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  • Brand : BIOFRON

  • Catalogue Number : BF-T3009

  • Specification : 98%

  • CAS number : 480-18-2

  • Formula : C15H12O7

  • Molecular Weight : 304.25

  • PUBCHEM ID : 439533

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



Off-white crystalline powder

Botanical Source

Albizia julibrissin,Acacia catechu,Gleditsia sinensis,Cinnamomum cassia,Olea europaea

Structure Type



Standards;Natural Pytochemical;API




Dihydroquercetin/(3R)-2-(3,4-Dihydroxyphenyl)-3,5,7-trihydroxy-2,3-dihydro-4H-chromen-4-one/(2R,3R)-3,3',4',5,7-Pentahydroxyflavanone/4H-1-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-2,3-dihydro-3,5,7-trihydroxy-, (2R,3R)-/Distylin/(+)-Taxifolin/(2S,3S)-2-(3,4-Dihydroxyphenyl)-3,5,7-trihydroxy-2,3-dihydro-4H-chromen-4-one/4H-1-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-2,3-dihydro-3,5,7-trihydroxy-, (2R-trans)-/5-18-05-00451/4H-1-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-2,3-dihydro-3,5,7-trihydroxy-, (2S,3S)-/Taxifolin/(-)-taxifolin/Taxifoliol/(2R,3R)-2-(3,4-Dihydroxyphenyl)-3,5,7-trihydroxy-2,3-dihydro-4H-chromen-4-one




1.7±0.1 g/cm3



Flash Point

264.2±25.0 °C

Boiling Point

687.6±55.0 °C at 760 mmHg

Melting Point

230-233°C (dec.)


InChl Key

WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:480-18-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Cerebral amyloid angiopathy (CAA) induces various forms of cerebral infarcts and hemorrhages from vascular amyloid-β accumulation, resulting in acceleration of cognitive impairment, which is currently untreatable. Soluble amyloid-β protein likely impairs cerebrovascular integrity as well as cognitive function in early stage Alzheimer’s disease. Taxifolin, a flavonol with strong anti-oxidative and anti-glycation activities, has been reported to disassemble amyloid-β in vitro but the in vivo relevance remains unknown. Here, we investigated whether taxifolin has therapeutic potential in attenuating CAA, hypothesizing that inhibiting amyloid-β assembly may facilitate its clearance through several elimination pathways. Vehicle- or taxifolin-treated Tg-SwDI mice (commonly used to model CAA) were used in this investigation. Cognitive and cerebrovascular function, as well as the solubility and oligomerization of brain amyloid-β proteins, were investigated. Spatial reference memory was assessed by water maze test. Cerebral blood flow was measured with laser speckle flowmetry and cerebrovascular reactivity evaluated by monitoring cerebral blood flow changes in response to hypercapnia. Significantly reduced cerebrovascular pan-amyloid-β and amyloid-β1-40 accumulation was found in taxifolin-treated Tg-SwDI mice compared to vehicle-treated counterparts (n = 5). Spatial reference memory was severely impaired in vehicle-treated Tg-SwDI mice but normalized after taxifolin treatment, with scoring similar to wild type mice (n = 10-17). Furthermore, taxifolin completely restored decreased cerebral blood flow and cerebrovascular reactivity in Tg-SwDI mice (n = 4-6). An in vitro thioflavin-T assay showed taxifolin treatment resulted in efficient inhibition of amyloid-β1-40 assembly. In addition, a filter trap assay and ELISA showed Tg-SwDI mouse brain homogenates exhibited significantly reduced levels of amyloid-β oligomers in vivo after taxifolin treatment (n = 4-5), suggesting the effects of taxifolin on CAA are attributable to the inhibition of amyloid-β oligomer formation. In conclusion, taxifolin prevents amyloid-β oligomer assembly and fully sustains cognitive and cerebrovascular function in a CAA model mice. Taxifolin thus appears a promising therapeutic approach for CAA.


Alzheimer’s disease; Cerebral amyloid angiopathy; Oligomer; Taxifolin; Treatment


Taxifolin inhibits amyloid-β oligomer formation and fully restores vascular integrity and memory in cerebral amyloid angiopathy.


