Cucurbitacin I is a natural selective inhibitor of JAK2/STAT3, with potent anti-cancer activity.

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].

Shanghai Jinpan Biotech Co Ltd 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].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

514.65

C₃₀H₄₂O₇

2222-07-3

葫芦素 I

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 : ≥ 100 mg/mL (194.31 mM)

* “≥” means soluble, but saturation unknown.

*

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

  此方案可获得 ≥ 3 mg/mL (5.83 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 30.0 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% (20% SBE-β-CD in saline)

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

  此方案可获得 ≥ 3 mg/mL (5.83 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 30.0 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
• 3.

  请依序添加每种溶剂： 10% DMSO    90% corn oil

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

  此方案可获得 ≥ 3 mg/mL (5.83 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 30.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

• [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 Apr 11;289(15):10607-19.

Mice^[4]
BALB/c nude (nu/nu) female mice are used. U251 cells (5×10⁶ cells in 50 μL of serum-free DMEM) are inoculated subcutaneously into the right flank of 5-week-old female mice after acclimatization for a week. Tumor growth is measured daily with calipers. When the tumors reach a mean volume of 90-120 mm³, animals are randomized into groups. In the first experiment, 16 mice are randomly assigned to Cucurbitacin I (1 mg/kg/day in 20% DMSO in PBS) or drug vehicle control (20% DMSO in PBS) and dosed intraperitoneally with 100 μL of vehicle or drug once daily for 18 days, whereas, in the second, 20 mice are assigned to four groups. Control animals receive 20% DMSO in PBS vehicle, whereas treated animals are injected with Cucurbitacin I (1 mg/kg/day) in 20% DMSO in PBS, CQ (25 mg/kg/day) in 20% DMSO in PBS, and Cucurbitacin I (1 mg/kg/day) plus CQ (25 mg/kg/day) in 20% DMSO in PBS and dosed intraperitoneally with 100 μL of vehicle or drug once daily for 15 days^[4].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

• [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 Apr 11;289(15):10607-19.