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5,7-Diacetoxy-8-methoxyflavone

$1,280

  • Brand : BIOFRON

  • Catalogue Number : BN-O1550

  • Specification : 98%(HPLC)

  • CAS number : 23246-80-2

  • Formula : C20H16O7

  • Molecular Weight : 368.3

  • PUBCHEM ID : 71307299

  • Volume : 5mg

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Catalogue Number

BN-O1550

Analysis Method

Specification

98%(HPLC)

Storage

-20℃

Molecular Weight

368.3

Appearance

Yellow powder

Botanical Source

This product is isolated and purified from the roots of Scutellaria baicalensis

Structure Type

Category

SMILES

CC(=O)OC1=CC(=C(C2=C1C(=O)C=C(O2)C3=CC=CC=C3)OC)OC(=O)C

Synonyms

wogonin diacetate/5,7-Diacetoxy-8-methoxyflavone/5,7-Diacetoxy-8-methoxy-2-phenyl-chromen-4-on/4H-1-Benzopyran-4-one, 5,7-bis(acetyloxy)-8-methoxy-2-phenyl-/8-Methoxy-4-oxo-2-phenyl-4H-chromene-5,7-diyl diacetate/5,7-diacetoxy-8-methoxy-2-phenyl-chromen-4-one

IUPAC Name

Density

1.3±0.1 g/cm3

Solubility

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

Flash Point

238.3±30.2 °C

Boiling Point

540.9±50.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

MPPVJYIDQFOAJU-UHFFFAOYSA-N

WGK Germany

RID/ADR

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#:23246-80-2) 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

26983361

Abstract

Identification of genome-wide patterns of divergence provides insight on how genomes are influenced by selection and can reveal the potential for local adaptation in spatially structured populations. In Atlantic cod – historically a major marine resource – Northeast-Arctic- and Norwegian coastal cod are recognized by fundamental differences in migratory and non-migratory behavior, respectively. However, the genomic architecture underlying such behavioral ecotypes is unclear. Here, we have analyzed more than 8.000 polymorphic SNPs distributed throughout all 23 linkage groups and show that loci putatively under selection are localized within three distinct genomic regions, each of several megabases long, covering approximately 4% of the Atlantic cod genome. These regions likely represent genomic inversions. The frequency of these distinct regions differ markedly between the ecotypes, spawning in the vicinity of each other, which contrasts with the low level of divergence in the rest of the genome. The observed patterns strongly suggest that these chromosomal rearrangements are instrumental in local adaptation and separation of Atlantic cod populations, leaving footprints of large genomic regions under selection. Our findings demonstrate the power of using genomic information in further understanding the population dynamics and defining management units in one of the world’s most economically important marine resources.

Title

Three chromosomal rearrangements promote genomic divergence between migratory and stationary ecotypes of Atlantic cod

Author

Paul R. Berg,a,1 Bastiaan Star,1 Christophe Pampoulie,2 Marte Sodeland,3,4 Julia M. I. Barth,1 Halvor Knutsen,1,3,4 Kjetill S. Jakobsen,1 and Sissel Jentoft1,4

Publish date

2016;

PMID

24973221

Abstract

Metformin, a well known antidiabetic agent that improves peripheral insulin sensitivity, also elicits anti-inflammatory actions, but its mechanism is unclear. Here, we investigated the mechanism responsible for the anti-inflammatory effect of metformin action in lipopolysaccharide (LPS)-stimulated murine macrophages. Metformin inhibited LPS-induced production of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in a concentration-dependent manner and in parallel induction of activating transcription factor-3 (ATF-3), a transcription factor and member of the cAMP-responsive element-binding protein family. ATF-3 knockdown abolished the inhibitory effects of metformin on LPS-induced proinflammatory cytokine production accompanied with reversal of metformin-induced suppression of mitogen-activated protein kinase (MAPK) phosphorylation. Conversely, AMP-activated protein kinase (AMPK) phosphorylation and NF-κB suppression by metformin were unaffected by ATF-3 knockdown. ChIP-PCR analysis revealed that LPS-induced NF-κB enrichments on the promoters of IL-6 and TNF-α were replaced by ATF-3 upon metformin treatment. AMPK knockdown blunted all the effects of metformin (ATF-3 induction, proinflammatory cytokine inhibition, and MAPK inactivation), suggesting that AMPK activation by metformin is required for and precedes ATF-3 induction. Oral administration of metformin to either mice with LPS-induced endotoxemia or ob/ob mice lowered the plasma and tissue levels of TNF-α and IL-6 and increased ATF-3 expression in spleen and lungs. These results suggest that metformin exhibits anti-inflammatory action in macrophages at least in part via pathways involving AMPK activation and ATF-3 induction.

KEYWORDS

Inflammation, Interleukin 6 (IL-6), Lipopolysaccharide (LPS), Macrophage, Tumor Necrosis Factor (TNF), ATF-3, Metformin

Title

Metformin Suppresses Lipopolysaccharide (LPS)-induced Inflammatory Response in Murine Macrophages via Activating Transcription Factor-3 (ATF-3) Induction*

Author

Juyoung Kim,‡,1 Hyun Jeong Kwak,‡,1 Ji-Young Cha,§ Yun-Seung Jeong,§ Sang Dahl Rhee,¶ Kwang Rok Kim,¶ and Hyae Gyeong Cheon‡‖,2

Publish date

2014 Aug 15

PMID

28423573

Abstract

The functional role of AF1q/MLLT11, an oncogenic factor involved in a translocation t(1;11)(q21;q23) responsible for acute myeloid leukaemia, has been investigated in hematological and solid malignancies and its expression was found to be linked to tumor progression and poor clinical outcome. In addition to its oncogenic function, AF1q has been shown to play a role in the onset of basal and drug-induced apoptosis in cancer cells of different histotypes, including ovarian cancer. Through in vitro, ex vivo, and in silico approaches, we demonstrated here that AF1q is also endowed with protumorigenic potential in ovarian cancer. In ovarian cancer cell lines, stable AF1q overexpression caused activation of epithelial-to-mesenchymal transition and increased motility/migratory/invasive abilities accompanied by gene expression changes mainly related to Wnt signaling and to signaling pathways involving in ERK/p38 activation. The potential role of AF1q in ovarian cancer progression was confirmed by immunohistochemical and in silico analyses performed in ovarian tumor specimens which revealed that the protein was absent in normal ovarian epithelium and became detectable when atypical proliferation was present. Moreover, AF1q was significantly lower in borderline ovarian tumors (i.e., tumors of low malignant potential without stromal invasion) than in invasive tumors, thus corroborating the association between high AF1q expression and increased migratory/invasive cell behavior and confirming its potential role in ovarian cancer progression. Our findings demonstrated, for the first time, that AF1q is endowed with protumorigenic activity in ovarian cancer, thus highlighting a dual behavior (i.e., protumorigenic and proapoptotic functions) of the protein in the malignancy.

KEYWORDS

AF1q/MLLT11, ovarian cancer, borderline ovarian tumor/BOT, low malignant potential ovarian tumor, EMT

Title

Involvement of AF1q/MLLT11 in the progression of ovarian cancer

Author

Paola Tiberio,1 Ludmila Lozneanu,1,2 Valentina Angeloni,1 Elena Cavadini,1 Patrizia Pinciroli,3 Maurizio Callari,1,4 Maria Luisa Carcangiu,5 Domenica Lorusso,6 Francesco Raspagliesi,6 Valentina Pala,1 Maria Grazia Daidone,1 and Valentina Appierto1

Publish date

2017 Apr 4;


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