WZB117 is a glucose transporter 1 (Glut1) inhibitor, which downregulates glycolysis, induces cell-cycle arrest, and inhibits cancer cell growth in vitro and in vivo.

Glucose uptake assays show that WZB117 inhibits glucose transport in cancer cells in a dose-dependent manner. The inhibition of glucose transport induced by WZB117 occurres within 1 minute after the assay started, suggesting that the inhibitory activity is likely to be via a direct and fast mechanism. Cell viability assay shows that WZB117 inhibits cancer cell proliferation with an IC₅₀ of approximately 10 μM. The inhibitory activity of WZB117 on cancer cell growth is also confirmed with a clonogenic assay, which also indicates that the inhibition is irreversible in nature. WZB117 treatment results in significantly more cell growth inhibition in lung cancer A549 cells than in nontumorigenic lung NL20 cells. Similar results are also observed in breast cancer MCF7 cells and their nontumorigenic MCF12A cells. When WZB117 is added to cancer cells grown under hypoxic conditions, more cell growth inhibition is observed than under normoxic conditions^[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.

The animal study shows that after daily intraperitoneal injection of WZB117 at 10 mg/kg body weight, the sizes of the compound-treated tumors are on average more than 70% smaller than those of the mock (PBS/DMSO)-treated tumors. Notably, 2 of the 10 compound-treated tumors disappear during the treatment and never grow back even at the end of the study. Body weight measurement and analysis reveal that the mice treated with WZB117 lost about 1 to 2 grams of body weight compared with the mock-treated mice with most of the weight loss in the fat tissue. Blood counts and analysis of mice at the end of the study show that lymphocytes and platelets are changed in the compound-treated mice compared with the vehicle-treated mice, but the cell counts remained in the normal ranges. One of the concerns for using glucose transport inhibitors is that the inhibitor might produce hyperglycemia in the treated mice^[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.

368.31

C₂₀H₁₃FO₆

1223397-11-2

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 : ≥ 150 mg/mL (407.27 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: ≥ 2.5 mg/mL (6.79 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (6.79 mM，饱和度未知) 的澄清溶液。

  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% (20% SBE-β-CD in saline)

  Solubility: ≥ 2.5 mg/mL (6.79 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (6.79 mM，饱和度未知) 的澄清溶液。

  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 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: ≥ 2.5 mg/mL (6.79 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (6.79 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]. Liu Y, et al. A small-molecule inhibitor of glucose transporter 1 downregulates glycolysis, induces cell-cycle arrest, and inhibits cancer cell growth in vitro and in vivo. Mol Cancer Ther. 2012 Aug;11(8):1672-82.

Human non-small cell lung cancer (NSCLC) cell lines H1299 and A549, human breast ductal carcinoma MCF7, as well as human nontumorigenic NL20 lung and MCF12A breast cells are maintained in cell culture media. Cells are treated with WZB117 for 24 or 48 hours. WZB117 (10 μM) is used in the experiments unless otherwise noted. Mock-treated and glucose deprivation samples served as negative and positive controls, respectively. In glucose deprivation, Dulbecco’s Modified Eagle’s Media (DMEM) with reduced glucose concentration (2 mM or 8% of glucose concentration in the regular cell culture medium) is prepared by mixing glucose-free DMEM with regular DMEM^[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^[1]
Male NU/J nude mice of 6 to 8 weeks of age are used. To determine the in vivo anticancer efficacy of WZB117 on human tumor xenograft growth, NSCLC A549 cells in exponential growth phase are harvested, washed, precipitated, and resuspended in PBS. Each mouse is injected subcutaneously with 5×10⁶ cancer cells in the flank. Compound treatment started 3 days after the cancer cells injection and when all tumors become palpable. Tumor cell–injected mice are randomly divided into 2 groups: control group (n=10) treated with PBS/DMSO (1:1, v/v) and WZB117 treatment group (n=10) treated with WZB117 (10 mg/kg body weight) dissolved in PBS/DMSO solution (1:1, v/v). Mice are given intraperitoneal injection with either PBS/DMSO vehicle or WZB117 (10 mg/kg) daily for 10 weeks. Tumor sizes are measured every 7 days with calipers, and tumor volume is calculated^[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.

• [1]. Liu Y, et al. A small-molecule inhibitor of glucose transporter 1 downregulates glycolysis, induces cell-cycle arrest, and inhibits cancer cell growth in vitro and in vivo. Mol Cancer Ther. 2012 Aug;11(8):1672-82.