Sequoiaflavone
Sequoiaflavone is a biflavonoid compound with multiple activities. Sequoiaflavone suppresses hepatic CYP1A1/(7-Ethoxycoumarin O-deethylase) ECOD, prevents Aβ1-42 fibrillization (IC50 = 0.29 μM) and disaggregates amyloid fibrils (EC50 = 2.04 μM), inhibits Alternaria alternata and inhibits human recombinant PDE5A1 overexpressed in COS-7 cells (IC50 = 19.9 μM) to exert NO-independent vasodilation. Sequoiaflavone can be used in Alzheimer's disease, peripheral circulatory disorder, and antifungal research.
For research use only. We do not sell to patients.
- CAS No.: 21763-71-3
- Formula: C31H20O10
- Molecular Weight:552.48
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| MCF7 | IC50 |
58.4 μM
Compound: 6
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Cytotoxicity against human MCF7 cells measured after 24 hrs by MTT assay
Cytotoxicity against human MCF7 cells measured after 24 hrs by MTT assay
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[PMID: 34875389] |
| PC-3 | GI50 |
43.29 μM
Compound: 18
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Growth inhibition of human PC3 cells by colorimetric MTT assay
Growth inhibition of human PC3 cells by colorimetric MTT assay
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[PMID: 25736997] |
In Vitro
Sequoiaflavone (100 μM; 4 h) fully inhibits spore germination of Alternaria alternata with an ED50 of 18 μM[1].
Sequoiaflavone (100 μM; 7 h) exerts obvious inhibitory effects on germ tube growth of Fusarium culmorum with an ED50 of 12 μM[1].
Sequoiaflavone (100 μM; 24 h) shows no detectable antifungal activity against Cladosporium oxysporum [1].
Sequoiaflavone (0.08 mg/mL) potently inhibits ECOD activity by 75.2%, leaving just 24.8% residual enzyme activity versus the 100% control level in rat liver microsomes[2].
Sequoiaflavone inhibits formation of Aβ fibrils with an IC50 of 0.29 μM[3].
Sequoiaflavone inhibits human recombinant PDE5A1 with an IC50 of 19.9 μM in COS-7 cells[4].
Sequoiaflavone blocks PDE5A1 activity to slow cGMP degradation in COS-7 cells[4].
Sequoiaflavone produces vasodilation via a NO-independent pathway in COS-7 cells[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 21763-71-3
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Molecular Weight 552.48
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Formula C31H20O10
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SMILES
O=C1C=C(C2=CC=C(O)C=C2)OC3=C(C4=CC(C5=CC(C6=C(O)C=C(OC)C=C6O5)=O)=CC=C4O)C(O)=CC(O)=C13
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Amyloid: Congo Red Amyloid Staining
Congo red amyloid staining is a histochemical method used to detect extracellular amyloid deposits in tissue sections based on the affinity of Congo red dye for β-pleated sheet-rich protein aggregates. When bound to amyloid, Congo red produces characteristic apple-green birefringence under polarized light microscopy, which is widely regarded as a diagnostic feature of amyloid deposition in histopathology. The diagnostic principle relies on the combination of dye binding (congophilia) and optical anisotropy under polarized illumination, which distinguishes amyloid from most non-amyloid eosinophilic extracellular deposits in routine histological evaluation. Amyloid identification by Congo red staining remains a cornerstone in diagnostic pathology despite the availability of adjunct methods such as immunohistochemistry and mass spectrometry, particularly because of its ability to localize deposits directly within tissue architecture. The specificity of Congo red-positive deposits is incre
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Alzheimer’s Disease Modeling
Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by a progressive decline in cognitive functions and loss of specific types of neurons and synapses. Alzheimer's symptoms can be simulated in mice by injecting drugs (such as Aβ) or genetically modified.
Purity & Documentation
References
[1]. Krauze-Baranowska M, et al. Antifungal activity of biflavones from Taxus baccata and Ginkgo biloba. Z Naturforsch C J Biosci. 2003 Jan-Feb;58(1-2):65-9. [Content Brief]
[2]. Fidelis QC, et al. Flavonoids and other compounds from Ouratea ferruginea (Ochnaceae) as anticancer and chemopreventive agents. Molecules. 2012 Jul 3;17(7):7989-8000. [Content Brief]
[3]. Choi EY, et al. Polyphenolic Biflavonoids Inhibit Amyloid-Beta Fibrillation and Disaggregate Preformed Amyloid-Beta Fibrils. Biomol Ther (Seoul). 2020 Mar 1;28(2):145-151. [Content Brief]
[4]. Dell'Agli M, et al. Inhibition of cGMP-phosphodiesterase-5 by biflavones of Ginkgo biloba. Planta Med. 2006 Apr;72(5):468-70. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)