Shipping to United States We Offer Worldwide Shipping
Login Wishlist

Genistein 7,4′-di-O-β-D-glucopyranoside

$896

  • Brand : BIOFRON

  • Catalogue Number : BD-P0249

  • Specification : 98.0%(HPLC)

  • CAS number : 36190-98-4

  • Formula : C27H30O15

  • Molecular Weight : 594.52

  • PUBCHEM ID : 91431845

  • Volume : 25mg

Available on backorder

Quantity
Checkout Bulk Order?

Catalogue Number

BD-P0249

Analysis Method

HPLC,NMR,MS

Specification

98.0%(HPLC)

Storage

2-8°C

Molecular Weight

594.52

Appearance

Powder

Botanical Source

Structure Type

Flavonoids

Category

SMILES

C1=CC(=CC=C1C2=COC3=CC(=CC(=C3C2=O)O)OC4C(C(C(C(O4)CO)O)O)O)OC5C(C(C(C(O5)CO)O)O)O

Synonyms

5-hydroxy-7-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-3-[4-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyphenyl]chromen-4-one

IUPAC Name

5-hydroxy-7-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-3-[4-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyphenyl]chromen-4-one

Applications

Density

Solubility

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

Flash Point

Boiling Point

Melting Point

InChl

InChI=1S/C27H30O15/c28-7-16-20(32)22(34)24(36)26(41-16)39-11-3-1-10(2-4-11)13-9-38-15-6-12(5-14(30)18(15)19(13)31)40-27-25(37)23(35)21(33)17(8-29)42-27/h1-6,9,16-17,20-30,32-37H,7-8H2/t16-,17-,20-,21-,22+,23+,24-,25-,26-,27-/m1/s1

InChl Key

OUJDQONJYHNTDX-UMUUNPGWSA-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#:36190-98-4) 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

26991497

Abstract

Background
Chinese populations have a higher proportion of intracerebral hemorrhage (ICH) in total strokes. However, the reasons are not fully understood.

Methods
To assess the differences in frequency of major risk factors between ICH and ischemic stroke (IS) in Chinese versus white populations of European descent, we systematically sought studies conducted since 1990 that compared frequency of risk factors between ICH and IS in Chinese or white populations. For each risk factor, in Chinese and Whites separately, we calculated study-specific and random effects pooled prevalence and odds ratios (ORs) for ICH versus IS.

Results
Six studies among 36190 Chinese, and seven among 52100 white stroke patients studied hypertension, diabetes, atrial fibrillation (AF), ischemic heart disease (IHD), hypercholesterolemia, smoking and alcohol. Pooled prevalence of AF was significantly lower in Chinese. Pooled ORs for ICH versus IS were mostly similar in Chinese and Whites. However, in Chinese-but not Whites-mean age was lower (62 versus 69 years), while hypertension and alcohol were significantly more frequent in ICH than IS (ORs 1.38, 95% CI 1.18-1.62, and 1.46, 1.12-1.91). Hypercholesterolemia and smoking were significantly less frequent in ICH in Whites, but not Chinese, while IHD, AF and diabetes were less frequent in ICH in both.

Conclusions
Different risk factor distributions in ICH and IS raise interesting possibilities about variation in mechanisms underlying the different distributions of pathological types of stroke between Chinese and Whites. Further analyses in large, prospective studies, including adjustment for potential confounders, are needed to consolidate and extend these findings.

Title

Comparing Risk Factor Profiles between Intracerebral Hemorrhage and Ischemic Stroke in Chinese and White Populations: Systematic Review and Meta-Analysis

Author

Chung-Fen Tsai,1,2 Niall Anderson,3 Brenda Thomas,2 and Cathie L. M. Sudlow2,4,* Terence J Quinn, Editor

