1. Protein Tyrosine Kinase/RTK Immunology/Inflammation NF-κB Metabolic Enzyme/Protease Apoptosis
  2. VEGFR Reactive Oxygen Species (ROS) Caspase Apoptosis
  3. trans-Trimethoxyresveratrol

trans-Trimethoxyresveratrol  (Synonyms: trans-trismethoxy Resveratrol; (E)-Resveratrol trimethyl ether; trans-3,5,4'-Trimethoxystilbene)

目录号: HY-N1408 纯度: 99.35%
COA 产品使用指南 技术支持

Trans-Trimethoxyresveratrol (trans-trismethoxy Resveratrol; (E)-Resveratrol trimethyl ether; trans-3,5,4'-Trimethoxystilbene) 是 Resveratrol (HY-16561) 的一种具有口服活性的天然衍生物。与 Resveratrol 相比,Trans-Trimethoxyresveratrol 具有更强的抗癌特性,能够更好地抑制癌细胞增殖、诱导细胞周期停滞、减少转移、并诱导细胞凋亡 (apoptosis)。Trans-Trimethoxyresveratrol 可通过 VEGFR2 发挥抗血管作用,导致微管和微管蛋白解聚。Trans-Trimethoxyresveratrol 可用于抗血管新生和癌症 (如非小细胞肺癌和骨肉瘤) 的研究。

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trans-Trimethoxyresveratrol

trans-Trimethoxyresveratrol Chemical Structure

CAS No. : 22255-22-7

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Trans-Trimethoxyresveratrol (trans-trismethoxy Resveratrol; (E)-Resveratrol trimethyl ether; trans-3,5,4'-Trimethoxystilbene) is an orally active natural derivative of Resveratrol (HY-16561). Trans-Trimethoxyresveratrol has an enhanced anticancer profile compared to Resveratrol, exhibiting higher potency than resveratrol, with improved cancer cell proliferation inhibition, induction of cell cycle arrest, decreased metastasis, and increased apoptosis. Trans-Trimethoxyresveratrol causes microtubule disassembling and tubulin depolymerization and exerts anti-angiogenic effects through VEGFR2. Trans-Trimethoxyresveratrol can be used for the studies of anti-angiogenic and anti-cancer (such as non-small cell lung cancer and osteosarcoma)[1][2][3][4][5][6].

IC50 & Target[2]

Caspase 3

 

VEGFR2

 

