Shipping to United States We Offer Worldwide Shipping
Login Wishlist

Fustin

$905

  • Brand : BIOFRON

  • Catalogue Number : AV-C10405

  • Specification : 98%

  • CAS number : 20725-03-5

  • Formula : C15H12O6

  • Molecular Weight : 288.3

  • PUBCHEM ID : 5317435

  • Volume : 5mg

Available on backorder

Quantity
Checkout Bulk Order?

Catalogue Number

AV-C10405

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

288.3

Appearance

Powder

Botanical Source

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

C1=CC(=C(C=C1C2C(C(=O)C3=C(O2)C=C(C=C3)O)O)O)O

Synonyms

2-(3,4-Dihydroxyphenyl)-3,7-dihydroxy-2,3-dihydro-4H-chromen-4-one/3,7,3',4'-tetrahydroxyflavone/5-Deoxydihydrouercetin/3',4',7-TRIHYDROXYFLAVANONOL/3,3',4',7-tetrahydroxyflavanone/4H-1-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-2,3-dihydro-3,7-dihydroxy-/DIHYDROFISETIN/2,3-Dihydrofisetin/2,3-DIHYDROFISETH/FUSTIN/3,7,3',4'-tetrahydroxyflavanone

IUPAC Name

(2R,3R)-2-(3,4-dihydroxyphenyl)-3,7-dihydroxy-2,3-dihydrochromen-4-one

Applications

Density

1.6±0.1 g/cm3

Solubility

Flash Point

249.2±25.0 °C

Boiling Point

644.2±55.0 °C at 760 mmHg

Melting Point

216-217ºC

InChl

InChI=1S/C15H12O6/c16-8-2-3-9-12(6-8)21-15(14(20)13(9)19)7-1-4-10(17)11(18)5-7/h1-6,14-18,20H/t14-,15+/m0/s1

InChl Key

FNUPUYFWZXZMIE-LSDHHAIUSA-N

WGK Germany

RID/ADR

HS Code Reference

2933990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:20725-03-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

17603285

Abstract

6-Hydroxydopamine (6-OHDA) is a neurotoxin and is commonly used to generate experimental models of Parkinson’s disease (PD). In this study, we investigated the signaling molecules involved in the 6-OHDA-induced cell death using a neuronal catecholaminergic cell line (SK-N-SH cells), and the protective effect of fustin, a flavonoid from Rhus verniciflua Stokes, on 6-OHDA-induced neuronal death. 6-OHDA significantly increased levels of reactive oxygen species (ROS), intracellular Ca(2+) ([Ca(2+)](i)), and p38 phosphorylation. In addition, this ROS increase by 6-OHDA was reduced by pretreatment with N-acetylcysteine (NAC), a free radical scavenger, but not by bis-(o-aminophenoxy)-ethane-N,N,N,N-tetraacetic acid (BAPTA), a Ca(2+) chelator. However, the [Ca(2+)](i) increase induced by 6-OHDA was suppressed by NAC. Moreover, pretreatment with NAC or BAPTA significantly prevented the 6-OHDA-induced increases in p38 phosphorylation, Bax/Bcl-2 ratio, and caspase-3 activity. Although 6-OHDA-increased phosphorylation of p38 was prevented by NAC or BAPTA, inhibition of p38 by SB203580 did not suppress ROS, Bax/Bcl-2 ratio, or caspase-3 activity increases, and only partially prevented 6-OHDA-induced cell death, thus demonstrating that p38 activation is a component of a signaling pathway leading to the initiation of 6-OHDA-induced cell death, which acts in parallel with an ROS-Ca(2+)-Bcl-2-caspase-3 pathway. Moreover, fustin not only suppressed 6-OHDA-induced cell death in a concentration-dependent manner but also blocked 6-OHDA-induced increases in ROS, [Ca(2+)](i), Bax/Bcl-2 ratio, caspase-3 activity, and p38 phosphorylation. These results suggest that fustin exerts neuroprotection against 6-OHDA-induced cell death.

Title

Protective effects of fustin, a flavonoid from Rhus verniciflua Stokes, on 6-hydroxydopamine-induced neuronal cell death.

Author

Park BC1, Lee YS, Park HJ, Kwak MK, Yoo BK, Kim JY, Kim JA.

Publish date

2007 Jun 30

PMID

19533734

Abstract

Natural flavonoids ameliorate amyloid-beta peptide (Abeta)-induced neurotoxicity. We examined whether the fustin flavonoid affects Abeta-induced learning impairment in mice. Repeated treatment with fustin significantly attenuated Abeta (1-42)-induced conditioned fear and passive avoidance behaviors. This effect was comparable to that of EGb761, a standard extract of ginkgo. Fustin treatment significantly prevented decreases in acetylcholine (ACh) levels, choline acetyltransferase (ChAT) activity, and ChAT gene expression induced by Abeta (1-42). Fustin also consistently suppressed increases in acetyl cholinesterase (AChE) activity and AChE gene expression induced by Abeta (1-42). In addition, fustin significantly attenuated Abeta (1-42)-induced selective decreases in muscarinic M1 receptor gene expression and muscarinic M1 receptor binding activity (as determined by [(3)H]pirenzepine binding) by modulating extracellular signal-regulated kinase 1/2 (ERK 1/2) and cAMP response-element binding protein (CREB) phosphorylation and brain-derived neurotrophic factor (BDNF) expression. These effects of fustin were reversed by treatment with dicyclomine, a muscarinic M1 receptor antagonist, and SL327, a selective ERK inhibitor, but not by chelerythrine, a pan-protein kinase C (PKC) inhibitor. Taken together, our results suggest that fustin attenuates Abeta (1-42)-impaired learning, and that the ERK/CREB/BDNF pathway is important for the M1 receptor-mediated cognition-enhancing effects of fustin.

Copyright 2009 Wiley-Liss, Inc.

Title

Fustin flavonoid attenuates beta-amyloid (1-42)-induced learning impairment.

Author

Jin CH1, Shin EJ, Park JB, Jang CG, Li Z, Kim MS, Koo KH, Yoon HJ, Park SJ, Choi WC, Yamada K, Nabeshima T, Kim HC.

Publish date

2009 Dec