2. Cell Cycle/DNA Damage Stem Cell/Wnt PI3K/Akt/mTOR
  3. Wnt CDK GSK-3
  4. DIF-3

DIF-3 是一个有口服活性的抗癌剂。DIF-3 通过激活 GSK-3β 促进细胞周期蛋白 D1 和 c-Myc 的降解，从而降低其表达水平。DIF-3 抑制细胞中 Wnt/β-catenin 信号通路相关蛋白。DIF-3 诱导活性氧 (ROS) 和细胞自噬 (autophagy)。DIF-3 在 HT1080 细胞中抑制克氏锥虫生长。DIF-3 在体外和体内均发挥抗肿瘤作用。

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DIF-3

DIF-3 Chemical Structure

CAS No. : 113411-17-9

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规格 价格 是否有货 数量
10 mM * 1 mL in DMSO ￥3450
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1 mg ￥1150
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5 mg ￥3000
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10 mg ￥4800
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DIF-3 相关抗体

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GSK-3 GSK-3α GSK-3β

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

DIF-3 is an orally active anticancer agent. DIF-3 reduces the expression levels of cyclin D1 and c-Myc by facilitating their degradation via activation of GSK-3β. DIF-3 inhibits Wnt/β-catenin signaling pathway-related proteins in cells. DIF-3 induces reactive oxygen species (ROS) and autophagy. DIF suppresses the growth of Trypanosoma. cruzi in HT1080 cells. DIF-3 exerts antitumor effects both in vitro and in vivo[1][2][3][4].

细胞效力
(Cellular Effect)
Cell Line Type Value Description References
S2 IC50
4.6 μM
Compound: 2, DIF-3
Immunosuppressive activity in Drosophila S2 cells expressing att-luc reporter gene assessed as inhibition of peptidoglycan-induced attacin production pre-treated for 1.5 hrs before peptidoglycan stimulation for 8 hrs by luciferase reporter gene assay
Immunosuppressive activity in Drosophila S2 cells expressing att-luc reporter gene assessed as inhibition of peptidoglycan-induced attacin production pre-treated for 1.5 hrs before peptidoglycan stimulation for 8 hrs by luciferase reporter gene assay
[PMID: 26122773]
体外研究
(In Vitro)

DIF-3 (10-30 μM, 24-48 h) 以剂量依赖性方式抑制人类结肠癌细胞的增殖[1]。
DIF-3 (30 μM, 24 h) 将人类结肠癌细胞的细胞周期停滞在 G0/G1 期[1]。
DIF-3 (10-30 μM, 1-24 h) 通过激活 GSK-3β 诱导人类结肠癌细胞中细胞周期蛋白 D1 和 c-Myc 的蛋白水解[1]。
DIF-3 (10-30 μM, 1-24 h) 抑制人类结肠癌细胞中的 Wnt/β-catenin 信号通路相关蛋白[1]。
DIF-3 (10 μM，4 h) 抑制溶血磷脂酸 (LPA) 诱导的小鼠骨肉瘤 LM8 细胞迁移[2]。
DIF-3 (20 μM, 0.25-24 h) 抑制 mTOR 信号传导并诱导 K562 CML 细胞自噬[3]。
DIF-3 (20 μM) 诱导 K562 细胞中的线粒体膜电位 (MMP) (0-10 min)、ATP 含量降低 (6 h) 和 ROS 产生 (0-30 min)[3]。
DIF-3 (10 μM, 3 d) 抑制 HT1080 细胞中克氏锥虫的生长，IC50 为 3.95 μM[4]。

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

DIF-3 相关抗体:

Cell Proliferation Assay[1]

Cell Line: HCT-116, DLD-1
Concentration: 10, 20, 30 μM
Incubation Time: 24, 48 h
Result: Strongly inhibited proliferation in a dose-dependent manner in both cell lines.
HCT-116 cells were more sensitive to DIF-3 than DLD-1 cells.

Cell Cycle Analysis[1]

Cell Line: HCT-116, DLD-1
Concentration: 30 μM
Incubation Time: 24 h
Result: Significantly increased the number of cells in G0/G1 phase and decreased those in S phase in both cell lines.
Also significantly increased the number of cells in G2 phase when HCT-116 cells were employed, this effect was not observed by using DLD-1 cells.

Cell Migration Assay [2]

Cell Line: LM8
Concentration: 10 μM
Incubation Time: 4 h
Result: Suppressed LPA-induced cell migration, whereas did not significantly affected cell migration in the absence of LPA.

Cell Autophagy Assay[3]

Cell Line: K562
Concentration: 20 μM
Incubation Time: 0.25, 0.5, 1, 3, 6, 24 h for mTOR study; 6, 16, 36, 48 h for Cathepsin B activity study
Result: Induced the rapid dephosphorylation of mTOR at Ser2481. Inhibited the mTOR pathway and leads to a rapid and robust conversion of LC3-I to LC3-II.
Increased autophagy was accompanied by the late activation of cathepsin B.

Western Blot Analysis[1]

Cell Line: HCT-116
Concentration: 10, 20, 30 μM
Incubation Time: 1, 3, 6, 12, 24 h
Result: Induced a rapid and marked reduction in the amount of cyclin D1 protein and c-Myc protein in a time and dose-dependent manner.
Had no effect on the expression level of β-catenin (30 μM for 24 h).
Reduced the amount of TCF7L2 which increased gradually over time in control cells, in a time and dose-dependent manner.
Reduction of TCF7L2 was associated with the transcriptional inhibition of cyclin D1 mRNA in HCT-116 cells.

