo:

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： 10% DMSO    40% PEG300    5% Tween-80    45% saline

  Solubility: 2.5 mg/mL (4.49 mM); Suspended solution; Need ultrasonic

  此方案可获得 2.5 mg/mL (4.49 mM) 的均匀悬浊液，悬浊液可用于口服和腹腔注射。

  以 1 mL 工作液为例，取 100 μL 25.0 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

• 2.

  请依序添加每种溶剂： 10% DMSO    90% corn oil

  Solubility: ≥ 2.5 mg/mL (4.49 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (4.49 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 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

• [1]. Hsu YC, et al. Therapeutic ROS targeting of GADD45γ in the induction of G2/M arrest in primary human colorectal cancer cell lines by cucurbitacin E. Cell Death Dis. 2014 Apr 24;5:e1198.

  [2]. Murtaza M, et al. Cucurbitacin E reduces obesity and related metabolic dysfunction in mice by targeting JAK-STAT5 signaling pathway. PLoS One. 2017 Jun 9;12(6):e0178910.

The colorectal cancer (CRC) cells are seeded into 96-well culture plates at 5000 cells/well. The cells are treated with 0, 2.5, 5, and 7.5 μM Cucurbitacin E for 1-3 days. MTT dye (1 mg/mL) is added to each well for at least 4 h of treatment. The reaction is stopped by the addition of DMSO, and optical density is measured at 540 nm on a multi-well plate reader. Background absorbance of the medium in the absence of cells is subtracted. All samples are assayed in triplicate, and the mean for each experiment is calculated. Results are expressed as a percentage of control, which is considered as 100%. Each assay is carried out in triplicate, and the results are expressed as the mean^[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.

Mice^[2]
C57BL/6 male mice are used. The mice are designated as metabolic syndrome mice (HFD-MetS-mice). Briefly, the mice are randomly assigned into two groups according to their diet for 8 weeks (n = 10-12): high fat diet group (HFD) (60% fat, 20% carbohydrate, 20% protein) or the matched low fat, standard diet group (SD) (10% fat, 70% carbohydrate, 20% protein). After eight weeks on high fat diet, the mice with significant obese phenotype and fasting blood glucose levels ≥126 mg/dL are considered MetS mice. The MetS mice are continued on the HFD throughout the study. The MetS mice are then randomly divided into three additional groups, according to the treatment administered by oral gavage for 10 weeks (n=10-12): a low dose 0.25 mg/kg/day of Cucurbitacin E designated as HFD+Cucurbitacin E (L) or high dose 0.5 mg/kg/day of Cucurbitacin E, designated as HFD+Cucurbitacin E (H) or 50 mg/kg/day Orlistat (HFD+Orlistat). Animals on SD are administered 0.5% CMC by oral gavage^[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.

• [1]. Hsu YC, et al. Therapeutic ROS targeting of GADD45γ in the induction of G2/M arrest in primary human colorectal cancer cell lines by cucurbitacin E. Cell Death Dis. 2014 Apr 24;5:e1198.

  [2]. Murtaza M, et al. Cucurbitacin E reduces obesity and related metabolic dysfunction in mice by targeting JAK-STAT5 signaling pathway. PLoS One. 2017 Jun 9;12(6):e0178910.