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Synonym name:
Catalogue No.: BP0584
Cas No.: 24211-30-1
Formula: C17H16O5
Mol Weight: 300.31
Botanical Source: the leaves of Rhododendron farrerae and other Rhododendron spp., from Cyrtomium spp., Phormium tenax and Angophora spp.
Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle
Can be supplied from milligrams to grams.
For Reference Standard and R&D, Not for Human Use Directly.
Inquire for bulk scale.
Description:
Farrerol has antioxidative, anti-bacterial, anti-inflammatory, antiangiogenic activities, it is a potential candidate for the intervention of endothelial-injury-associated cardiovascular diseases. Farrerol inactivates KEAP-1 or activates the Akt, p38 and ERK to facilitate the release of Nrf2 from Keap1 and subsequent reduces the intracellular production of reactive oxygen species via the induction of HO-1 expression. Farrerol can inhibit angiogenesis through down regulation of Akt/mTOR, Erk and Jak2/Stat3 signal pathway, and can inhibit IL-1β-induced inflammatory responses in osteoarthritis chondrocytes by blocking PI3K/Akt/NF-κB signaling pathway.
References:
Chem Biol Interact. 2015 Jun 22.
The antioxidative potential of farrerol occurs via the activation of Nrf2 mediated HO-1 signaling in RAW 264.7 cells.
Farrerol, (S)-2,3-dihydro-5,7-dihydroxy-2-(4-hydroxyphenyl)-6,8-dimethyl-4-benzopyrone, isolated from rhododendron, has been shown to have antioxidative potential, but the molecular mechanism underlying this activity remains unclear. The inducible expression of heme oxygenase-1 (HO-1), a potent antioxidative and cytoprotective enzyme, is known to play an important role in cytoprotection in a variety of pathological models.
METHODS AND RESULTS:
In this study, we evaluated the antioxidative potential of Farrerol against oxidative damage and investigated its antioxidative mechanism in RAW 264.7 cells. The molecular mechanism underlying the cytoprotective function of Farrerol was determined by analyzing intracellular signaling pathways, transcriptional activation and the inhibitory effect of HO-1 on ROS production. Farrerol induced antioxidant enzymes mRNA expression, HO-1 protein expression and nuclear translocation of NF-E2-related factor 2 in RAW 264.7 macrophage cells. Farrerol down-regulated the expression of the Keap1 protein and the thiol reducing agents attenuated Farrerol-induced HO-1 expression. Further investigation utilizing Western blotting and specific inhibitors of Akt, p38, JNK and ERK demonstrated that Akt, p38, and ERK axis of signaling pathway mediates HO-1 expression. Moreover, tert-butyl hydroperoxide (t-BHP)-induced oxidative damage was ameliorated by Farreroltreatment in a dose-dependent manner, which was abolished by Akt, p38, ERK and HO-1 inhibitors (Snpp). It is hence likely that Farrerol inactivated KEAP-1 or activated the Akt, p38 and ERK to facilitate the release of Nrf2 from Keap1 and subsequent reduced the intracellular production of reactive oxygen species via the induction of HO-1 expression.
CONCLUSIONS:
These results support the central role of HO-1 in the cytoprotective effect of Farrerol.
Microb Pathog. 2013 Dec;65:1-6.
Farrerol regulates antimicrobial peptide expression and reduces Staphylococcus aureus internalization into bovine mammary epithelial cells.
Mastitis, defined as inflammation of the mammary gland, is an infectious disease with a major economic influence on dairy industry. Staphylococcus aureus is a common gram-positive pathogen that frequently causes subclinical, chronic infection of the mammary gland in dairy cows. Farrerol, a traditional Chinese medicine isolated from rhododendron, has been shown to have anti-bacterial activity. However, the effect of Farrerol on S. aureus infection in mammary epithelium has not been studied in detail. The aim of this study was to investigate the effect of Farrerol on the invasion of bovine mammary epithelial cells (bMEC) by S. aureus.
