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Oxyresveratrol 3′-O-β-D-glucopyranoside

$672

  • Brand : BIOFRON

  • Catalogue Number : BD-P0187

  • Specification : 97.5%(HPLC)

  • CAS number : 144525-40-6

  • Formula : C20H22O9

  • Molecular Weight : 406.4

  • PUBCHEM ID : 6475174

  • Volume : 10mg

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Catalogue Number

BD-P0187

Analysis Method

HPLC,NMR,MS

Specification

97.5%(HPLC)

Storage

2-8°C

Molecular Weight

406.4

Appearance

Powder

Botanical Source

Structure Type

Phenols

Category

SMILES

C1=CC(=C(C=C1O)O)C=CC2=CC(=CC(=C2)OC3C(C(C(C(O3)CO)O)O)O)O

Synonyms

(2S,3R,4S,5S,6R)-2-[3-[(E)-2-(2,4-dihydroxyphenyl)ethenyl]-5-hydroxyphenoxy]-6-(hydroxymethyl)oxane-3,4,5-triol

IUPAC Name

(2S,3R,4S,5S,6R)-2-[3-[(E)-2-(2,4-dihydroxyphenyl)ethenyl]-5-hydroxyphenoxy]-6-(hydroxymethyl)oxane-3,4,5-triol

Applications

Density

Solubility

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

Flash Point

Boiling Point

Melting Point

InChl

InChI=1S/C20H22O9/c21-9-16-17(25)18(26)19(27)20(29-16)28-14-6-10(5-13(23)7-14)1-2-11-3-4-12(22)8-15(11)24/h1-8,16-27H,9H2/b2-1+/t16-,17-,18+,19-,20-/m1/s1

InChl Key

GGQVPULXXVQLRT-CUYWLFDKSA-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#:144525-40-6) 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

19877685

Abstract

In addition to addiction, the repeated use of (+)-methamphetamine [(+)-METH], (+)amphetamine [(+)-AMP], or (±)-methylenedioxymethamphetamine [(±)-MDMA, commonly called ecstasy] can lead to life-threatening medical problems including cardiovascular injury, severe depression, and psychosis. Currently, there are no specific pharmacotherapies to treat these medical problems. In this study, we report the design and synthesis of two haptens, (S)-(+)-3-(9-carboxynonyloxy)methamphetamine [3a, (+)-METHMO10] and (S)-(+)-3-(5-carboxypentyloxy)methamphetamine [3b, (+)-METH MO6], and their use in generating high affinity (low KD value) monoclonal antibodies (mAbs) against (+)-METH, (+)-AMP, and/or (+)-MDMA. Based on results from the determination of mAb KD values and ligand specificity, the mAbs generated from hapten 3a showed the greatest promise for generating active and passive immunotherapies for treating overdose or addiction from (+)-METH-like stimulants.

Title

The Synthesis of Haptens and Their Use for the Development of Monoclonal Antibodies for Treating Methamphetamine Abuse

Author

F. Ivy Carroll,1,* Philip Abraham,1 Paul K. Gong,1 Ramakrishna R. Pidaparthi,1 Bruce E. Blough,1 Yingni Che,2 Amber Hampton,2 Melinda Gunnell,2 Jackson O. Lay, Jr.,3 Eric C. Peterson,2 and S. Michael Owens2

