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Glabratine

$1,376

  • Brand : BIOFRON

  • Catalogue Number : BN-O0941

  • Specification : 97%(HPLC)

  • CAS number : 142750-47-8

  • Formula : C27H34N2O9

  • Molecular Weight : 530.57

  • PUBCHEM ID : 101620039

  • Volume : 5mg

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Catalogue Number

BN-O0941

Analysis Method

HPLC,NMR,MS

Specification

97%(HPLC)

Storage

2-8°C

Molecular Weight

530.57

Appearance

Powder

Botanical Source

Structure Type

Category

Standards;Natural Pytochemical;API

SMILES

COC(=O)C1=CN2CCC3=C(C2CC1C(CO)C=C)NC4=C3C(=CC=C4)OC5C(C(C(C(O5)CO)O)O)O

Synonyms

(2S,12bS)-2-((R)-1-Hydroxymethyl-allyl)-8-((2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-hydroxymethyl-tetrahydro-pyran-2-yloxy)-1,2,6,7,12,12b-hexahydro-indolo[2,3-a]quinolizine-3-carboxylic acid methyl ester

IUPAC Name

methyl (12bS)-2-(1-hydroxybut-3-en-2-yl)-8-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-1,2,6,7,12,12b-hexahydroindolo[2,3-a]quinolizine-3-carboxylate

Density

Solubility

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

Flash Point

Boiling Point

Melting Point

InChl

InChI=1S/C27H34N2O9/c1-3-13(11-30)15-9-18-22-14(7-8-29(18)10-16(15)26(35)36-2)21-17(28-22)5-4-6-19(21)37-27-25(34)24(33)23(32)20(12-31)38-27/h3-6,10,13,15,18,20,23-25,27-28,30-34H,1,7-9,11-12H2,2H3/t13?,15?,18-,20+,23+,24-,25+,27+/m0/s1

InChl Key

USUGTFYUSIJKAR-BDLUZLCISA-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#:142750-47-8) 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

23940744

Abstract

Background
A 2011 report from the National Lung Screening Trial indicates that three annual low-dose computed tomography (LDCT) screenings for lung cancer reduced lung cancer mortality by 20% compared to chest X-ray among older individuals at high risk for lung cancer. Discussion has shifted from clinical proof to financial feasibility. The goal of this study was to determine whether LDCT screening for lung cancer in a commercially-insured population (aged 50-64) at high risk for lung cancer is cost-effective and to quantify the additional benefits of incorporating smoking cessation interventions in a lung cancer screening program.

Methods and Findings
The current study builds upon a previous simulation model to estimate the cost-utility of annual, repeated LDCT screenings over 15 years in a high risk hypothetical cohort of 18 million adults between age 50 and 64 with 30+ pack-years of smoking history. In the base case, the lung cancer screening intervention cost $27.8 billion over 15 years and yielded 985,284 quality-adjusted life years (QALYs) gained for a cost-utility ratio of $28,240 per QALY gained. Adding smoking cessation to these annual screenings resulted in increases in both the costs and QALYs saved, reflected in cost-utility ratios ranging from $16,198 per QALY gained to $23,185 per QALY gained. Annual LDCT lung cancer screening in this high risk population remained cost-effective across all sensitivity analyses.

Conclusions
The findings of this study indicate that repeat annual lung cancer screening in a high risk cohort of adults aged 50-64 is highly cost-effective. Offering smoking cessation interventions with the annual screening program improved the cost-effectiveness of lung cancer screening between 20% and 45%. The cost-utility ratios estimated in this study were in line with other accepted cancer screening interventions and support inclusion of annual LDCT screening for lung cancer in a high risk population in clinical recommendations.

Title

A Cost-Utility Analysis of Lung Cancer Screening and the Additional Benefits of Incorporating Smoking Cessation Interventions

Author

Andrea C. Villanti, 1 , 2 Yiding Jiang, 3 David B. Abrams, 1 , 2 , 4 and Bruce S. Pyenson 3 , *

Publish date

2013

PMID

30805487

Abstract

Background and objectives
Methotrexate (MTX) is a chemotherapeutic agent that functions as a folic acid antagonist. The frequency of high dose methotrexate (HDMTX)-associated toxicity is variable. In this study, we investigated the frequency of myelotoxicity and hepatotoxicity 7 days after HDMTX infusion.