Western Blot Analysis[1]

Cell Line: HCT-116
Concentration: 30 μM
Incubation Time: 1 h
Result: Effects could be attenuated by MG132 (HY-13259) and SB216763 (HY-12012), indicating the involvement of GSK-3β in degradation of cyclin D1 and c-Myc.
体内研究
(In Vivo)

DIF-3 (150 mg/kg；口服；每天一次，每周 5 天，持续 4 周) 可抑制 Mutyh-/- 小鼠中氧化应激 (0.2% KBrO3) 诱发的肿瘤[1]。

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

Animal Model: Mutyh-/- mice (KBrO3 dissolved in water at a concentration of 2 g/L was administered to 4-week-old mice for 12 weeks)[1]
Dosage: 150 mg/kg
Administration: Oral gavage (p.o.); once a day for 5 days/week over 4 weeks
Result: Markedly reduced the number of intestinal tumors, especially the number of large tumors with a diameter of >2.0 mm.
No differences in the appearance, activity, body weight, or blood cell counts.
The numbers of TCF7L2-and cyclin D1-positive nuclei in tumors were significantly decreased.
分子量

272.72

Formula

C13H17ClO4
CAS 号
性状

固体

颜色

White to off-white

运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

溶解性数据
细胞实验： 

DMSO 中的溶解度 : 100 mg/mL (366.68 mM; 超声助溶; 吸湿的 DMSO 对产品的溶解度有显著影响，请使用新开封的 DMSO)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 3.6668 mL 18.3338 mL 36.6676 mL
5 mM 0.7334 mL 3.6668 mL 7.3335 mL
查看完整储备液配制表

* 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 (protect from light)。-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。

  • 摩尔计算器

  • 稀释计算器

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量
=
浓度
×
体积
×
分子量 *

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

浓度 (start)

C1

×
体积 (start)

V1

=
浓度 (final)

C2

×
体积 (final)

V2

动物实验：

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

  • 方案 一

    请依序添加每种溶剂： 10% DMSO    90% Corn Oil

    Solubility: ≥ 2.5 mg/mL (9.17 mM); 澄清溶液

    此方案可获得 ≥ 2.5 mg/mL（饱和度未知）的澄清溶液，此方案实验周期在半个月以上的动物实验酌情使用。

    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。

动物溶解方案计算器
请输入动物实验的基本信息：

给药剂量

mg/kg

动物的平均体重

g

每只动物的给药体积

μL

动物数量

只
由于实验过程有损耗，建议您多配一只动物的量
请输入您的动物体内配方组成：
%
DMSO +
% 
+
%
Tween-80 +
%
Saline
如果您的动物是免疫缺陷鼠或者体弱鼠，建议 DMSO 中的在最后工作液体系中的占比尽量不超过 2%。
方案所需 助溶剂 包括：DMSO， ，均可在 MCE 网站选购。 ，Tween 80，均可在 MCE 网站选购。
计算结果
工作液所需浓度 : mg/mL
储备液配制方法 : mg 药物溶于 μL  DMSO（母液浓度为 mg/mL）。

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

您所需的储备液浓度超过该产品的实测溶解度，以下方案仅供参考，如有需要，请与 MCE 中国技术支持联系。
动物实验体内工作液的配制方法 : 取 μL DMSO 储备液，加入 μL 。 μL ，混合均匀至澄清，再加 μL Tween 80，混合均匀至澄清，再加 μL 生理盐水。
连续给药周期超过半月以上，请谨慎选择该方案。
请确保第一步储备液溶解至澄清状态，从左到右依次添加助溶剂。您可采用超声加热 （超声清洗仪，建议频次 20-40 kHz），涡旋吹打等方式辅助溶解。
纯度 & 产品资料
参考文献

DIF-3 相关分类

完整储备液配制表

* 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 (protect from light)。-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。

可选溶剂 浓度 溶剂体积 质量 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 3.6668 mL 18.3338 mL 36.6676 mL 91.6691 mL
5 mM 0.7334 mL 3.6668 mL 7.3335 mL 18.3338 mL
10 mM 0.3667 mL 1.8334 mL 3.6668 mL 9.1669 mL
15 mM 0.2445 mL 1.2223 mL 2.4445 mL 6.1113 mL
20 mM 0.1833 mL 0.9167 mL 1.8334 mL 4.5835 mL
25 mM 0.1467 mL 0.7334 mL 1.4667 mL 3.6668 mL
30 mM 0.1222 mL 0.6111 mL 1.2223 mL 3.0556 mL
40 mM 0.0917 mL 0.4583 mL 0.9167 mL 2.2917 mL
50 mM 0.0733 mL 0.3667 mL 0.7334 mL 1.8334 mL
60 mM 0.0611 mL 0.3056 mL 0.6111 mL 1.5278 mL
80 mM 0.0458 mL 0.2292 mL 0.4583 mL 1.1459 mL
100 mM 0.0367 mL 0.1833 mL 0.3667 mL 0.9167 mL
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

DIF-3113411-17-9DIF3DIF 3WntCDKGSK-3Cyclin dependent kinaseGlycogen synthase kinase-3Glycogen synthase kinase 3cyclin D1c-MycGSK-3βWnt/β-cateninDLD-1 cellsHeLaInhibitorinhibitorinhibit

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