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  3. 4-Methoxycinnamic acid ethyl ester

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

Cat. No.: HY-N0346
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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.

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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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Description

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

 

In Vitro

4-Methoxycinnamic acid ethyl ester (25-200 μg/mL, 0-48 h) inhibits the growth of HUVECs with an IC50 of 160 μg/mL and suppresses the migration ability of HUVECs through VEGF[2].
4-Methoxycinnamic acid ethyl ester (50-200 μg/mL, 6-24 h) dose-dependently impairs the ability of HUVECs to form tube-like structures on Matrigel[2].
4-Methoxycinnamic acid ethyl ester (50-200 μg/mL, 5 d) significantly inhibits the sprouting and growth of microvessels from rat aortic rings[2].
4-Methoxycinnamic acid ethyl ester (0.03-0.97 mM, 7 d) inhibits M. tuberculosis H37Ra, H37Rv, drug susceptible and multidrug resistant (MDR) clinical isolates (MIC: 0.242-0.485 mM) and is ineffective against common bacteria such as Mycobacterium smegmatis, Escherichia coli, and Staphylococcus aureus[3].
4-Methoxycinnamic acid ethyl ester (50 μM, 12 h) significantly reduces the phosphorylation levels of p-p65 (Ser536) and p-Akt (Ser473)[4].
4-Methoxycinnamic acid ethyl ester (50 μM, 24 h) significantly inhibits the migration and invasion ability of melanoma cells[4].
4-Methoxycinnamic acid ethyl ester (1-50 μM, 12-24 h) reverses the resistance of melanoma cells to Paclitaxel (HY-B0015)[4].
4-Methoxycinnamic acid ethyl ester (125-500 μM, 24 h) exhibits broad-spectrum antiviral activity against all four dengue serotypes (DENV-1, DENV-2, DENV-3, DENV-4), with EC50 values of 22.58 and 6.17 μM for DENV-2 in HepG2 and A549 cells, respectively[5].
4-Methoxycinnamic acid ethyl ester (100 μM, 1-24 h) inhibits de novo fatty acid synthesis, rather than glycolysis, to deplete ATP in ehrlich ascites cancer cells (EATCs)[6].
4-Methoxycinnamic acid ethyl ester (48 h) shows moderate cytotoxicity against MCF-7, HT-29, HCT-116 (IC50 = 42.1 μg/mL), U-937, PC-3 (IC50 = 39 μg/mL), K-562 cells[7].
4-Methoxycinnamic acid ethyl ester (50-200 μg/mL, 12-48 h) inhibits cell migration and induces apoptosis via the mitochondrial pathway in HCT-116 cells[7].
4-Methoxycinnamic acid ethyl ester (200 μg/mL, 8 h) significantly activates all tested caspases, including Caspase-9, Caspase-8, and Caspase-3/7 in HCT-116 cells[7].

MedChemExpress (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.
In Vivo

4-Methoxycinnamic acid ethyl ester (100-800 mg/kg, i.g., single dose) inhibited paw edema in a dose-dependent manner in rats[4].
4-Methoxycinnamic acid ethyl ester (200-800 mg/kg, i.g., once daily for 7 days) inhibits the formation of chronic granuloma in a dose-dependent manner in rats[2].
4-Methoxycinnamic acid ethyl ester (200-800 mg/kg, i.g., single dose) prolongs the tail-flick latency of rats in a dose-dependent manner, showing a significant analgesic effect[2].

MedChemExpress (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
Molecular Weight

206.24

Formula

C12H14O3

CAS No.
SMILES

O=C(OCC)/C=C/C1=CC=C(OC)C=C1

Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

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

Purity & Documentation
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4-Methoxycinnamic acid ethyl ester
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