1. Immunology/Inflammation NF-κB Apoptosis Protein Tyrosine Kinase/RTK Anti-infection
  2. COX NF-κB TNF Receptor Interleukin Related Apoptosis VEGFR Bacterial Dengue Virus Caspase
  3. 4-Methoxycinnamic acid ethyl ester

4-Methoxycinnamic acid ethyl ester  (Synonyms: Ethyl p-methoxycinnamate)

目录号: HY-N0346
产品使用指南 技术支持

4-Methoxycinnamic acid ethyl ester (Ethyl p-methoxycinnamate) 是一种口服有效的天然化合物。4-Methoxycinnamic acid ethyl ester 通过抑制环氧合酶 (COX-1 (IC50 = 1.12 μM) 和 COX-2 (IC50 = 0.83 μM))、NF-κB (IC50 = 88.7 μM) 及细胞因子产生 (TNF-α (IC50 = 96.84 μg/mL) 和 IL-1β (IC50 = 166.4 μg/mL)) 来发挥抗炎作用。4-Methoxycinnamic acid ethyl ester 抑制肿瘤细胞增殖、迁移和癌症代谢,并诱导细胞凋亡 (apoptosis)。4-Methoxycinnamic acid ethyl ester 抑制 VEGF 表达,从而抑制血管生成。4-Methoxycinnamic acid ethyl ester 对登革病毒和结核分枝杆菌具有显著的抑制作用。4-Methoxycinnamic acid ethyl ester 在大鼠中具有镇痛效果。

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4-Methoxycinnamic acid ethyl ester

4-Methoxycinnamic acid ethyl ester Chemical Structure

CAS No. : 1929-30-2

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Other Forms of 4-Methoxycinnamic acid ethyl ester:

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

4-Methoxycinnamic acid ethyl ester (Ethyl p-methoxycinnamate) is an orally active natural compound found. 4-Methoxycinnamic acid ethyl ester exerts anti-inflammatory effects by inhibiting cyclooxygenase (COX-1 (IC50 = 1.12 μM) and COX-2 (IC50 = 0.83 μM)), NF-κB (IC50 = 88.7 μM) and cytokine production (TNF-α (IC50 = 96.84 μg/mL) and IL-1β (IC50 = 166.4 μg/mL)). 4-Methoxycinnamic acid ethyl ester inhibits tumor cell proliferation, migration and cancer metabolism and induces apoptosis.4-Methoxycinnamic acid ethyl ester inhibits VEGF expression, thereby inhibiting angiogenesis. 4-Methoxycinnamic acid ethyl ester has a significant inhibitory effect on dengue virus and Mycobacterium tuberculosis. 4-Methoxycinnamic acid ethyl ester has analgesic effects in rats[1][2][3][4][5][6][7].

IC50 & Target[1][2][7]

COX-1

1.12 μM (IC50)

COX-2

0.83 μM (IC50)

NF-κB

88.7 μM (IC50)

IL-1β

116.4 μg/mL (IC50)

Caspase-3

 

Caspase-7

 

Caspase-8

 

Caspase-9

 

体外研究
(In Vitro)

4-Methoxycinnamic acid ethyl ester (25-200 μg/mL, 0-48 h) 以 160 μg/mL 的 IC50 抑制 HUVECs 的生长,并通过 VEGF 抑制 HUVECs 的迁移能力[2]
4-Methoxycinnamic acid ethyl ester (50-200 μg/mL, 6-24 h) 剂量依赖性地损害 HUVECs 在 Matrigel 上形成管状结构的能力[2]
4-Methoxycinnamic acid ethyl ester (50-200 μg/mL, 5 d) 显著抑制大鼠主动脉环微血管的出芽和生长[2]
4-Methoxycinnamic acid ethyl ester (0.03-0.97 mM, 7 d) 抑制结核分枝杆菌 H37Ra、H37Rv、药物敏感和多重耐药 (MDR) 临床分离株 (MIC: 0.242-0.485 mM),并且对常见细菌如耻垢分枝杆菌、大肠杆菌和金黄色葡萄球菌无效[3]
4-Methoxycinnamic acid ethyl ester (50 μM, 12 h) 显著降低 p-p65 (Ser536) 和 p-Akt (Ser473) 的磷酸化水平[4]
4-Methoxycinnamic acid ethyl ester (50 μM, 24 h) 显著抑制黑色素瘤细胞的迁移和侵袭能力[4]
4-Methoxycinnamic acid ethyl ester (1-50 μM, 12-24 h) 逆转黑色素瘤细胞对 Paclitaxel (HY-B0015) 的耐药性[4]
4-Methoxycinnamic acid ethyl ester (125-500 μM, 24 h) 对所有四种登革热血清型 (DENV-1, DENV-2, DENV-3, DENV-4) 表现出广谱抗病毒活性,在 HepG2 和 A549 细胞中,对 DENV-2 的 EC50 值分别为 22.58 和 6.17 μM[5]
4-Methoxycinnamic acid ethyl ester (100 μM, 1-24 h) 抑制艾氏腹水癌细胞 (EATCs) 的从头脂肪酸合成 (而非糖酵解),从而耗竭 ATP[6]
4-Methoxycinnamic acid ethyl ester (48 h) 对 MCF-7、HT-29、HCT-116 (IC50 = 42.1 μg/mL)、U-937、PC-3 (IC50 = 39 μg/mL)、K-562 细胞显示出中等细胞毒性[7]
4-Methoxycinnamic acid ethyl ester (50-200 μg/mL, 12-48 h) 抑制 HCT-116 细胞的迁移,并通过线粒体途径诱导细胞凋亡[7]
4-Methoxycinnamic acid ethyl ester (200 μg/mL, 8 h) 在 HCT-116 细胞中显著激活所有测试的 Caspase,包括 Caspase-9、Caspase-8 和 Caspase-3/7[7]

