STF-31

上海金畔生物科技有限公司为生命科学和医药研发人员提供生物活性分子抑制剂、激动剂、特异性抑制剂、化合物库、重组蛋白,专注于信号通路和疾病研究领域。

STF-31  纯度: 96.97%

STF-31 是一种葡萄糖转运蛋白 1(GLUT1) 的选择性抑制剂, IC50 为 1 μM。

STF-31

STF-31 Chemical Structure

CAS No. : 724741-75-7

规格 价格 是否有货 数量
10 mM * 1 mL in DMSO ¥1210 In-stock
10 mg ¥1100 In-stock
50 mg ¥4400 In-stock
100 mg   询价  
200 mg   询价  

* Please select Quantity before adding items.

STF-31 相关产品

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生物活性

STF-31 is a selective inhibitor of glucose transporter 1 (GLUT1), with an IC50 of 1μM[1][2].

IC50 & Target[2]

GLUT1

1 μM (IC50)

体外研究
(In Vitro)

STF-31 (0.01-10 μM; 10 days) is specifically toxic to RCC4 cells, whereas RCC4/VHL cells are relatively unaffected. RCC4/VHL cells treated with STF-31 (5 μM; 10 days) largely recovery, whereas RCC4 cells under the same conditions does not[1].
STF-31 (1.25-5 μM; 3 days) does not induce autophagy, apoptosis, or DNA damage. STF-31 causes a necrotic cell death[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.

Cell Viability Assay[1]

Cell Line: Wild-type RCC4 cells (RCC4/VHL) and RCC4 cells without VHL
Concentration: 0.01, 0.1, 1, 10 μM
Incubation Time: 10 days
Result: Reduced viability of RCC4 cells without VHL in a concentration-dependent manner when compared to their wild-type counterparts.

体内研究
(In Vivo)

Soluble analog of STF-31 (11.6 mg/kg; i.p.) treatment delays tumor growth in mice with VHL-deficient RCC tumor xenografts[1].
STF-31 (10 mg/kg; i.p.; twice daily for 2 days, followed by once daily for another 3 days) does not affect normal mice body weight, behavior, and ERG responses. STF-31 reduces light-induced CX3CR1gfp/+ mice microglial activation and retinal degeneration[3].

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.

Animal Model: Twelve-week old C57BL/6J and CX3CR1gfp/+ mice[3]
Dosage: 10 mg/kg
Administration: I.p. injections; twice daily for 2 days, followed by once daily for another 3 days
Result: Improved photoreceptor survival and reduced microglial activation of CX3CR1gfp/+ mice, and not induced any C57BL/6J mice retinal cell death.

分子量

423.53

Formula

C23H25N3O3S

CAS 号

724741-75-7

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
In Vitro: 

DMSO : ≥ 34 mg/mL (80.28 mM)

* “≥” means soluble, but saturation unknown.

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 2.3611 mL 11.8055 mL 23.6111 mL
5 mM 0.4722 mL 2.3611 mL 4.7222 mL
10 mM 0.2361 mL 1.1806 mL 2.3611 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: 2.5 mg/mL (5.90 mM); Clear solution; Need ultrasonic

    此方案可获得 2.5 mg/mL (5.90 mM) 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 (5.90 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (5.90 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
*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献
  • [1]. Chan DA, et al. Targeting GLUT1 and the Warburg effect in renal cell carcinoma by chemical synthetic lethality. Sci Transl Med. 2011 Aug 3;3(94):94ra70.

    [2]. Dedda CD, et al. Pharmacological Targeting of GLUT1 to Control Autoreactive T Cell Responses. International Journal of Molecular Sciences. 2019 Oct 8; 20(19):4962.

    [3]. Wang L, et al. Glucose transporter 1 critically controls microglial activation through facilitating glycolysis. Molecular Neurodegeneration, 2019 Jan 11; 14(1):2.

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