Baohuoside I(Synonyms: 宝藿苷 I; Icariin-II; Icariside-II)

天然产物 糖类和糖苷 Saccharides and Glycosides

Baohuoside I;(Synonyms: 宝藿苷 I; Icariin-II; Icariside-II) 纯度: 99.15%

Baohuoside I 是从朝鲜淫羊藿中得到的黄酮类化合物,作为 CXCR4 的抑制剂,能够抑制 CXCR4 的表达,诱导凋亡,具有抗肿瘤活性。

Baohuoside I(Synonyms: 宝藿苷 I; Icariin-II;  Icariside-II)

Baohuoside I Chemical Structure

CAS No. : 113558-15-9

规格 价格 是否有货 数量
10;mM;*;1 mL in DMSO ¥1320 In-stock
5 mg ¥800 In-stock
10 mg ¥1200 In-stock
50 mg ¥4800 In-stock
100 mg ¥6500 In-stock
200 mg ; 询价 ;
500 mg ; 询价 ;

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Baohuoside I 相关产品

bull;相关化合物库:

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生物活性

Baohuoside I, a flavonoid isolated from Epimedium koreanum Nakai, acts as an inhibitor of CXCR4, downregulates CXCR4 expression, induces apoptosis and shows anti-tumor activity.

IC50 Target

CXCR4

;

体外研究
(In Vitro)

Baohuoside I is an inhibitor of CXCR4, and downregulates CXCR4 expression at 12-25 μM. Baohuoside I (0-25 μM) suppresses NF-κB activation in a dose-dependent manner, suppresses CXCL12 induced the invasion of cervical cancer cells. Baohuoside I also inhibits invasion of breast cancer cells[1]. Baohuoside I inhibits A549 cell viability, with IC50s of 25.1 μM at 24 h, 11.5 μM and 9.6 μM at 48 h and 72 h, respectively. Baohuoside I ((25 μM) suppresses the caspase cascade in A549 cells, elevates ROS levels and activates JNK and p38MAPK signaling cascade[2]. Baohuoside I (3.125, 6.25, 12.5, 25.0 and 50.0 µg/mL) significantly and dose-dependently blocks the growth of esophageal squamous cell carcinoma Eca109 cells, with an IC50 of 4.8 µg/mL at 48 h[3].

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

体内研究
(In Vivo)

Baohuoside I (25 mg/kg) decreases β-catenin protein levels, cyclin D1 and survivin expression in nude mice[3].

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

分子量

514.52

Formula

C27H30O10

CAS 号

113558-15-9

中文名称

宝藿苷 I;淫羊藿次苷 Ⅱ;宝霍苷 I

运输条件

Room temperature in continental US; may vary elsewhere.

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

DMSO : ≥ 32 mg/mL (62.19 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 1.9436 mL 9.7178 mL 19.4356 mL
5 mM 0.3887 mL 1.9436 mL 3.8871 mL
10 mM 0.1944 mL 0.9718 mL 1.9436 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: ≥ 2.08 mg/mL (4.04 mM); Clear solution

    此方案可获得 ≥ 2.08 mg/mL (4.04 mM,饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例,取 100 μL 20.8 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: ≥ 2.08 mg/mL (4.04 mM); Clear solution

    此方案可获得 ≥ 2.08 mg/mL (4.04 mM,饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例,取 100 μL 20.8 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: ≥ 2.08 mg/mL (4.04 mM); Clear solution

    此方案可获得 ≥ 2.08 mg/mL (4.04 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 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中,混合均匀。

*以上所有助溶剂都可在 MCE 网站选购。
参考文献
  • [1]. Kim B, et al. Baohuoside I suppresses invasion of cervical and breast cancer cells through the downregulation of CXCR4 chemokine receptor expression. Biochemistry. 2014 Dec 9;53(48):7562-9.

    [2]. Song J, et al. Reactive oxygen species-mediated mitochondrial pathway is involved in Baohuoside I-induced apoptosis in human non-small cell lung cancer. Chem Biol Interact. 2012 Jul 30;199(1):9-17.

    [3]. Wang L, et al. The flavonoid Baohuoside-I inhibits cell growth and downregulates survivin and cyclin D1 expression in esophageal carcinoma via β-catenin-dependent signaling. Oncol Rep. 2011 Nov;26(5):1149-56.

Cell Assay
[2]

The cytotoxicity effect of Baohuoside I on A549 cells is determined by MTT assay. Cells (1×104 cells/well) are seeded in a 96-well plate, and treated with Baohuoside I (6.25, 12.5, and 25 μM) or 1 mM NAC for 24, 48 or 72 h. After MTT containing medium is removed, the crystals that have formed are dissolved by the addition of DMSO to each well. After mixing, the absorbance of the cells is measured at 540 nm by using Multiskan Spectrum Microplate Reader[2].

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

Animal Administration
[3]

Mice[3]
Female Balb/c nude mice (4- to 6-weeks-old) are used in the assay. Subconfluent Eca109-Luc cells are harvested and resuspended in PBS to a final density of 2 × 107 cells/mL. Prior to injection, cells are resuspended in PBS and analyzed by 0.4% trypan blue exclusion assay (viable cells >90%). For subcutaneous injection, 1 × 107 Eca109-Luc cells in 200 µL PBS are injected into the left flank of each mouse using 27G needles. At 1 week after tumor cell injection, Baohuoside I (25 mg/kg per mouse) is injected intralesionally once a day, whereas the 10 mice intended for vehicle treatment are administered an equal volume of PBS[3].

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

参考文献
  • [1]. Kim B, et al. Baohuoside I suppresses invasion of cervical and breast cancer cells through the downregulation of CXCR4 chemokine receptor expression. Biochemistry. 2014 Dec 9;53(48):7562-9.

    [2]. Song J, et al. Reactive oxygen species-mediated mitochondrial pathway is involved in Baohuoside I-induced apoptosis in human non-small cell lung cancer. Chem Biol Interact. 2012 Jul 30;199(1):9-17.

    [3]. Wang L, et al. The flavonoid Baohuoside-I inhibits cell growth and downregulates survivin and cyclin D1 expression in esophageal carcinoma via β-catenin-dependent signaling. Oncol Rep. 2011 Nov;26(5):1149-56.