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5,7-Dihydroxy-3’,4’,5’-trimethoxyflavone

$580

  • Brand : BIOFRON

  • Catalogue Number : AV-B04202

  • Specification : 98%

  • CAS number : 18103-42-9

  • Formula : C18H16O7

  • Molecular Weight : 344.32

  • PUBCHEM ID : 5379265

  • Volume : 5mg

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Catalogue Number

AV-B04202

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

344.32

Appearance

Powder

Botanical Source

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

COC1=CC(=CC(=C1OC)OC)C2=CC(=O)C3=C(C=C(C=C3O2)O)O

Synonyms

tricetin 3',4',5'-trimethyl ether/5,7-Dihydroxy-3',4',5'-trimethoxyflavone/3',4',5'-trimethyltricetin/5,7-dihydroxy-2-(3,4,5-trimethoxyphenyl)chromen-4-one

IUPAC Name

5,7-dihydroxy-2-(3,4,5-trimethoxyphenyl)chromen-4-one

Applications

522

Density

1.387g/cm3

Solubility

Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

206.2ºC

Boiling Point

562.4ºC at 760mmHg

Melting Point

266-276ºC

InChl

InChI=1S/C18H16O7/c1-22-15-4-9(5-16(23-2)18(15)24-3)13-8-12(21)17-11(20)6-10(19)7-14(17)25-13/h4-8,19-20H,1-3H3

InChl Key

CPCPHNWWTJLXKQ-UHFFFAOYSA-N

WGK Germany

RID/ADR

HS Code Reference

2914500000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:18103-42-9) 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

23720814

Abstract

Little is known about the role(s) of endogenous Gal-1 during arthritis. In this study we queried whether anti-arthritic functions for this effector of endogenous anti-inflammation could be unveiled, by studying collagen-induced arthritis (CIA) in Gal-1?/? mice.

Gal-1?/? and C57BL/6J (WT) mice received an immunisation of chicken type II collagen (CII) in complete Freund’s adjuvant (FA) followed by a booster on day 21, which consisted of CII in incomplete FA. Animals were monitored for signs of arthritis from day 14 onwards. Clinical and histological signs of arthritis were recorded and humoral and cellular immune responses against CII were analysed.

A distinct disease penetrance was apparent, with ~70% of Gal-1?/? mice developing arthritis compared to ~50% in WT animals. Gal-1?/? mice also exhibited an accelerated disease onset and more severe arthritis characterised by significantly elevated clinical scores. Post-mortem analyses (day 42) revealed higher levels of IgG1 and IgG2b anti-CII immunoglobulin isotypes in the serum of Gal-1 null animals compared to WT. Lastly, T cell responses following ex-vivo stimulation with CII revealed a greater degree of proliferation in T cells of Gal-1?/? mice compared to WT, which was associated with increased production of IL-17 and IL-22.

These data provide the novel notion that endogenous Gal-1 is an inhibitory factor in the development of arthritis affecting disease severity. We have also highlighted the importance of endogenous Gal-1 in regulating T cell reactivity during experimental arthritis.

Title

Endogenous galectin-1 exerts tonic inhibition on experimental arthritis

Author

Asif J Iqbal,*,1 Dianne Cooper,*,1 Alexander Vugler,† Beatrice R. Gittens,* Adrian Moore,† and Mauro Perretti*

Publish date

2014 Apr 1.

PMID

2191003

Abstract

A total of 117 nasal aspirates were cultured for respiratory syncytial virus (RSV) and tested for RSV antigen by a direct fluorescent-antibody (DFA) test (Bartels Immunodiagnostic Supplies, Inc., Bellevue, Wash.), the Directigen enzyme immunoassay (EIA; Becton Dickinson Microbiology Systems, Cockeysville, Md.), the TestPack EIA (Abbott Laboratories, North Chicago, Ill.), and RSV EIA (Abbott). Agreement of two of five methods or a positive RSV culture were required to validate a result. A total of 57 of 117 (48.7%) specimens were culture positive in HEp-2 cells, A549 cells, or both. A total of 5 of 117 (4.3%) additional specimens met the criteria of a positive specimen; i.e., 62 of 117 (53.0%) specimens were positive. Results obtained from 77 of 117 (65.8%) specimens were concordant for all five methods. The sensitivities, specificities, and positive and negative predictive values for the culture and DFA methods were 91.9, 100, 100, and 91.7% and 91.9, 96.4, 96.6, and 91.4%, respectively. The sensitivities, specificities, and positive and negative predictive values for the three EIA procedures, Directigen, TestPack, and RSV EIA, were 75.8, 80.0, 81.0, and 74.6%; 93.6, 100, 100, and 93.2%; and 71.0, 100, 100, and 75.3%, respectively. New self-contained EIA configurations and the DFA method offer attractive alternatives to the culture method. Technical simplicity, rapid turnaround time, performance, and cost must all be considered when selecting a system for RSV detection.

Title

Evaluation of five methods for respiratory syncytial virus detection.

Author

D C Halstead, S Todd, and G Fritch

Publish date

1990 May;

PMID

20923877

Abstract

Epstein Barr virus latent membrane protein 1 (LMP1) induces NF-κB activation through transformation effector sites (TES) 1 and 2, both of which are critical for B-lymphocyte transformation. TES2 principally activates canonical NF-κB, which we confirm is NF-κB essential modifier (NEMO)-dependent and requires an intact ubiquitin binding in A20 binding inhibitor of NF-κB and NEMO (UBAN) domain. LMP1 TES2 activated NF-κB in Jurkat cell lines harboring NEMO truncated at 372 (A45) or NEMO with an in-frame deletion of 133-224 (2C), whereas TNFα, 12-O-Tetradecanoylphorbol-13-acetate, human T-cell leukemia virus 1 Tax, and CD40 did not. In both A45 and 2C Jurkat cell lines, LMP1 TES2-mediated NF-κB activation was blocked by siRNAs to TNFα receptor-associated factor 6 and NEMO, by IκB kinase inhibitors, and by the IκBα superrepressor, indicating that the NEMO mutants function to support canonical NF-κB activation. Expression of A45 or 2C mutants in NEMO-deficient murine embryonic fibroblasts reproduced the Jurkat phenotypes: LMP1 TES2 activated NF-κB in fibroblasts lacking NEMO amino acids 133-224 or 373-419, but TNFα and Tax did not. Further analysis indicated that TES2 did not activate NF-κB in cells expressing the double deletion mutant Δ133-224/Δ372-419. These data provide further evidence of the essential role for NEMO in LMP1 TES2 NF-κB activation and highlight the importance of unique domains within NEMO for sensing distinct NF-κB stimuli.

KEYWORDS

IκB kinase γ, tumor necrosis factor alpha, human T-cell leukemia virus 1 Tax, CD40

Title

Epstein-Barr latent membrane protein 1 transformation site 2 activates NF-κB in the absence of NF-κB essential modifier residues 133-224 or 373-419

Author

Daniela Boehm, Benjamin E. Gewurz, Elliott Kieff,1 and Ellen Cahir-McFarland1

Publish date

2010 Oct 19;