Patients and methods
This study included children diagnosed with acute lymphoblastic leukemia (ALL) between January 2010 and April 2015. The patient blood counts and biochemical parameters measured before and after 7 days of HDMTX infusion were retrospectively recorded. We assessed HDMTX infusions for 48 children. The number of patients and drug doses included the following: 17 children receiving 1 g/m2 (68 infusions), 14 children receiving 2 g/m2 (56 infusions), and 17 children receiving 5 g/m2 (68 infusions). The classification of toxicity was made based on the Common Terminology Criteria for Adverse Events (CTCAE) 2010 criteria. Myelotoxicity was defined as a hemoglobin level <10 g/L and absolute neutrophil count <1 × 109/L or platelet count <75 × 109/L. The presence of transaminase levels ≥5 times the upper limit was considered to be hepatotoxicity grade ≥3. The MTX levels at 42 h in patients with and without toxicity were compared to evaluate the correlation between MTX levels, hematologic parameters, and transaminase levels. Results Myelotoxicity was observed in 35.2%, 37.5%, and 33.8% of the infusions, and hepatotoxicity grade ≥3 was detected in 13.2%, 12.5%, and 11.7% of the infusions in patients receiving 1, 2 and 5 g/m2 HDMTX after 7 days, respectively. There was no statistically significant difference between MTX levels at 42 h in patients with and without toxicity (P > .05, for all). There was no correlation between hematologic parameters and transaminase levels and MTX levels at 42 h.

Conclusion
Hematologic toxicity was the most common toxicity observed. The data indicate the hematologic toxicity increased after repeated cycles in patients receiving 5 g/m2. However, the hepatic toxicity decreased with additional cycles. Our results show the level of MTX at 42 h is not effective to identify toxicity.

KEYWORDS

Children, Leukemia, High dose methotrexate, Myelotoxicity, Hepatotoxicity

Title

The frequency of hepatotoxicity and myelotoxicity in leukemic children with different high doses of methotrexate

Author

Zeynep Canan ozdemir,∗ AySe Bozkurt Turhan, Yeter Duzenli Kar, and ozcan Bor

Publish date

2016 Dec;

PMID

25252978

Abstract

In contrast with advances in massively parallel DNA sequencing1, high-throughput protein analyses2-4 are often limited by ensemble measurements, individual analyte purification and hence compromised quality and cost-effectiveness. Single-molecule (SM) protein detection achieved using optical methods5 is limited by the number of spectrally nonoverlapping chromophores. Here, we introduce a single molecular interaction-sequencing (SMI-Seq) technology for parallel protein interaction profiling leveraging SM advantages. DNA barcodes are attached to proteins collectively via ribosome display6 or individually via enzymatic conjugation. Barcoded proteins are assayed en masse in aqueous solution and subsequently immobilized in a polyacrylamide (PAA) thin film to construct a random SM array, where barcoding DNAs are amplified into in situ polymerase colonies (polonies)7 and analyzed by DNA sequencing. This method allows precise quantification of various proteins with a theoretical maximum array density of over one million polonies per square millimeter. Furthermore, protein interactions can be measured based on the statistics of colocalized polonies arising from barcoding DNAs of interacting proteins. Two demanding applications, G-protein coupled receptor (GPCR) and antibody binding profiling, were demonstrated. SMI-Seq enables “library vs. library” screening in a one-pot assay, simultaneously interrogating molecular binding affinity and specificity.

Title

Multiplex single-molecule interaction profiling of DNA barcoded proteins

Author

Liangcai Gu,1 Chao Li,2 John Aach,1 David E. Hill,1,3 Marc Vidal,1,3 and George M. Church1,2

Publish date

2014 Dec 27.


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