| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 50mg |
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| 250mg | |||
| Other Sizes |
| Targets |
- ERK1/2, JNK1/2, NF-κB [1]
- Nrf2/Keap1 [2] - Akt/mTOR, Erk, Jak2/Stat3 [3] - Epithelial mesenchymal transition (EMT) inducers [4] - AKT, NF-κB [5] - Nrf2, Autophagy-related targets [6] |
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| ln Vitro |
AKT, ERK1/2, JNK1/2, and NF-κB p65 phosphorylation are inhibited by farrerol [1]. In the small star cell line, farrerol augments β-amyloid-induced redox and regulation via Nrf2/Keap1 [1]. By inhibiting Akt/mTOR, Erk, and Jak2/Stat3 signaling, farrerol prevents venogenesis [3]. By controlling the production of inducible factors, farrerol prevents lung squamous glucose from going through the semi-epithelial-mesenchymal transition [4]. Hepatotoxicity in respiratory tract digestion is repaired by Nrf2 and autophagy [6].
- In colon epithelial cells and macrophages, Farrerol inhibited TNBS-induced activation of ERK1/2, JNK1/2, and NF-κB pathways. It reduced the expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and chemokines, and suppressed the phosphorylation of ERK1/2, JNK1/2, and NF-κB p65. [1] - In microglia cells, Farrerol attenuated β-amyloid-induced oxidative stress by upregulating Nrf2 nuclear translocation and downstream antioxidant enzymes (HO-1, NQO1). It also inhibited the production of inflammatory mediators (iNOS, COX-2, TNF-α, IL-1β) via regulating Nrf2/Keap1 pathway. [2] - In vascular endothelial cells, Farrerol inhibited angiogenesis by suppressing Akt/mTOR, Erk, and Jak2/Stat3 signaling pathways. It reduced cell proliferation, migration, and tube formation of endothelial cells. [3] - In lung squamous cell carcinoma cells, Farrerol downregulated the expression of EMT inducers (Snail, Slug, Twist), inhibited cell invasion and migration, and reversed epithelial-mesenchymal transition. [4] - In dopaminergic neuron-like cells and microglia, Farrerol suppressed LPS-induced activation of AKT and NF-κB pathways, reduced the release of inflammatory factors, and protected dopaminergic neurons from damage. [5] - In hepatocytes, Farrerol activated Nrf2 pathway and promoted autophagy, which alleviated APAP-induced oxidative stress and hepatocyte injury. [6] |
| ln Vivo |
Farrerol protects dopaminergic neurons in lipopolysaccharide-induced neural models of Parkinson's disease by decreasing the activation of AKT and NF-κB signaling feedback [5].
- In TNBS-induced colitis mice, Farrerol (administered at 20 and 40 mg/kg) improved colonic histopathological changes, reduced colonic mucosal damage, and decreased the levels of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) in colon tissues. It also inhibited the phosphorylation of ERK1/2, JNK1/2, and NF-κB p65 in colon tissues. [1] - In LPS-induced Parkinson's disease rats, Farrerol (administered at 10, 20, and 40 mg/kg) protected dopaminergic neurons in the substantia nigra pars compacta, increased dopamine levels in the striatum, and reduced microglial activation. It suppressed the activation of AKT and NF-κB pathways in brain tissues. [5] - In APAP-induced hepatotoxicity mice, Farrerol (administered at 25 and 50 mg/kg) reduced serum ALT and AST levels, alleviated hepatic histological damage, and decreased oxidative stress markers (ROS, MDA) in liver tissues. It activated Nrf2 pathway and promoted autophagy in liver tissues. [6] |
| Enzyme Assay |
- For ERK1/2, JNK1/2, and NF-κB activity detection: Cell or tissue lysates were prepared and subjected to SDS-PAGE electrophoresis. Proteins were transferred to membranes, blocked, and incubated with primary antibodies against phosphorylated ERK1/2, JNK1/2, and NF-κB p65, followed by secondary antibodies. The immunoreactive bands were detected using chemiluminescence, and band intensities were quantified. [1]
- For Nrf2 activity assay: Nuclear and cytoplasmic extracts were prepared from cells. The expression of Nrf2 in nuclear fractions was detected by western blot as described above. The activity of Nrf2 downstream enzymes (HO-1, NQO1) was measured using specific assay kits according to standard protocols. [2] - For Akt/mTOR, Erk, and Jak2/Stat3 activity detection: Cell lysates were analyzed by western blot with antibodies against phosphorylated Akt, mTOR, Erk, Jak2, and Stat3. The relative phosphorylation levels were calculated by normalizing to total protein expression. [3] - For autophagy-related enzyme activity: Cell or tissue lysates were assayed for LC3-II/LC3-I ratio and Beclin-1 expression via western blot. The activity of autophagic flux was evaluated by detecting the degradation of p62. [6] |
| Cell Assay |
- Colon epithelial cells and macrophages were seeded in culture plates and treated with TNBS (to induce inflammation) and different concentrations of Farrerol (0, 10, 20, 40 μM) for 24 hours. Cell viability was measured by CCK-8 assay. The expression of pro-inflammatory cytokines and signaling pathway proteins was detected by western blot and qRT-PCR. [1]