Publish date

2010 Nov 26.

PMID

18192498

Abstract

Chronic or excessive (+)-methamphetamine (METH) use often leads to addiction and toxicity to critical organs like the brain. With medical treatment as a goal, a novel single chain variable fragment (scFv) against METH was engineered from anti-METH monoclonal antibody mAb6H4 (IgG, κ light chain, KD = 11 nM) and found to have similar ligand affinity (KD = 10 nM) and specificity as mAb6H4. The anti-METH scFv (scFv6H4) was cloned, expressed in yeast, purified and formulated as a naturally occurring mixture of monomer (~75%) and dimer (~25%). To test the in vivo efficacy of the scFv6H4, male Sprague Dawley rats (n=5) were implanted with 3-day sc osmotic pumps delivering 3.2 mg/kg/day METH. After reaching steady-state METH concentrations, an i.v. dose of scFv6H4 (36.5 mg/kg, equimolar to the METH body burden) was administered along with a [3H]-scFv6H4 tracer. Serum pharmacokinetic (PCKN) analysis of METH and [3H]-scFv6H4 showed that the scFv6H4 caused an immediate 65-fold increase in the METH concentrations and a 12-fold increase in the serum METH area under the concentration-time curve from 0-480 min after scFv6H4 administration. The scFv6H4 monomer was quickly cleared or converted to multivalent forms with an apparent t1/2λz of 5.8 min. In contrast, the larger scFv6H4 multivalent forms (dimers, trimers, etc.) showed a much longer t1/2λz (228 min), and the significantly increased METH serum molar concentrations correlated directly with scFv6H4 serum molar concentrations. Considered together these data suggested that the scFv6H4 multimers (and not the monomer) were responsible for the prolonged redistribution of METH into the serum.

Title

Development and Preclinical Testing of a High Affinity Single Chain Antibody against (+)-Methamphetamine

Author

Eric C. Peterson, Elizabeth M. Laurenzana, William T. Atchley, Howard Hendrickson, and S. Michael Owens

Publish date

2009 Nov 4.

PMID

28452408

Abstract

Background
Coronary heart disease (CHD) is the most common cause of death globally, although mortality rates are falling. Psychological symptoms are prevalent for people with CHD, and many psychological treatments are offered following cardiac events or procedures with the aim of improving health and outcomes. This is an update of a Cochrane systematic review previously published in 2011.

Objectives
To assess the effectiveness of psychological interventions (alone or with cardiac rehabilitation) compared with usual care (including cardiac rehabilitation where available) for people with CHD on total mortality and cardiac mortality; cardiac morbidity; and participant‐reported psychological outcomes of levels of depression, anxiety, and stress; and to explore potential study‐level predictors of the effectiveness of psychological interventions in this population.

Search methods
We updated the previous Cochrane Review searches by searching the following databases on 27 April 2016: CENTRAL in the Cochrane Library, MEDLINE (Ovid), Embase (Ovid), PsycINFO (Ovid), and CINAHL (EBSCO).

Selection criteria
We included randomised controlled trials (RCTs) of psychological interventions compared to usual care, administered by trained staff, and delivered to adults with a specific diagnosis of CHD. We selected only studies estimating the independent effect of the psychological component, and with a minimum follow‐up of six months. The study population comprised of adults after: a myocardial infarction (MI), a revascularisation procedure (coronary artery bypass graft (CABG) or percutaneous coronary intervention (PCI)), and adults with angina or angiographically defined coronary artery disease (CAD). RCTs had to report at least one of the following outcomes: mortality (total‐ or cardiac‐related); cardiac morbidity (MI, revascularisation procedures); or participant‐reported levels of depression, anxiety, or stress.

Data collection and analysis
Two review authors independently screened titles and abstracts of all references for eligibility. A lead review author extracted study data, which a second review author checked. We contacted study authors to obtain missing information.

Main results
This review included 35 studies which randomised 10,703 people with CHD (14 trials and 2577 participants added to this update). The population included mainly men (median 77.0%) and people post‐MI (mean 65.7%) or after undergoing a revascularisation procedure (mean 27.4%). The mean age of participants within trials ranged from 53 to 67 years. Overall trial reporting was poor, with around a half omitting descriptions of randomisation sequence generation, allocation concealment procedures, or the blinding of outcome assessments. The length of follow‐up ranged from six months to 10.7 years (median 12 months). Most studies (23/35) evaluated multifactorial interventions, which included therapies with multiple therapeutic components. Ten studies examined psychological interventions targeted at people with a confirmed psychopathology at baseline and two trials recruited people with a psychopathology or another selecting criterion (or both). Of the remaining 23 trials, nine studies recruited unselected participants from cardiac populations reporting some level of psychopathology (3.8% to 53% with depressive symptoms, 32% to 53% with anxiety), 10 studies did not report these characteristics, and only three studies excluded people with psychopathology.

