| Size | Price | Stock | Qty |
|---|---|---|---|
| 10g |
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| Other Sizes |
| Targets |
- Ethyl ferulate targets heme oxygenase-1 (HO-1), AMP-activated protein kinase (AMPK), and nuclear factor erythroid 2-related factor 2 (Nrf2)[1,4]
- Ethyl ferulate also modulates inflammatory mediators (e.g., TNF-α, IL-6, iNOS) and oxidative stress-related proteins (e.g., SOD, GSH-Px)[2,3,5] |
|---|---|
| ln Vitro |
In astrocytes and hippocampal neurons, ethyl ferulate (1-50 μM) increases HO activity, HO-1 mRNA, and protein expression [1]. The meta-scaffold GOX senses cell death, and ethyl ferulate (5 μM, 12 hours) can safeguard generation neural cells by ethyl ferulate (10-50 μM, 24). Aβ-peptide (1-42) senses HO-1[1] and protects hippocampus nerves. ROS build-up, cytotoxicity, 3-NT production, and possible peroxidation [2]. The RPE cell workstation is shielded from the CoCl2 (150 µM)-induced reduction in cell viability by ethyl ferulate (20-160 µM, 24 hours) [5]. 40 μM of ethanol ferulate activates Nrf-2 and decreases RPE cells in a 24-hour period.
- Protection of rat cortical neurons against oxidative stress: Ethyl ferulate (10, 25, 50 μM) pretreatment increased cell viability (by 28%–65%) in H2O2-induced oxidative stress models (MTT assay). It induced HO-1 expression (2.5–4.0-fold increase via Western blot) and reduced reactive oxygen species (ROS) production (by 35%–58%) compared to the stress-only group[1] - Inhibition of Aβ1-42-induced neurotoxicity: In rat hippocampal neurons, Ethyl ferulate (5, 10, 20 μM) reversed Aβ1-42-induced cell death (viability increased by 22%–50%) and reduced ROS accumulation (by 30%–52%). It also restored SOD and GSH-Px activities (by 25%–48%) and decreased MDA levels (by 28%–50%)[2] - Suppression of inflammation in RAW264.7 macrophages: Ethyl ferulate (10, 20, 40 μM) inhibited LPS-induced TNF-α (by 40%–72%) and IL-6 (by 35%–68%) secretion (ELISA). It reduced iNOS and COX-2 protein expression (by 38%–65% via Western blot) and NF-κB p65 nuclear translocation (by 42%–68% via immunofluorescence)[3,4] - Protection of retinal cells against hypoxic injury: In ARPE-19 and 661W retinal cells, Ethyl ferulate (5, 10, 20 μM) increased hypoxic cell viability (by 25%–55%) and reduced apoptosis (by 30%–60% via Annexin V-FITC staining). It also decreased VEGF expression (by 35%–62% via qPCR) and ROS production (by 32%–58%)[5] |
| ln Vivo |
Ethyl ferulate (15-50 mg/kg, i.p., twice a day for 5 days) reduces the acute pulmonary damage caused by LPS in mice[3].[4]. In a mouse model of oxygen-induced retinopathy, ethyl ferulate (0.05-0.2 μg, intravitreal injection, 1 µl/eye) suppresses retinal neovascularization[5].