细胞效力
(Cellular Effect)
Cell Line Type Value Description References
BT-549 IC50
15.6 μM
Compound: 3
Cytotoxicity against human BT549 cells assessed as growth inhibition measured after 48 hrs by XTT assay
Cytotoxicity against human BT549 cells assessed as growth inhibition measured after 48 hrs by XTT assay
[PMID: 23547843]
BXPC-3 GI50
0.35 μg/mL
Compound: 1b
Growth inhibition of human BxPC3 cells after 48 hrs by sulforhodamine B assay
Growth inhibition of human BxPC3 cells after 48 hrs by sulforhodamine B assay
[PMID: 19719153]
Caco-2 IC50
11.95 μM
Compound: 9
Cytotoxicity against human Caco-2 cells after 3 days by [3H]thymidine incorporation assay
Cytotoxicity against human Caco-2 cells after 3 days by [3H]thymidine incorporation assay
[PMID: 20627379]
DU-145 GI50
1.5 μg/mL
Compound: 1b
Growth inhibition of human DU145 cells after 48 hrs by sulforhodamine B assay
Growth inhibition of human DU145 cells after 48 hrs by sulforhodamine B assay
[PMID: 19719153]
HCT-116 IC50
5.7 μM
Compound: 8E
Cytotoxicity against human HCT116 cells after 24 hrs by MTT assay
Cytotoxicity against human HCT116 cells after 24 hrs by MTT assay
[PMID: 21215623]
HEK293 IC50
28.3 μM
Compound: 5H6
Inhibition of TNFalpha induced NF-kappaB activation in human 293 cells after 24 hrs by luciferase reporter gene assay
Inhibition of TNFalpha induced NF-kappaB activation in human 293 cells after 24 hrs by luciferase reporter gene assay
[PMID: 18487053]
HeLa IC50
13.3 μM
Compound: 3
Cytotoxicity against human HeLa cells assessed as growth inhibition measured after 48 hrs by XTT assay
Cytotoxicity against human HeLa cells assessed as growth inhibition measured after 48 hrs by XTT assay
[PMID: 23547843]
HepG2 IC50
> 100 μM
Compound: TMS; 66
Anticancer activity against human HepG2 cells assessed as cell growth inhibition incubated for 24 hrs by MTT assay
Anticancer activity against human HepG2 cells assessed as cell growth inhibition incubated for 24 hrs by MTT assay
[PMID: 32485531]
HT-29 IC50
14 μM
Compound: TMS; 66
Anticancer activity against human HT-29 cells assessed as cell growth inhibition incubated for 24 hrs by MTT assay
Anticancer activity against human HT-29 cells assessed as cell growth inhibition incubated for 24 hrs by MTT assay
[PMID: 32485531]
HT-29 IC50
16.1 μM
Compound: 9
Cytotoxicity against human HT-29 cells after 3 days by [3H]thymidine incorporation assay
Cytotoxicity against human HT-29 cells after 3 days by [3H]thymidine incorporation assay
[PMID: 20627379]
IMR-90 IC50
2.1 μM
Compound: 8E
Cytotoxicity against human IMR90 cells after 24 hrs by MTT assay
Cytotoxicity against human IMR90 cells after 24 hrs by MTT assay
[PMID: 21215623]
K562 IC50
6.39 μM
Compound: TMRV
Cytotoxicity against Homo sapiens (human) K562 cells assessed as growth inhibition after 48 hr by MTT assay
Cytotoxicity against Homo sapiens (human) K562 cells assessed as growth inhibition after 48 hr by MTT assay
10.1007/s00044-012-0159-y
KB IC50
10.3 μM
Compound: 2
Cytotoxicity against human KB cells after 48 hrs
Cytotoxicity against human KB cells after 48 hrs
[PMID: 17000031]
KB IC50
17.7 μM
Compound: 3
Cytotoxicity against human KB cells assessed as growth inhibition measured after 48 hrs by XTT assay
Cytotoxicity against human KB cells assessed as growth inhibition measured after 48 hrs by XTT assay
[PMID: 23547843]
LLC-PK1 IC50
20 μM
Compound: 3
Cytotoxicity against pig LLC-PK1 cells assessed as growth inhibition measured after 48 hrs by XTT assay
Cytotoxicity against pig LLC-PK1 cells assessed as growth inhibition measured after 48 hrs by XTT assay
[PMID: 23547843]
MCF7 IC50
1.1 μM
Compound: 8E
Cytotoxicity against human MCF7 cells after 24 hrs by MTT assay
Cytotoxicity against human MCF7 cells after 24 hrs by MTT assay
[PMID: 21215623]
MCF7 IC50
8.41 μM
Compound: TMRV
Cytotoxicity against Homo sapiens (human) MCF7 cells assessed as growth inhibition after 48 hr by MTT assay
Cytotoxicity against Homo sapiens (human) MCF7 cells assessed as growth inhibition after 48 hr by MTT assay
10.1007/s00044-012-0159-y
NCI-H460 GI50
0.62 μg/mL
Compound: 1b
Growth inhibition of human NCI-H460 cells after 48 hrs by sulforhodamine B assay
Growth inhibition of human NCI-H460 cells after 48 hrs by sulforhodamine B assay
[PMID: 19719153]
SF-268 GI50
0.56 μg/mL
Compound: 1b
Growth inhibition of human SF268 cells after 48 hrs by sulforhodamine B assay
Growth inhibition of human SF268 cells after 48 hrs by sulforhodamine B assay
[PMID: 19719153]
SK-BR-3 IC50
111.8 μM
Compound: TMS; 66
Anticancer activity against human SK-BR-3 cells assessed as cell growth inhibition incubated for 24 hrs by MTT assay
Anticancer activity against human SK-BR-3 cells assessed as cell growth inhibition incubated for 24 hrs by MTT assay
[PMID: 32485531]
SK-MEL IC50
12.2 μM
Compound: 3
Cytotoxicity against human SK-MEL cells assessed as growth inhibition measured after 48 hrs by XTT assay
Cytotoxicity against human SK-MEL cells assessed as growth inhibition measured after 48 hrs by XTT assay
[PMID: 23547843]
SK-OV-3 IC50
55.5 μM
Compound: 3
Cytotoxicity against human SKOV3 cells assessed as growth inhibition measured after 48 hrs by XTT assay
Cytotoxicity against human SKOV3 cells assessed as growth inhibition measured after 48 hrs by XTT assay
[PMID: 23547843]
SW480 IC50
54 μM
Compound: 3
Antiproliferative activity against human SW480 cells assessed as cell viability using propidium iodide staining after 48 hrs
Antiproliferative activity against human SW480 cells assessed as cell viability using propidium iodide staining after 48 hrs
[PMID: 20395019]
Vero IC50
26.7 μM
Compound: 3
Cytotoxicity against african green monkey Vero cells assessed as growth inhibition measured after 48 hrs by XTT assay
Cytotoxicity against african green monkey Vero cells assessed as growth inhibition measured after 48 hrs by XTT assay
[PMID: 23547843]
体外研究
(In Vitro)