METHODS AND RESULTS:
The expression of antimicrobial peptide genes by bMEC were assessed in the presence or absence of S. aureus infection. Our results demonstrated that Farrerol (4-16 μg/ml) reduced > 55% the internalization of S. aureus into bMEC. We also found that Farrerol was able to down-regulate the mRNA expression of tracheal antimicrobial peptide (TAP) and bovine neutrophil β-defensin 5 (BNBD5) in bMEC infected with S. aureus. The Nitric oxide (NO) production of bMEC after S. aureus stimulation was decreased by Farrerol treatment. Furthermore, Farrerol treatment suppressed S. aureus-induced NF-κB activation in bMEC.
CONCLUSIONS:
These results demonstrated that Farrerol modulated TAP and BNBD5 gene expression in mammary gland, enhances bMEC defense against S. aureus infection and could be useful in protection against bovine mastitis.
Eur J Pharmacol. 2015 Oct 5;764:443-7.
Anti-inflammatory effects of farrerol on IL-1β-stimulated human osteoarthritis chondrocytes.
The present study aimed to investigate the anti-inflammatory effects and the underlying molecular mechanism of Farrerol on IL-1β-stimulated human osteoarthritis chondrocytes.
METHODS AND RESULTS:
Chondrocytes were pretreated with Farrerol 1h before IL-1β stimulation. The effects of Farrerol on NO and PGE2 production were tested by Griess reagent and ELISA. The effects of Farrerol on COX-2, iNOS, Akt, phosphorylated Akt, and NF-κB activation were measured by western blot analysis. The results showed that Farrerol remarkably inhibited IL-1β-induced NO and PGE2 production, as well as COX-2 and iNOS expression. Farrerol also inhibited IL-1β-induced NF-κB activation. Furthermore, Farrerol significantly inhibited IL-1β-induced phosphorylation of PI3K and Akt.
CONCLUSIONS:
In conclusion, these results indicated that Farrerol inhibited IL-1β-induced inflammatory responses in osteoarthritis chondrocytes by blocking PI3K/Akt/NF-κB signaling pathway.
HPLC of Farrerol
HNMR of Farrerol
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
86.9900
2.8213
2.6101
.1999
3.0073
28.0599
Low
89.3717
3.0275
No
No
Yes
No
Yes
No
0.6
Yes
No
Yes
No
Natural products, as important sources of drug discovery, have attracted much attention due to their structural diversity and biological activity. Farrerol is a flavonoid compound isolated from rhododendron (Rhododendron spp.), and in recent years, it has become a hot topic in pharmacological research due to its multiple biological activities. Rhododendron not only exhibits significant antioxidant, anti-inflammatory, and antitumor activities, but also possesses multiple pharmacological effects such as neuroprotective and hepatoprotective effects, demonstrating broad potential for medicinal development. Especially in research on the treatment of breast cancer and other tumors, azelucine demonstrates a complex yet effective mechanism of action by regulating multiple key molecular targets. This paper will systematically review the chemical structure, origins, pharmacological activity, mechanism of action, and druggability evaluation of rheudoxine, aiming to provide theoretical basis and research directions for its clinical application and new drug development.
Farrerol (CAS No.: 24211-30-1) is a flavonoid compound with a molecular formula of C_17H_14O_5 and a molecular weight of 300.31. Its structural features include a typical flavonoid backbone with multiple hydroxyl substituents, which give it excellent antioxidant activity. The LogP value of ajudazine is 2.82, indicating moderate lipid solubility, which is beneficial for cell membrane penetration. The topological polar surface area (TPSA) is 86.99, indicating moderate polarity that facilitates binding to biological targets. Low water solubility (0.1999 mg/mL) indicates limited solubility in the aqueous phase, which may affect its bioavailability. The blood-brain barrier has relatively low permeability, indicating that its distribution in the central nervous system is somewhat limited. The hERG channel inhibition test was negative, indicating a low risk of cardiotoxicity. The Ames test scored 0.6, indicating a low genotoxicity risk.