Publish date

2016

PMID

29785028

Abstract

Chronic lymphocytic leukemia (CLL) is a frequent hematological neoplasm in which underlying epigenetic alterations are only partially understood. Here we analyze the reference epigenome of seven primary CLLs and the regulatory chromatin landscape of 107 primary cases in the context of normal B-cell differentiation. We identify that the CLL chromatin landscape is largely influenced by distinct dynamics during normal B-cell maturation. Beyond this, we define extensive catalogues of regulatory elements de novo reprogrammed in CLL as a whole and in its major clinico-biological subtypes classified by IGHV somatic hypermutation levels. We uncover that IGHV-unmutated CLLs harbor more active and open chromatin than IGHV-mutated cases. Furthermore, we show that de novo active regions in CLL are enriched for NFAT, FOX and TCF/LEF transcription factor family binding sites. Although most genetic alterations are not associated with consistent epigenetic profiles, CLLs with MYD88 mutations and trisomy 12 show distinct chromatin configurations. Furthermore, we observe that non-coding mutations in IGHV-mutated CLLs are enriched in H3K27ac-associated regulatory elements outside accessible chromatin. Overall, this study provides an integrative portrait of the CLL epigenome, identifies extensive networks of altered regulatory elements and sheds light on the relationship between the genetic and epigenetic architecture of the disease.

Title

The reference epigenome and regulatory chromatin landscape of chronic lymphocytic leukemia

Author

Renee Beekman,1,2 Vicente Chapaprieta,3 Núria RussiNol,1 Roser Vilarrasa-Blasi,3 Núria Verdaguer-Dot,3 Joost H.A. Martens,4 Marti Duran-Ferrer,3 Marta Kulis,5 Francois Serra,6,7,8 Biola M. Javierre,9 Steven W. Wingett,9 Guillem Clot,1,2 Ana C. Queiros,1 Giancarlo Castellano,10 Julie Blanc,6,11 Marta Gut,6,11 Angelika Merkel,6,11 Simon Heath,6,11 Anna Vlasova,12 Sebastian Ullrich,12 Emilio Palumbo,12 Anna Enjuanes,1,2 David Martin-Garcia,1,2 Silvia Beà,1,2 Magda Pinyol,1,2 Marta Aymerich,2,13 Romina Royo,14 Montserrat Puiggros,14 David Torrents,14,15 Avik Datta,16 Ernesto Lowy,16 Myrto Kostadima,16 Maša Roller,16 Laura Clarke,16 Paul Flicek,16 Xabier Agirre,2,17 Felipe Prosper,2,17,18 Tycho Baumann,2,19 Julio Delgado,2,19 Armando Lopez-Guillermo,2,19 Peter Fraser,9,20 Marie-Laure Yaspo,21 Roderic Guigo,12 Reiner Siebert,22 Marc A. Marti-Renom,6,7,8,15 Xose S. Puente,2,23 Carlos Lopez-Otin,2,23 Ivo Gut,6,11 Hendrik G. Stunnenberg,4 Elias Campo,1,2,3,5,24 and Jose I. Martin-Subero1,2,3

Publish date

2019 Feb 5.

PMID

14002760

Abstract

youmans, anne S. (Northwestern University Medical School, Chicago, Ill.) and guy p. youmans. Effect of mycosuppressin on the respiration and growth of Mycobacterium tuberculosis. J. Bacteriol. 84:708-715. 1962.—A substance, called mycosuppressin, was found in the lungs of guinea pigs and rabbits vaccinated with BCG or with a particulate immunizing fraction isolated from mycobacterial cells, and was not found in lungs of unvaccinated animals. Mycosuppressin inhibited the endogenous respiration and the growth of the virulent H37Rv strain of Mycobacterium tuberculosis. It also inhibited the endogenous respiration of the avirulent H37Ra strain and the saprophyte, M. smegmatis, but it increased the respiration of M. phlei. The oxidation by the H37Rv strain of lactate, pyruvate, glycerol, and glucose was also inhibited. Cytochrome oxidase activity was suppressed. Mycosuppressin was most stable at pH 6 to 7. It was nondialyzable, stable at 98 C, and not affected by lyophilization or freezing. It was soluble, in alcohol and acetone, insoluble in ether and water. Under appropriate conditions, mycosuppressin combined with, or was adsorbed to, mycobacterial cells, and was inactivated by serum and bovine serum albumin. It did not inhibit but, instead increased markedly, the respiration of Staphylococcus aureus and Escherichia coli.

Title

EFFECT OF MYCOSUPPRESSIN ON THE RESPIRATION AND GROWTH OF MYCOBACTERIUM TUBERCULOSIS

Author

Anne S. Youmans and Guy P. Youmans

Publish date

1962 Oct