Catalogue Number
BD-P0372
Analysis Method
HPLC,NMR,MS
Specification
95.0%(HPLC)
Storage
-20℃
Molecular Weight
502.43
Appearance
Powder
Botanical Source
Structure Type
Flavonoids
Category
SMILES
C1=CC(=CC=C1C2=COC3=C(C2=O)C=CC(=C3)OC4C(C(C(C(O4)COC(=O)CC(=O)O)O)O)O)O
Synonyms
3-oxo-3-[[(2R,3S,4S,5R,6S)-3,4,5-trihydroxy-6-[3-(4-hydroxyphenyl)-4-oxochromen-7-yl]oxyoxan-2-yl]methoxy]propanoic acid
IUPAC Name
3-oxo-3-[[(2R,3S,4S,5R,6S)-3,4,5-trihydroxy-6-[3-(4-hydroxyphenyl)-4-oxochromen-7-yl]oxyoxan-2-yl]methoxy]propanoic acid
Density
1.595g/cm3
Solubility
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Flash Point
284ºC
Boiling Point
824.8ºC at 760 mmHg
Melting Point
InChl
InChI=1S/C24H22O12/c25-12-3-1-11(2-4-12)15-9-33-16-7-13(5-6-14(16)20(15)29)35-24-23(32)22(31)21(30)17(36-24)10-34-19(28)8-18(26)27/h1-7,9,17,21-25,30-32H,8,10H2,(H,26,27)/t17-,21-,22+,23-,24-/m1/s1
InChl Key
MTXMHWSVSZKYBT-ASDZUOGYSA-N
WGK Germany
RID/ADR
HS Code Reference
2934990000
Personal Projective Equipment
Correct Usage
For Reference Standard and R&D, Not for Human Use Directly.
Meta Tag
provides coniferyl ferulate(CAS#:124590-31-4) 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.
30225135
The asymmetric unit of the title compound {systematic name: 3-[(tert-butyldiphenylsilyl)oxy]propane-1,2-diol, C19H26O3Si}, contains eight chiral molecules (Z′ = 8). These molecules are connected via a complex system of hydrogen bonds into an infinite assembly along the [100] axis; hydrophobic tert-butyl and phenyl groups form an external coating of the assembly. These assemblies are packed by weak intermolecular interactions in a peculiar formation resembling a ‘header bond’ masonry brick wall. Disorder of flexible fragments increases with temperature but the same crystal structure exists from 120 to 220 K (and most probably to the melting point at 334 K).
crystal structure, (S)-1-O-t-butyldiphenylsilylglycerol, chiral, high Z′ structure, disorder
Crystal structure of (S)-1-O-tert-butyldiphenylsilylglycerol: eight chiral molecules in a triclinic cell
Bogdan Doboszewski,a Alexander Y. Nazarenko,b,* Victor N. Nemykin,c and Maria Joselice e Silvad
2018 Sep 1;
19430104
Objective
To determine the extent of viral resistance over time among non-clade B HIV-1 infected patients in Uganda maintained on first line highly active antiretroviral therapy (HAART) following virologic failure.
Methods
Genotyping was performed on sixteen patients with virologic failure who were enrolled in an open label randomized clinical trial of short-cycle treatment interruption.
Results
All patients receiving efavirenz containing HAART had at least 1 efavirenz resistance mutation develop during follow-up. The majority 13/15 (86%) developed lamivudine resistance during follow-up but no thymidine analogue mutations (TAMS) developed during a median duration of virologic failure of 325.5 days.
Conclusions
Genotypic resistance to both efavirenz and lamivudine developed early during the course of treatment after virologic failure. TAMs did not emerge early despite moderate exposure time to thymidine analogs during virologic failure.
human immunodeficiency virus (HIV), antiretroviral drug resistance, virologic failure
Steven J. Reynolds,1,2 Cissy Kityo,3 Frank Mbamanya,3 Robin Dewar,4 Francis Ssali,3 Thomas C. Quinn,1,2 Peter Mugyenyi,3 and Mark Dybul5
Steven J. Reynolds,1,2 Cissy Kityo,3 Frank Mbamanya,3 Robin Dewar,4 Francis Ssali,3 Thomas C. Quinn,1,2 Peter Mugyenyi,3 and Mark Dybul5
2009 Sep 24.
25558175
Purpose
To analyze the spectrum of sequence variants in the MYO7A and USH2A genes in a group of Italian patients affected by Usher syndrome (USH).
Methods
Thirty-six Italian patients with a diagnosis of USH were recruited. They received a standard ophthalmologic examination, visual field testing, optical coherence tomography (OCT) scan, and electrophysiological tests. Fluorescein angiography and fundus autofluorescence imaging were performed in selected cases. All the patients underwent an audiologic examination for the 0.25-8,000 Hz frequencies. Vestibular function was evaluated with specific tests. DNA samples were analyzed for sequence variants of the MYO7A gene (for USH1) and the USH2A gene (for USH2) with direct sequencing techniques. A few patients were analyzed for both genes.
Results
In the MYO7A gene, ten missense variants were found; three patients were compound heterozygous, and two were homozygous. Thirty-four USH2A gene variants were detected, including eight missense variants, nine nonsense variants, six splicing variants, and 11 duplications/deletions; 19 patients were compound heterozygous, and three were homozygous. Four MYO7A and 17 USH2A variants have already been described in the literature. Among the novel mutations there are four USH2A large deletions, detected with multiplex ligation dependent probe amplification (MLPA) technology. Two potentially pathogenic variants were found in 27 patients (75%). Affected patients showed variable clinical pictures without a clear genotype-phenotype correlation.
Conclusions
Ten variants in the MYO7A gene and 34 variants in the USH2A gene were detected in Italian patients with USH at a high detection rate. A selective analysis of these genes may be valuable for molecular analysis, combining diagnostic efficiency with little time wastage and less resource consumption.
MYO7A and USH2A gene sequence variants in Italian patients with Usher syndrome
Andrea Sodi,1 Alessandro Mariottini,2 Ilaria Passerini,2 Vittoria Murro,1 Iryna Tachyla,corresponding author1 Benedetta Bianchi,3 Ugo Menchini,1 and Francesca Torricelli2
2014;