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

Cell Migration Assay [2]

Cell Line: HUVECs
Concentration: 50, 100, 200 μg/mL
Incubation Time: 0, 6 and 12 h
Result: Effectively prevented the migration of endothelial cells to the damaged area.

Western Blot Analysis[4]

Cell Line: B16F10 G5-Luc and SK-Mel 28
Concentration: 50 μM
Incubation Time: 12 h (B16F10 G5-Luc) and 24 h (SK-Mel 28)
Result: Significantly reduced the phosphorylation levels of p-p65 (Ser536) and p-Akt (Ser473).
Upregulated the expression of γ-H2AX with Paclitaxel.

Cell Migration Assay [4]

Cell Line: B16F10 G5-Luc
Concentration: 50 μM
Incubation Time: 12 h
Result: Significantly inhibited the migration.

Cell Invasion Assay[4]

Cell Line: B16F10 G5-Luc
Concentration: 50 μM
Incubation Time: 12 h
Result: Significantly reduced the number of cells passing through Matrigel.

Western Blot Analysis[4]

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.

RT-PCR[6]

Cell Line: EATCs
Concentration: 100 μM
Incubation Time: 1, 6 and 12 h
Result: Significantly downregulated the mRNA expression of key enzymes in fatty acid synthesis, including Acly, Acc1, and Fasn.
Was no significant effect on the mRNA expression of key fatty acid oxidation enzymes Cpt1a and Cpt1b.
Significantly downregulated the expression levels of SREBP1 mRNA.

Western Blot Analysis[6]

Cell Line: EATCs
Concentration: 100 μM
Incubation Time: 1, 6 and 12 h
Result: Significantly reduced the phosphorylation level of c-Myc protein Ser62 site.
Downregulated the expression of key enzymes in fatty acid synthesis (Acly, Acc1, Fasn).

Apoptosis Analysis[7]

Cell Line: HCT-116
Concentration: 50, 100, 200 μg/mL
Incubation Time: 48 h
Result: Dose-dependently induced chromatin condensation in HCT-116 cells.
Dose-dependent lost mitochondrial membrane potential.
体内研究
(In Vivo)

4-Methoxycinnamic acid ethyl ester (100-800 mg/kg, 单次灌胃) 在大鼠体内以剂量依赖性方式抑制足爪水肿[1]
4-Methoxycinnamic acid ethyl ester (200-800 mg/kg, 每日灌胃一次,连续 7 天) 在大鼠体内以剂量依赖性方式抑制慢性肉芽肿的形成[2]
4-Methoxycinnamic acid ethyl ester (200-800 mg/kg, 单次灌胃) 以剂量依赖性方式延长大鼠的甩尾潜伏期,显示出显著的镇痛效果[2]

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

Animal Model: Carrageenan-induced paw edema model established in male Sprague Dawely (SD) rats (150-200 g)[1]
Dosage: 100, 200, 400 and 800 mg/kg
Administration: Oral gavage (i.g.), single dose
Result: Inhibited paw edema in a dose-dependent manner, with the minimum effective dose (MIC) being 100 mg/kg.
No toxic reactions were observed at 2000 mg/kg.
Animal Model: Cotton pellet granuloma assay established in male Sprague Dawely (SD) rats (200-250 g)[2]
Dosage: 200, 400, 800 mg/kg
Administration: Oral gavage (i.g.), once daily for 7 days
Result: Reached inhibition rate by 51.65% at 800 mg/kg.
Inhibited the production of key pro-inflammatory cytokines IL-1β and TNF-α.
Animal Model: Tail flick assay established in male Sprague Dawely (SD) rats (200-250 g)[2]
Dosage: 200, 400, 800 mg/kg
Administration: Oral gavage (i.g.), single dose
Result: Prolonged the tail-flick latency of rats in a dose-dependent manner
分子量

206.24

Formula

C12H14O3

CAS 号
结构分类
初始来源
运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.

纯度 & 产品资料
参考文献
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    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.

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