Saito S1,2, Yamamoto Y3, Maki T4, Hattori Y5, Ito H6, Mizuno K7, Harada-Shiba M3,8, Kalaria RN9, Fukushima M10, Takahashi R4, Ihara M11.

Publish date

2017 Apr 4


28579433 DOI: 10.1016/j.bbrc.2017.06.002 [Indexed for MED


Taxifolin, a flavonoid compound, has been reported to stimulate osteogenic differentiation in osteoblasts. The present study investigated whether taxifolin affects the osteogenic differentiation of human bone marrow mesenchymal stem cells (hBMSCs) and the molecular mechanisms involved. The proliferation and osteogenic differentiation of hBMSCs in the presence of taxifolin were examined by CCK-8 assay, alkaline phosphatase (ALP) activity, ALP staining and Alizarin red staining. The expression of osteogenic differentiation markers were detected by real-time quantitative PCR (RT-PCR) analysis and western blot assay. The activation of potential related pathways was examined by luciferase reporter assay, immunofluorescence and western blot analysis. Taxifolin treatment increased osteogenic differentiation of hBMSCs without cytotoxicity. Luciferase reporter assay showed that taxifolin could not activate estrogen receptor pathway, but inhibit TNF-α-induced NF-κB signaling pathway activation in osteogenic induction condition. Moreover, the nucleus translocation of NF-κB under TNF-α treatment was inhibited by taxifolin treatment. The taxifolin-induced osteogenic differentiation effects of hBMSCs were abolished by TNF-α treatment. In conclusion, our results suggested that taxifolin could promote osteogenesis of hBMSCs, partially through antagonism of NF-κB signaling pathway.
Copyright © 2017 Elsevier Inc. All rights reserved.


Flavonoid; MSC; NF-κB; Osteogenesis; Taxifolin


Taxifolin enhances osteogenic differentiation of human bone marrow mesenchymal stem cells partially via NF-κB pathway.


Wang YJ1, Zhang HQ2, Han HL3, Zou YY3, Gao QL1, Yang GT1.q

Publish date

2017 Aug 12




Taxifolin is a flavonoid. It has been used as a chemopreventive agent and supplement. It may have some beneficial effects to treat prostate cancer by suppressing androgen production in Leydig cells. The objective of the present study was to study the effects of taxifolin on androgen production of rat Leydig cells isolated from immature testis and some rat and human testosterone biosynthetic enzyme activities. Rat Leydig cells were incubated with 100μM taxifolin without (basal) or with 10ng/ml luteinizing hormone (LH), 10mM 8-bromoadenosine 3′,5′-cyclic monophosphate (8BR), and steroid enzyme substrates (20μM): 22R-hydroxychloesterol, pregnenolone, progesterone, and androstenedione. The medium concentrations of 5α-androstane-3α, 17β-diol (DIOL) and testosterone were measured. Taxifolin significantly suppressed basal, LH-stimulated, 8BR-stimulated, pregnenolone-mediated, and progesterone-mediated androgen production by Leydig cells. Further study demonstrated that taxifolin inhibited rat 3β-hydroxysteroid dehydrogenase and 17α-hydroxylase/17, 20-lyase with IC50 values of 14.55±0.013 and 16.75±0.011μM, respectively. Taxifolin also inhibited these two enzyme activities in human testis with IC50 value of about 100μM. Taxifolin was a competitive inhibitor for these two enzymes when steroid substrates were used. In conclusion, taxifolin may have benefits for the treatment of prostate cancer.
Copyright © 2018. Published by Elsevier B.V.


17α-hydroxylase/17,20-lyase; 3β-hydroxysteroid dehydrogenase; Leydig cells; Steroidogenesis; Taxifolin


Taxifolin suppresses rat and human testicular androgen biosynthetic enzymes.


Ge F1, Tian E2, Wang L2, Li X1, Zhu Q1, Wang Y1, Zhong Y3, Ge RS4.

Publish date

2018 Mar

Description :

Taxifolin exhibits important anti-tyrosinase activity. Taxifolin exhibits significant inhibitory activity against collagenase with an IC50 value of 193.3 μM.