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(-)-Vestitol

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Brand : BIOFRON
Catalogue Number : BD-D0570
Specification : HPLC≥98%
CAS number : 35878-41-2
Formula : C15H12O6 
Molecular Weight : 288.3
PUBCHEM ID : 182259
Volume : 5mg

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Catalogue Number

BD-D0570

Analysis Method

HPLC,NMR,MS

Specification

HPLC≥98%

Storage

2-8°C

Molecular Weight

288.3

Appearance

Powder

Botanical Source

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

COC1=CC(=C(C=C1)C2CC3=C(C=C(C=C3)O)OC2)O

Synonyms

(3R)-3-(2-hydroxy-4-methoxyphenyl)-3,4-dihydro-2H-chromen-7-ol/2H-1-Benzopyran-7-ol, 3,4-dihydro-3-(2-hydroxy-4-methoxyphenyl)-/3-(2-hydroxy-4-methoxyphenyl)-3,4-dihydro-2H-chromen-7-ol/3-(2-Hydroxy-4-methoxyphenyl)-7-chromanol/2H-1-Benzopyran-7-ol, 3,4-dihydro-3-(2-hydroxy-4-methoxyphenyl)-, (±)-

IUPAC Name

(3R)-3-(2-hydroxy-4-methoxyphenyl)-3,4-dihydro-2H-chromen-7-ol

Density

1.3±0.1 g/cm3

Solubility

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

Flash Point

206.9±28.7 °C

Boiling Point

418.5±45.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C16H16O4/c1-19-13-4-5-14(15(18)8-13)11-6-10-2-3-12(17)7-16(10)20-9-11/h2-5,7-8,11,17-18H,6,9H2,1H3/t11-/m0/s1

InChl Key

XRVFNNUXNVWYTI-NSHDSACASA-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#:35878-41-2) 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

20826800

Abstract

The β subunit of high voltage-activated Ca2+ (Cav) channels targets the pore-forming α1 subunit to the plasma membrane and tunes the biophysical phenotype of the Cav channel complex. We used a combination of molecular biology and whole-cell patch clamp to investigate the functional role of a long N-terminal polyacidic motif (NPAM) in a Cavβ subunit of the human parasite Schistosoma mansoni (βSm), a motif that does not occur in other known Cavβ subunits. When expressed in human embryonic kidney cells stably expressing Cav2.3, βSm accelerates Ca2+/calmodulin-independent inactivation of Cav2.3. Deleting the first 44 amino acids of βSm, a region that includes NPAM, significantly slows the predominant time constant of inactivation (τfast) under conditions that prevent Ca2+/CaM-dependent inactivation (βSm: τfast = 66 ms; βSmΔ2-44: τfast = 111 ms, p < 0.01). Interestingly, deleting the amino acids that are N-terminal to NPAM (2-24 or 2-17) results in faster inactivation than with an intact N terminus (τfast = 42 ms with βSmΔ2-17; τfast = 40 ms with βSmΔ2-24, p < 0.01). This suggests that NPAM is the structural determinant for accelerating Ca2+/calmodulin-independent inactivation. We also created three chimeric subunits that contain the first 44 amino acids of βSm attached to mammalian β1b, β2a, and β3 subunits. For any given mammalian β subunit, inactivation was faster if it contained the N terminus of βSm than if it did not. Co-expression of the mammalian α2δ-1 subunit resulted in doubling of the inactivation rate, but the effects of NPAM persisted. Thus, it appears that the schistosome Cav channel complex has acquired a new function that likely contributes to reducing the amount of Ca2+ that enters the cells in vivo. This feature is of potential interest as a target for new antihelminthics.

KEYWORDS

Biophysics, Calcium Channels, Calmodulin, Neuroscience, Parasitology, Protein Domains, Schistosoma

Title

The N Terminus of a Schistosome β Subunit Regulates Inactivation and Current Density of a Cav2 Channel

Author

Vicenta Salvador-Recatalà, Robert M. Greenberg

Publish date

2010 Nov 12

PMID

18040998

Abstract

Background
The reasons for race/ethnicity (R/E) differences in breast cancer survival have been difficult to disentangle.

Methods
Surveillance, Epidemiology, and End Results (SEER)-Medicare data were used to identify 41,020 women aged ≥68 years with incident breast cancer between 1994-1999 including African American (2479), Hispanic (1172), Asian/ Pacific Island (1086), and white women (35,878). A Cox proportional hazards model assessed overall and stage-specific (0/I, II/III, and IV) R/E differences in breast cancer survival after adjusting for mammography screening, tumor characteristics at diagnosis, biologic markers, treatment, comorbidity, and demographics.

Results
African American women had worse survival than white women, although controlling for predictor variables reduced this difference among all stage breast cancer (hazards ratio [HR], 1.08; 95% confidence interval [95% CI], 0.97-1.20). Adjustment for predictors reduced, but did not eliminate, disparities in the analysis limited to women diagnosed with stage II/III disease (HR, 1.30; 95% CI, 1.10-1.54). Screening mammography, tumor characteristics at diagnosis, biologic markers, and treatment each produced a similar reduction in HRs for women with stage II/III cancers. Asian and Pacific Island women had better survival than white women before and after accounting for all predictors (adjusted all stages HR, 0.61 [95% CI, 0.47-0.79]; adjusted stage II/III HR, 0.61 [95% CI, 0.47-0.79]). Hispanic women had better survival than white women in all and stage II/III analysis (all stage HR, 0.88; 95% CI, 0.75-1.04) and stage II/III analysis (HR, 0.88; 95% CI, 0.75-1.04), although these findings did not reach statistical significance. There was no significant difference in survival by R/E noted among women diagnosed with stage IV disease.

Conclusions
Predictor variables contribute to, but do not fully explain, R/E differences in breast cancer survival for elderly American women. Future analyses should further investigate the role of biology, demographics, and disparities in quality of care.

KEYWORDS

breast cancer, survival, race/ethnicity, mammography screening, tumor severity, biology, treatment, comorbidities, demographics

Title

Racial and Ethnic Differences in Breast Cancer Survival: How Much Is Explained by Screening, Tumor Severity, Biology, Treatment, Comorbidities, and Demographics?

Author

Elana Curtis, Chris Quale, David Haggstrom, Rebecca Smith-Bindman

Publish date

2009 Apr 29.

PMID

24860344

Abstract

The title compound, C14H12FN3O, adopts an E conformation with respect to the azomethine bond. The pyridyl and fluoro­benzene rings make dihedral angles of 38.58 (6) and 41.61 (5)° respectively with the central C(=O)N2CC unit, resulting in a non-planar mol­ecule. The inter­molecular inter­actions comprise two classical N—H⋯O and N—H⋯N hydrogen bonds and four non-classical C—H⋯O and C—H⋯F hydrogen bonds. These inter­actions are augmented by a weak π-π inter­action between the benzene and pyridyl rings of neighbouring mol­ecules, with a centroid-centroid distance of 3.9226 (10) a. This leads to a three-dimensional supra­molecular assembly in the crystal system. The F atom is disordered over two sites in a 0.559 (3): 0.441 (3) ratio, through a 180° rotation of the fluoro­benzene ring.

Title

N′-[(E)-1-(2-Fluoro­phen­yl)ethyl­idene]pyridine-4-carbohydrazide

Author

P. B. Sreeja, M. Sithambaresan, N. Aiswarya, M. R. Prathapachandra Kurup

Publish date

2014 May 1;