Trans-Trimethoxyresveratrol 对多种肿瘤细胞具有显著的细胞毒性,对 A549 细胞的 IC50 为 0.8 g/mL,对 MDA-MB-231 细胞的 IC50 为 1.2 μM,对 LNCaP 细胞的 IC50 为 2.5 μM[1]
Trans-Trimethoxyresveratrol (1-100 μM,24-72 h) 在抑制内皮细胞增殖、出芽、胶原凝胶侵袭和形态发生方面的效力是白藜芦醇的 30-100 倍 (ID50 = 0.3-3.0 μM)[2]
Trans-Trimethoxyresveratrol (1 μM,3 h) 可显著破坏微管网络并抑制管腔形成[2]
Trans-Trimethoxyresveratrol (1 μM,24 h) 仅在亚融合的内皮细胞中诱导凋亡,并在离体大鼠主动脉环测定中诱导未成熟血管的凋亡退化[2]
Trans-Trimethoxyresveratrol (0.1 μM,6 h) 能快速 (30 分钟内) 使斑马鱼胚胎中的血流停止,且已形成的血管可在 6 小时内消失[2]
Trans-Trimethoxyresveratrol (300 pmol/implant,48 h) 可抑制鸡胚脉管区的血管生长,并导致该区域已存在的血管消失[2]
Trans-Trimethoxyresveratrol (3-100 μM,20 h) 可下调 VEGFR2 并诱导斑马鱼胚胎的 G2/M 期细胞周期阻滞[3]
Trans-Trimethoxyresveratrol (0.5-50 μM,48 h) 通过上调 miR-345 和 miR-498 抑制 MAPK/Akt/Bcl-2 通路,从而降低 H1299 和 PC-9/GR 细胞对 Gefitinib (HY-50895) 的耐药性[4]
Trans-Trimethoxyresveratrol (1-10 μM,0-24 h) 可诱导 ROS 生成和 DNA 损伤,激活 p53/PUMA/Bax 通路,并增强 143B 细胞的凋亡敏感性[6]

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

RT-PCR[3]

Cell Line: zebrafish embryos
Concentration: 10 μM
Incubation Time: 20 h
Result: Suppressed transcription of VEGFR2.

Cell Cycle Analysis[3]

Cell Line: zebrafish embryos
Concentration: 3, 10, 30 and 100 μM
Incubation Time: 20 h
Result: Induced cell-cycle arrest at G2/M phase.

Western Blot Analysis[4]

Cell Line: H1299 and PC-9/GR cells
Concentration: 0.5, 5 and 50 μM
Incubation Time: 48 h
Result: Decreased the Bcl-2/Bax and p-Akt/Akt while Increased PC-9/GR.

RT-PCR[4]

Cell Line: H1299 and PC-9/GR cells
Concentration: 5 μM
Incubation Time: 48 h
Result: Increased the levels of miR-345 and miR-498.
Increased the Bax and caspase-3, and decreased Bcl-2.

