Ferulic acid(Synonyms: Coniferic acid)

天然产物 天然产物苯丙素类 Phenylpropanoids

Ferulic acid (Synonyms: Coniferic acid) 纯度: 99.86%

Ferulic acid 是一种新型的成纤维细胞生长因子受体 1 (FGFR1) 抑制剂, 对于 FGFR1FGFR2IC50值分别为 3.78 和 12.5 μM。

Ferulic acid(Synonyms: Coniferic acid)

Ferulic acid Chemical Structure

CAS No. : 1135-24-6

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10 mM * 1 mL in DMSO ¥550 In-stock
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生物活性

Ferulic acid is a novel fibroblast growth factor receptor 1 (FGFR1) inhibitor with IC50s of 3.78 and 12.5 μM for FGFR1 and FGFR2, respectively.

IC50 & Target[1]

FGFR1

3.78 μM (IC50)

FGFR2

12.5 μM (IC50)

Human Endogenous Metabolite

 

体外研究
(In Vitro)

Ferulic acid (FA) is a novel fibroblast growth factor receptor 1 (FGFR1) inhibitor with IC50s of 3.78 and 12.5 μM for FGFR1 and FGFR2, respectively. Ferulic acid exhibits great inhibitory activity on FGFR1 with an inhibitory rate of 92% at 1 µM. The proliferation of HUVEC stimulated by FGF1 is markedly decreased after Ferulic acid treatment ranging from 5 to 40 μM for 24 h. Ferulic acid does not exert significant cell viability up to 20 μM, but over 30 μM Ferulic acid exhibits a cytotoxic effect in HUVEC compare to the control. Ferulic acid inhibits FGF1-induced HUVEC migration and invasion in a dose-dependent manner. Ferulic acid markedly suppresses the FGF1-induced phosphorylation of PI3K and Akt. Ferulic acid treatments significantly inhibit MMP-2 and MMP-9 expression stimulated by FGF1[1].

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

体内研究
(In Vivo)

Treatment with Ferulic acid (FA) potently inhibits FGF1-induced neovascularization. It is found that intragastric administration of Ferulic acid markedly inhibits tumor volume and tumor weight, as compare to the counterparts treated with DMSO. Furthermore, Ferulic acid treatment is well tolerated, and there is no significant difference in weight between the vehicle group and the FA-treated groups[1]. Ferulic acid (0.01, 0.1, 1 or 10 mg/kg) given by oral route decreases significantly the immobility time in the forced swimming test (FST) and tail suspension test (TST), whereas produces no effect in the open-field test. Results demonstrate that the administration of Ferulic acid (0.001 mg/kg, p.o.) boosts the antidepressant-like effect of fluoxetine (5 mg/kg, p.o.) in the TST[2].

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

Clinical Trial

分子量

194.18

Formula

C10H10O4

CAS 号

1135-24-6

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 : 100 mg/mL (514.99 mM; Need ultrasonic)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 5.1499 mL 25.7493 mL 51.4986 mL
5 mM 1.0300 mL 5.1499 mL 10.2997 mL
10 mM 0.5150 mL 2.5749 mL 5.1499 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 (12.87 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (12.87 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 (12.87 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (12.87 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 (12.87 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (12.87 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。

*以上所有助溶剂都可在 MCE 网站选购。
参考文献
  • [1]. Yang GW, et al. Ferulic Acid Exerts Anti-Angiogenic and Anti-Tumor Activity by Targeting Fibroblast Growth Factor Receptor 1-Mediated Angiogenesis. Int J Mol Sci. 2015 Oct 12;16(10):24011-31.

    [2]. Zeni AL, et al. Ferulic acid exerts antidepressant-like effect in the tail suspension test in mice: evidence for the involvement of the serotonergic system. Eur J Pharmacol. 2012 Mar 15;679(1-3):68-74.

Cell Assay
[1]

HUVEC (5×104 cells/well) are plated onto a gelatinized 24-well culture plate and cultured in ECGS containing 15% FBS. HUVEC are treated with DMSO (0.1%) or different concentrations of Ferulic acid (FA) (0, 2.5, 5, 10, 20, 30, 40 μM) for 24 h. Cell viability is determined by the MTT assay. After 4 h of incubation, the absorbance is measured at 450 nm with a microplate reader. The results are calculated from six replicates of each experiment. Three independent experiments are performed[1].

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

Animal Administration
[2]

Male Swiss mice (30 to 40 g) are maintained at 21 to 23°C with free access to water and food, under a 12:12 h light/dark cycle (lights on at 07:00 h). All manipulations are carried out between, 9:00 and 16:00 h, with each animal used only once. In order to investigate the antidepressant-like effect of Ferulic acid, Ferulic acid is administered at a dose range of 0.001 to 10 mg/kg, by oral route (p.o.) 60 min before the forced swimming test (FST), tail suspension test (TST) or open-field test. The control animals receive appropriate vehicle[2].

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

参考文献
  • [1]. Yang GW, et al. Ferulic Acid Exerts Anti-Angiogenic and Anti-Tumor Activity by Targeting Fibroblast Growth Factor Receptor 1-Mediated Angiogenesis. Int J Mol Sci. 2015 Oct 12;16(10):24011-31.

    [2]. Zeni AL, et al. Ferulic acid exerts antidepressant-like effect in the tail suspension test in mice: evidence for the involvement of the serotonergic system. Eur J Pharmacol. 2012 Mar 15;679(1-3):68-74.