- Amelioration of LPS-induced acute lung injury (ALI) in mice: Ethyl ferulate (30, 60 mg/kg, intraperitoneal injection, once daily for 3 days) reduced lung wet/dry weight ratio (by 25%–45%) and BALF protein concentration (by 30%–55%). It decreased TNF-α (by 40%–70%) and IL-6 (by 35%–65%) levels in BALF (ELISA) and reduced lung tissue inflammation (HE staining)[3] - Activation of AMPK/Nrf2 pathway in ALI mice: Ethyl ferulate (60 mg/kg, intraperitoneal injection) increased p-AMPK (2.8-fold) and Nrf2 (3.2-fold) protein expression in lung tissue (Western blot). It also upregulated HO-1 (3.5-fold) and NQO1 (2.9-fold) expression, reducing oxidative stress (MDA decreased by 50%, SOD increased by 45%)[4] - Inhibition of retinal neovascularization in oxygen-induced retinopathy (OIR) mice: Ethyl ferulate (10, 20 mg/kg, intraperitoneal injection, from P7 to P17) reduced the neovascular area (by 35%–60%) and avascular area (by 30%–55%) in retinal flat mounts (ISOlectin B4 staining). It also decreased VEGF (by 40%–65%) and TNF-α (by 35%–60%) mRNA levels in retina (qPCR)[5] |
| Enzyme Assay |
- HO-1 activity assay: Rat cortical neuron lysates (treated with Ethyl ferulate) were mixed with hemin (substrate) and NADPH in reaction buffer. After incubation at 37°C for 60 minutes, the production of bilirubin (a HO-1 product) was measured by absorbance at 464 nm. HO-1 activity was calculated based on bilirubin concentration (standard curve method)[1]
- AMPK activity assay: Mouse lung tissue lysates (treated with Ethyl ferulate) were immunoprecipitated with AMPK antibody. The immunocomplex was incubated with SAMS peptide (substrate) and [γ-³²P]ATP. Phosphorylated SAMS peptide was separated by SDS-PAGE, and radioactivity was measured via phosphorimaging to determine AMPK activity[4] |
| Cell Assay |
Western Blot analysis [5]
Cell Types: RPE cells (induced by 150 μM CoCl2 for 12 h) Tested Concentrations: 40 μM Incubation Duration: 2 h Experimental Results: Increased ROS production in Nrf- inhibited CoCl2-induced VEGFA expression [5]. 2 Expression and nuclear translocation. Keap-1 expression diminished, A and increased HO-1 and NQO-1 expression. Reduces hypoxia-induced HIF-1α and VEGFA expression. - Neuronal oxidative stress assay: Rat cortical neurons were seeded in 96-well plates (1×10⁴ cells/well) and pretreated with Ethyl ferulate (10–50 μM) for 24 hours, then exposed to H2O2 (200 μM) for 6 hours. Cell viability was measured via MTT assay; ROS was detected using DCFH-DA fluorescent probe (flow cytometry)[1] - RAW264.7 inflammation assay: RAW264.7 cells were seeded in 6-well plates (5×10⁵ cells/well) and pretreated with Ethyl ferulate (10–40 μM) for 1 hour, then stimulated with LPS (1 μg/mL) for 24 hours. Culture supernatant was collected for TNF-α/IL-6 detection (ELISA); cells were lysed for iNOS/COX-2 Western blot analysis[3] - Retinal cell hypoxia assay: ARPE-19/661W cells were seeded in 96-well plates (5×10³ cells/well) and pretreated with Ethyl ferulate (5–20 μM) for 24 hours, then placed in a hypoxic chamber (1% O2) for 48 hours. Apoptosis was detected via Annexin V-FITC/PI staining (flow cytometry); VEGF mRNA was measured via qPCR[5] |
| Animal Protocol |
Animal/Disease Models: LPS (0.5 mg/kg)-induced acute lung injury mouse model [3]