Western Blot Analysis[6]

Cell Line: 143B cells
Concentration: 2.5 μM
Incubation Time: 1, 2, 4, 8, 16 and 24 h
Result: Activated caspases and increased PARP-1 cleavage.
Promoted the phosphorylation of p53, and upregulated PUMA and Bax.
Increased the level of γH2AX.
体内研究
(In Vivo)

Trans-Trimethoxyresveratrol (30 mg/kg,口服,每日一次,持续 30 天) 在 H1299 细胞诱导的异种移植小鼠模型中发挥抗肿瘤作用[4]
Trans-Trimethoxyresveratrol (1 mg/kg,口服,每两天一次,持续 4 周) 在 143B 细胞诱导的小鼠异种移植模型中显著抑制肿瘤生长[6]

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

Animal Model: H1299 cells induced xenograft model established in BALB/c nude mice[4]
Dosage: 30 mg/kg alone or with 25 mg/kg Gefitinib (HY-50895)
Administration: Oral administration (p.o.), once daily for 30 days
Result: The growth rates of tumour volume and weight were smaller but that the combined inhibition was more remarkable.
Animal Model: 143B cells induced xenograft model established in BALB/c nude mice[6]
Dosage: 1 mg/kg and 0.1 mg/kg TNF-related apoptosis-inducing ligand (TRAIL)
Administration: Oral administration (p.o.), every two days for 4 weeks
Result: Inhibited the development ofosteosarcoma without significant toxicity.
分子量

270.32

Formula

C17H18O3

CAS 号
性状

固体

颜色

White to off-white

结构分类
初始来源
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 2 years
-20°C 1 year
溶解性数据
细胞实验: 

DMSO 中的溶解度 : ≥ 50 mg/mL (184.97 mM; 吸湿的 DMSO 对产品的溶解度有显著影响,请使用新开封的 DMSO)

H2O 中的溶解度 : < 0.1 mg/mL (insoluble)

* "≥" 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 3.6993 mL 18.4966 mL 36.9932 mL
5 mM 0.7399 mL 3.6993 mL 7.3986 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, 2 years; -20°C, 1 year。-80°C储存时,请在2年内使用, -20°C储存时,请在1年内使用。

  • 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    40% PEG300    5% Tween-80    45% Saline

    Solubility: ≥ 2.5 mg/mL (9.25 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。

    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;再向上述体系中加入 50 μL Tween-80,混合均匀;然后再继续加入 450 μL 生理盐水 定容至 1 mL

    生理盐水的配制:将 0.9 g 氯化钠,溶解于 ddH₂O 并定容至 100 mL,可以得到澄清透明的生理盐水溶液。
  • 方案 二

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

    Solubility: ≥ 2.5 mg/mL (9.25 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。

    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。

    2 g SBE-β-CD(磺丁基醚 β-环糊精)粉末定容于 10 mL 的生理盐水中,完全溶解至澄清透明。
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

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)。
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

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, 2 years; -20°C, 1 year。-80°C储存时,请在2年内使用, -20°C储存时,请在1年内使用。

可选溶剂 浓度 溶剂体积 质量 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 3.6993 mL 18.4966 mL 36.9932 mL 92.4830 mL
5 mM 0.7399 mL 3.6993 mL 7.3986 mL 18.4966 mL
10 mM 0.3699 mL 1.8497 mL 3.6993 mL 9.2483 mL
15 mM 0.2466 mL 1.2331 mL 2.4662 mL 6.1655 mL
20 mM 0.1850 mL 0.9248 mL 1.8497 mL 4.6241 mL
25 mM 0.1480 mL 0.7399 mL 1.4797 mL 3.6993 mL
30 mM 0.1233 mL 0.6166 mL 1.2331 mL 3.0828 mL
40 mM 0.0925 mL 0.4624 mL 0.9248 mL 2.3121 mL
50 mM 0.0740 mL 0.3699 mL 0.7399 mL 1.8497 mL
60 mM 0.0617 mL 0.3083 mL 0.6166 mL 1.5414 mL
80 mM 0.0462 mL 0.2312 mL 0.4624 mL 1.1560 mL
100 mM 0.0370 mL 0.1850 mL 0.3699 mL 0.9248 mL
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trans-Trimethoxyresveratrol
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HY-N1408
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