- Microglia cells were pretreated with Farrerol (0, 5, 10, 20 μM) for 2 hours, then stimulated with β-amyloid for 24 hours. Oxidative stress markers (ROS, MDA, SOD) were measured using respective kits. Inflammatory mediator expression was analyzed by western blot and qRT-PCR. Nrf2 nuclear translocation was observed by immunofluorescence staining. [2] - Vascular endothelial cells were treated with Farrerol (0, 5, 10, 20 μM) for 24 hours. Cell proliferation was detected by EdU assay. Cell migration was evaluated by scratch wound healing assay and Transwell assay. Tube formation assay was performed on Matrigel-coated plates. Signaling pathway proteins were analyzed by western blot. [3] - Lung squamous cell carcinoma cells were treated with Farrerol (0, 10, 20, 40 μM) for 48 hours. Cell invasion and migration were detected by Transwell assay. The expression of EMT-related proteins (E-cadherin, N-cadherin, Snail, Slug, Twist) was analyzed by western blot and qRT-PCR. [4] - Dopaminergic neuron-like cells and microglia were pretreated with Farrerol (0, 5, 10, 20 μM) for 2 hours, then stimulated with LPS for 24 hours. Cell viability was measured by MTT assay. The release of inflammatory cytokines (TNF-α, IL-1β) was detected by ELISA. Signaling pathway proteins (p-AKT, p-NF-κB) were analyzed by western blot. [5] - Hepatocytes were pretreated with Farrerol (0, 10, 20, 40 μM) for 2 hours, then exposed to APAP for 24 hours. Cell viability was assessed by CCK-8 assay. Oxidative stress markers were measured using kits. Autophagy-related proteins (LC3-II/LC3-I, Beclin-1, p62) and Nrf2 pathway proteins were detected by western blot. [6] |
| Animal Protocol |
- TNBS-induced colitis mice model: Mice were randomly divided into control, model, and Farrerol (20, 40 mg/kg) groups. Colitis was induced by intrarectal administration of TNBS. Farrerol was dissolved in 0.5% carboxymethylcellulose sodium and administered intragastrically once daily for 7 days. At the end of the experiment, mice were sacrificed, colon tissues were collected for histopathological examination, western blot, and qRT-PCR analysis. [1]
- LPS-induced Parkinson's disease rats model: Rats were divided into control, model, and Farrerol (10, 20, 40 mg/kg) groups. Parkinson's disease was induced by intraperitoneal injection of LPS. Farrerol was dissolved in normal saline and administered intraperitoneally once daily for 14 days. After treatment, rats were subjected to behavioral tests. Brain tissues (substantia nigra pars compacta, striatum) were collected for immunohistochemistry, western blot, and dopamine content detection. [5] - APAP-induced hepatotoxicity mice model: Mice were divided into control, model, and Farrerol (25, 50 mg/kg) groups. Hepatotoxicity was induced by intraperitoneal injection of APAP. Farrerol was dissolved in 0.5% carboxymethylcellulose sodium and administered intragastrically 1 hour before APAP injection. Mice were sacrificed 24 hours after APAP administration. Serum and liver tissues were collected for biochemical analysis (ALT, AST), histopathological examination, and western blot analysis. [6] |
| References |
|
| Additional Infomation |
It has been reported that rhododendron dauricum, Rhododendron farrerae, and Daphne aurantiaca all contain farrolein, and there is relevant data available.
See also: ……See more …… - Farool is a natural flavonoid compound with potential anti-inflammatory, antioxidant, anti-angiogenic, antitumor, and neuroprotective activities [1-6] - In colitis, farool exerts a protective effect by inhibiting inflammatory signaling pathways and reducing the production of pro-inflammatory cytokines [1] - In neurodegenerative diseases, farool protects neurons by alleviating oxidative stress, inflammation, and neuronal damage [2,5] - In cancer, farool inhibits tumor progression by inhibiting angiogenesis and epithelial-mesenchymal transition [3,4] - In liver injury, farool reduces hepatotoxicity by activating antioxidant pathways and promoting autophagy [6] |
| Molecular Formula |
C17H16O5
|
|---|---|
| Molecular Weight |
300.3059
|
| Exact Mass |
300.099
|
| CAS # |
24211-30-1
|
| PubChem CID |
91144
|
| Appearance |
White to light yellow solid powder
|
| Density |
1.4±0.1 g/cm3
|
| Boiling Point |
583.0±50.0 °C at 760 mmHg
|
| Flash Point |
219.7±23.6 °C
|
| Vapour Pressure |
0.0±1.7 mmHg at 25°C
|
| Index of Refraction |
1.662
|
| LogP |
4.11
|
| Hydrogen Bond Donor Count |
3
|
| Hydrogen Bond Acceptor Count |
5
|
| Rotatable Bond Count |
1
|
| Heavy Atom Count |
22
|
| Complexity |
417
|
| Defined Atom Stereocenter Count |
0
|
| SMILES |
O1C2=C(C([H])([H])[H])C(=C(C([H])([H])[H])C(=C2C(C([H])([H])C1([H])C1C([H])=C([H])C(=C([H])C=1[H])O[H])=O)O[H])O[H]
|
| InChi Key |
DYHOLQACRGJEHX-UHFFFAOYSA-N
|
| InChi Code |
InChI=1S/C17H16O5/c1-8-15(20)9(2)17-14(16(8)21)12(19)7-13(22-17)10-3-5-11(18)6-4-10/h3-6,13,18,20-21H,7H2,1-2H3
|
| Chemical Name |
5,7-dihydroxy-2-(4-hydroxyphenyl)-6,8-dimethyl-2,3-dihydrochromen-4-one
|
| 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: This product requires protection from light (avoid light exposure) during transportation and storage. |
| 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 : ~125 mg/mL (~416.24 mM)
|
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (6.93 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 20.8 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: ≥ 2.08 mg/mL (6.93 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 20.8 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: ≥ 2.08 mg/mL (6.93 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 | 3.3299 mL | 16.6495 mL | 33.2989 mL | |
| 5 mM | 0.6660 mL | 3.3299 mL | 6.6598 mL | |
| 10 mM | 0.3330 mL | 1.6649 mL | 3.3299 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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