Exposure of the COLO205 cells to Cucurbitacin I significantly decreases cell viability. The anticancer activity of Cucurbitacin I is accomplished by downregulating p-STAT3 and MMP-9 expression^[1] . PE-induced cell enlargement and upregulation of ANF and β-MHC are significantly suppressed by pretreatment of the cardiomyocytes with Cucurbitacin I. Notably, Cucurbitacin I also impaires connective tissue growth factor (CTGF) and MAPK signaling, pro-hypertrophic factors, as well as TGF-β/Smad signaling, the important contributing factors to fibrosis^[2] . Incubation of the Seax cell line with the Jak/Stat3 inhibitor Cucurbitacin I result in a time- and concentration-dependent decrease of P-Stat3 and Stat3. In freshly isolated Sz cells (n=3), Cucurbitacin I induces a concentration-dependent decrease in Stat3 expression whereas P-Stat3 is undetectable. Finally, incubation of freshly isolated Sz cells (n=4) with 30 μM Cucurbitacin I for 6 hours induces apoptosis in the large majority (73-91%) of tumor cells^[3] .

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

No major side effects are noted throughout the study. It is shown that average tumor volumes at the end of the study are as follows: control, 616 mm³ (±130); CQ, 580 mm³ (±107); Cucurbitacin I, 346mm³ (±79); and combination, 220mm³ (±62). The differences in tumor volume between the Cucurbitacin I and control, combination and control, and combination and Cucurbitacin I arms are significant. Furthermore, combination-treated tumors exhibit a significantly lower average tumor weight at study termination than the control. Moreover, there was no effect on the body weights of mice^[4] .

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

514.65

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2222-07-3

葫芦素 I

CC(C)(C1=CC[C@@]2([H])[C@@]3(C[C@@H](O)[C@@H]([C@]3(C4)C)[C@@](C)(O)C(/C=C/C(C)(O)C)=O)C)C(C(O)=C[C@@]1([H])[C@]2(C)C4=O)=O

Room temperature in continental US; may vary elsewhere.

Powder-20°C3 years4°C2 yearsIn solvent-80°C6 months-20°C1 month

In Vitro: 

DMSO : ≥ 100 mg/mL (194.31 mM)

* "≥" means soluble, but saturation unknown.

Preparing
Stock Solutions

ConcentrationSolventMass1 mg5 mg10 mg1 mM1.9431 mL9.7153 mL19.4307 mL5 mM0.3886 mL1.9431 mL3.8861 mL10 mM0.1943 mL0.9715 mL1.9431 mL

*

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: ≥ 3 mg/mL (5.83 mM); Clear solution

  
  

• 2.

  
  

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

  Solubility: ≥ 3 mg/mL (5.83 mM); Clear solution

  
  

• 3.

  
  

  请依序添加每种溶剂： 10% DMSO    90% corn oil

  Solubility: ≥ 3 mg/mL (5.83 mM); Clear solution

  
  

*以上所有助溶剂都可在 MCE 网站选购。

• [1]. Song J, et al. Cucurbitacin I inhibits cell migration and invasion and enhances chemosensitivity in colon cancer. Oncol Rep. 2015 Apr;33(4):1867-71.

  [2]. van Kester MS, et al. Cucurbitacin I inhibits Stat3 and induces apoptosis in Sézary cells. J Invest Dermatol. 2008 Jul;128(7):1691-5.

  [3]. Jeong MH, et al. Cucurbitacin I Attenuates Cardiomyocyte Hypertrophy via Inhibition of Connective Tissue Growth Factor (CCN2) and TGF- β/Smads Signalings. PLoS One. 2015 Aug 21;10(8):e0136236.

  [4]. Yuan G, et al. Cucurbitacin I induces protective autophagy in glioblastoma in vitro and in vivo. J Biol Chem. 2014 A