Moderate quality evidence showed no risk reduction for total mortality (risk ratio (RR) 0.90, 95% confidence interval (CI) 0.77 to 1.05; participants = 7776; studies = 23) or revascularisation procedures (RR 0.94, 95% CI 0.81 to 1.11) with psychological therapies compared to usual care. Low quality evidence found no risk reduction for non‐fatal MI (RR 0.82, 95% CI 0.64 to 1.05), although there was a 21% reduction in cardiac mortality (RR 0.79, 95% CI 0.63 to 0.98). There was also low or very low quality evidence that psychological interventions improved participant‐reported levels of depressive symptoms (standardised mean difference (SMD) ‐0.27, 95% CI ‐0.39 to ‐0.15; GRADE = low), anxiety (SMD ‐0.24, 95% CI ‐0.38 to ‐0.09; GRADE = low), and stress (SMD ‐0.56, 95% CI ‐0.88 to ‐0.24; GRADE = very low).

There was substantial statistical heterogeneity for all psychological outcomes but not clinical outcomes, and there was evidence of small‐study bias for one clinical outcome (cardiac mortality: Egger test P = 0.04) and one psychological outcome (anxiety: Egger test P = 0.012). Meta‐regression exploring a limited number of intervention characteristics found no significant predictors of intervention effects for total mortality and cardiac mortality. For depression, psychological interventions combined with adjunct pharmacology (where deemed appropriate) for an underlying psychological disorder appeared to be more effective than interventions that did not (β = ‐0.51, P = 0.003). For anxiety, interventions recruiting participants with an underlying psychological disorder appeared more effective than those delivered to unselected populations (β = ‐0.28, P = 0.03).

Authors’ conclusions
This updated Cochrane Review found that for people with CHD, there was no evidence that psychological treatments had an effect on total mortality, the risk of revascularisation procedures, or on the rate of non‐fatal MI, although the rate of cardiac mortality was reduced and psychological symptoms (depression, anxiety, or stress) were alleviated; however, the GRADE assessments suggest considerable uncertainty surrounding these effects. Considerable uncertainty also remains regarding the people who would benefit most from treatment (i.e. people with or without psychological disorders at baseline) and the specific components of successful interventions. Future large‐scale trials testing the effectiveness of psychological therapies are required due to the uncertainty within the evidence. Future trials would benefit from testing the impact of specific (rather than multifactorial) psychological interventions for participants with CHD, and testing the targeting of interventions on different populations (i.e. people with CHD, with or without psychopathologies).

KEYWORDS

Aged, Female, Humans, Male, Middle Aged, Psychotherapy, Anxiety, Anxiety/therapy, Cause of Death, Coronary Disease, Coronary Disease/mortality, Coronary Disease/psychology, Depression, Depression/therapy, Myocardial Infarction, Myocardial Infarction/epidemiology, Myocardial Infarction/prevention & control, Myocardial Infarction/psychology, Myocardial Revascularization, Myocardial Revascularization/psychology, Myocardial Revascularization/statistics & numerical data, Randomized Controlled Trials as Topic, Reoperation, Stress, Psychological, Stress, Psychological/epidemiology

Title

Psychological interventions for coronary heart disease

Author

Suzanne H Richards, Lindsey Anderson, Caroline E Jenkinson, Ben Whalley, Karen Rees, Philippa Davies, Paul Bennett, Zulian Liu, Robert West, David R Thompson, and Rod S Taylorcorresponding author

Publish date

2017 Apr