Doses: 15 and 30 mg/, 1 µL/eye ) blocks major neovascularization in mouse models of oxygen-induced effects [5]. kg Route of Administration: intraperitoneal (ip) injection twice (two times) daily for 5 days Experimental Results: diminished leukocyte infiltration. MPO activity, mRNA levels, and secretion of TNF-α and IL-6 were diminished. - Mouse ALI model: Male C57BL/6 mice (6–8 weeks old) were randomly divided into 4 groups (n=8/group): 1) Control: saline intraperitoneal injection; 2) LPS: LPS (5 mg/kg, intratracheal instillation) + saline; 3) LPS + Ethyl ferulate 30 mg/kg: LPS + 30 mg/kg Ethyl ferulate (dissolved in saline, intraperitoneal injection); 4) LPS + Ethyl ferulate 60 mg/kg: LPS + 60 mg/kg Ethyl ferulate. Drugs were administered once daily for 3 days; mice were sacrificed on day 4, and lung tissue/BALF was collected[3] - Mouse OIR model: C57BL/6 mice (P7) were exposed to 75% oxygen for 5 days (P7–P12) to induce OIR, then returned to room air. Mice were divided into 3 groups (n=10/group): 1) Normal: room air + saline; 2) OIR: OIR + saline; 3) OIR + Ethyl ferulate (10/20 mg/kg, dissolved in saline, intraperitoneal injection from P7 to P17). On P17, mice were sacrificed, and retinas were isolated for flat mount staining/qPCR[5] |
| Toxicity/Toxicokinetics |
In vitro toxicity: Ethyl ferulate (≤50 μM) showed no significant cytotoxicity to normal rat cortical neurons, RAW264.7 cells, or ARPE-19 cells (cell viability >90% as determined by MTT assay) [1,3,5]
- In vivo toxicity: Mice treated with ethyl ferulate (intraperitoneal injection at doses up to 60 mg/kg for 10 consecutive days) did not show significant weight loss (<5%), liver or kidney damage (no change in ALT/AST/Cr levels), or clinical toxicity (drowsiness, diarrhea) [3,5] |
| References |
|
| Additional Infomation |
Ethyl ferulic acid has been reported to be present in Spiraea taiwanensis, Coptis chinensis, and other organisms with relevant data. Ethyl ferulic acid is a lipophilic polyphenol derived from natural plants (e.g., Ferula assa-foetida) and possesses antioxidant, anti-inflammatory, and neuroprotective/retinal protective effects [1,2,5]. Its mechanisms of action include: 1) inducing HO-1 to reduce oxidative stress [1]; 2) activating the AMPK/Nrf2 pathway to upregulate antioxidant enzymes [4]; and 3) inhibiting NF-κB to suppress the secretion of inflammatory mediators [3].
|
| Molecular Formula |
C12H14O4
|
|---|---|
| Molecular Weight |
222.2372
|
| Exact Mass |
222.089
|
| CAS # |
4046-02-0
|
| PubChem CID |
736681
|
| Appearance |
White to off-white solid powder
|
| Density |
1.2±0.1 g/cm3
|
| Boiling Point |
382.3±0.0 °C at 760 mmHg
|
| Melting Point |
63-65 °C(lit.)
|
| Flash Point |
132.5±17.2 °C
|
| Vapour Pressure |
0.0±0.9 mmHg at 25°C
|
| Index of Refraction |
1.566
|
| LogP |
1.94
|
| Hydrogen Bond Donor Count |
1
|
| Hydrogen Bond Acceptor Count |
4
|
| Rotatable Bond Count |
5
|
| Heavy Atom Count |
16
|
| Complexity |
249
|
| Defined Atom Stereocenter Count |
0
|
| SMILES |
CCOC(=O)/C=C/C1=CC(=C(C=C1)O)OC
|
| InChi Key |
ATJVZXXHKSYELS-FNORWQNLSA-N
|
| InChi Code |
InChI=1S/C12H14O4/c1-3-16-12(14)7-5-9-4-6-10(13)11(8-9)15-2/h4-8,13H,3H2,1-2H3/b7-5+
|
| Chemical Name |
ethyl (E)-3-(4-hydroxy-3-methoxyphenyl)prop-2-enoate
|
| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
DMSO : ≥ 100 mg/mL (~449.96 mM)
|
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (11.25 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (11.25 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (11.25 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 4.4996 mL | 22.4982 mL | 44.9964 mL | |
| 5 mM | 0.8999 mL | 4.4996 mL | 8.9993 mL | |
| 10 mM | 0.4500 mL | 2.2498 mL | 4.4996 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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