Rhododendron is mainly found in plants of the Azalea genus, especially in traditional Chinese medicinal herbs such as Dendrobium officinale and rhododendron. Its content is greatly influenced by plant species, growing environment, and harvest time. The extraction method typically uses organic solvent extraction combined with chromatography separation technology. Common extraction processes include:
In recent years, ultrasound-assisted extraction and microwave-assisted extraction technologies have also been applied to the extraction of rhododendron, improving extraction efficiency and purity.
Azelaic has a significant free radical scavenging ability, effectively reducing intracellular reactive oxygen species (ROS) levels and alleviating cellular damage caused by oxidative stress. In vitro experiments show that azelaine enhances cellular antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity, enhancing cells' ability to resist oxidative damage.
Azelaquin can inhibit the expression of inflammatory factors, including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and nitric oxide (NO), reducing inflammatory responses. Its mechanism involves inhibiting the nuclear factor κB (NF-κB) signaling pathway, blocking the transmission of pro-inflammatory signals, and reducing the release of inflammatory mediators.
Rhodendulin demonstrates the ability to inhibit proliferation and induce apoptosis across various tumor cell lines, and has attracted particular attention in breast cancer research. Its antitumor effects involve regulation of multiple signaling pathways, including activating the AMPK pathway, inhibiting STAT3 signaling, modulating the expression of BCL2 family proteins, and promoting cancer cell apoptosis. Additionally, azelaine can inhibit tumor cell migration and invasion, partly by reduced MMP2 enzyme activity.
Azedrin protects nerve cells from damage by inhibiting oxidative stress and inflammatory responses. Related studies have shown that it can alleviate neuroinflammation and apoptosis in neurodegenerative disease models, improve cognitive impairment, and demonstrate potential neuroprotective value.
Audericular has shown protective effects against various liver injury models, reducing hepatocyte necrosis and fibrosis. Its mechanisms include antioxidant, anti-inflammatory, and regulation of hepatocyte apoptosis, demonstrating potential as an adjunct therapy for liver diseases.
The multi-target mechanism of ajuazine forms the basis of its various pharmacological activities. For breast cancer, azelucine mainly regulates the following key targets:
In summary, aude juuantin achieves comprehensive regulation of tumor cells through synergistic action across multiple targets and pathways.
The druggability parameters of ajuazine indicate that it has certain potential for drug development. Its moderate molecular weight and lipophilic solubility facilitate absorption in the body and penetration of cell membranes. The TPSA value suggests moderate polarity, which may facilitate binding to target proteins. Lower water solubility may limit its oral bioavailability, requiring improvements through formulation optimization or drug carrier technology.
Low blood-brain barrier permeability means that rheudodon has limited distribution in the central nervous system, but this also reduces the risk of potential central toxicity. hERG channels show no inhibitory effect, indicating good cardiac safety. Ames test results showed a low genotoxicity risk and met safety requirements.
In terms of pharmacokinetics, current research is relatively limited. In vivo, metabolic pathways may involve liver phase I and II metabolic enzymes, and the activity and toxicity of these metabolites require further evaluation. Parameters such as half-life, oral absorption rate, and tissue distribution still require systematic research to guide clinical dosage formulation design and administration regimens.
As a multifunctional natural flavonoid compound, azelaoids exhibit broad pharmacological activity and good safety profiles, especially showing unique advantages in the anti-tumor field. The multi-target mechanism of action for breast cancer provides a theoretical foundation for its clinical development. Future research should focus on the following aspects:
With advances in molecular biology and medicinal chemistry, the mechanism of action of ajuantazine will become clearer, laying a solid foundation for its transformation into clinical drugs.
As a natural flavonoid compound derived from azalea flowers, azelaine demonstrates broad medicinal value due to its multi-target and multi-pathway pharmacological activity. Its research achievements in antioxidant, anti-anti-inflammatory, anti-tumor, neuroprotection, and liver protection provide important examples for natural product pharmacology. Although challenges such as poor water solubility and insufficient pharmacokinetic data remain, with the application of modern drug development technologies, ajuazumin is expected to become a candidate molecule for novel antitumor and multifunctional protective drugs. Future in-depth research will drive its clinical translation, benefiting more patients.
Shenshuai
Wenjing
Hedandan
