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3,4-Dimethoxyphenyl glucoside


  • Brand : BIOFRON

  • Catalogue Number : BN-O1604

  • Specification : 98%(HPLC)

  • CAS number : 84812-00-0

  • Formula : C14H20O8

  • Molecular Weight : 316.3

  • PUBCHEM ID : 10313649

  • Volume : 5mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

This product is isolated and purified from the herbs of Phyllanthus emblica

Structure Type



Standards;Natural Pytochemical;API




Phenethyl |A-D-Glucopyranoside/Phenylethyl 2-Glucoside/3,4-Dimethoxyphenyl β-D-glucopyranoside/β-D-Glucopyranoside, 3,4-dimethoxyphenyl/|A-Phenylethyl |A-D-Glucoside/2-Phenylethyl |A-D-Glucoside/3,4-Dimethoxyphenyl Beta-D-glucopyranoside/|A-Phenylethanol Glucoside/Phenethyl |A-D-Glucoside




1.4±0.1 g/cm3


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

Flash Point

278.3±30.1 °C

Boiling Point

536.5±50.0 °C at 760 mmHg

Melting Point


InChl Key


WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:84812-00-0) 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.




Minimal residual disease (MRD) testing by higher performance techniques such as flow cytometry and polymerase chain reaction (PCR) can be used to detect the proportion of remaining leukemic cells in bone marrow or peripheral blood during and after the first phases of chemotherapy in children with acute lymphoblastic leukemia (ALL). The results of MRD testing are used to reclassify these patients and guide changes in treatment according to their future risk of relapse.

We conducted a systematic review of the economic literature, cost-effectiveness analysis, and budget-impact analysis to ascertain the cost-effectiveness and economic impact of MRD testing by flow cytometry for management of childhood precursor B-cell ALL in Ontario.

A systematic literature search (1998-2014) identified studies that examined the incremental cost-effectiveness of MRD testing by either flow cytometry or PCR. We developed a lifetime state-transition (Markov) microsimulation model to quantify the cost-effectiveness of MRD testing followed by risk-directed therapy to no MRD testing and to estimate its marginal effect on health outcomes and on costs. Model input parameters were based on the literature, expert opinion, and data from the Pediatric Oncology Group of Ontario Networked Information System. Using predictions from our Markov model, we estimated the 1-year cost burden of MRD testing versus no testing and forecasted its economic impact over 3 and 5 years.

In a base-case cost-effectiveness analysis, compared with no testing, MRD testing by flow cytometry at the end of induction and consolidation was associated with an increased discounted survival of 0.0958 quality-adjusted life-years (QALYs) and increased discounted costs of $4,180, yielding an incremental cost-effectiveness ratio (ICER) of $43,613/QALY gained. After accounting for parameter uncertainty, incremental cost-effectiveness of MRD testing was associated with an ICER of $50,249/QALY gained. In the budget-impact analysis, the 1-year cost expenditure for MRD testing by flow cytometry in newly diagnosed patients with precursor B-cell ALL was estimated at $340,760. We forecasted that the province would have to pay approximately $1.3 million over 3 years and $2.4 million over 5 years for MRD testing by flow cytometry in this population.

Compared with no testing, MRD testing by flow cytometry in newly diagnosed patients with precursor B-cell ALL represents good value for money at commonly used willingness-to-pay thresholds of $50,000/QALY and $100,000/QALY.


Minimal Residual Disease Evaluation in Childhood Acute Lymphoblastic Leukemia: An Economic Analysis


Health Quality Ontario

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Enterococcus durans NCIM5427 (ED-27), capable of producing an intracellular acid stable lipase, was isolated from fish processing waste. Its growth and subsequent lipase production was optimized by Box Behneken design (optimized conditions: 5 % v/v fish waste oil (FWO), 0.10 mg/ml fish waste protein hydrolysates (FWPH) at 48 h of fermentation time). Under optimized conditions, ED-27 showed a 3.0 fold increase (207.6 U/ml to 612.53 U/ml) in lipase production, as compared to un-optimized conditions. Cell growth and lipase production was modeled using Logistic and Luedeking-Piret model, respectively; and lipase production by ED-27 was found to be growth-associated. Lipase produced by ED-27 showed stability at low pH ranges from 2 to 5 with its optimal activity at 30 °C , pH 4.6; showed metal ion dependent activity wherein its catalytic activity was activated by barium, sodium, lithium and potassium (10 mM); reduced by calcium and magnesium (10 mM). However, iron and mercury (5 mM) completely inactivated the enzyme. In addition, modifying agents like SDS, DTT, β-ME (1%v/v) increased activity of lipase of ED-27; while, PMSF, DEPC and ascorbic acid resulted in a marked decrease. ED-27 had maximum cell growth of 9.90309 log CFU/ml under optimized conditions as compared to 13 log CFU/ml in MRS. The lipase produced has potential application in poultry and slaughterhouse waste management.


Enterococcus durans NCIM5427, Acidic lipase, Kinetic modeling, Optimization, Fish waste


Kinetic modeling, production and characterization of an acidic lipase produced by Enterococcus durans NCIM5427 from fish waste


Vrinda Ramakrishnan, Louella Concepta Goveas, Prakash M. Halami,corresponding author and Bhaskar Narayancorresponding author

Publish date

2015 Mar




Ketamine and propofol are two well-known, powerful anesthetic agents, yet at first sight this appears to be their only commonality. Ketamine is a dissociative anesthetic agent, whose main mechanism of action is considered to be N-methyl-d-aspartate (NMDA) antagonism; whereas propofol is a general anesthetic agent, which is assumed to primarily potentiate currents gated by γ-aminobutyric acid type A (GABAA) receptors. However, several experimental observations suggest a closer relationship. First, the effect of ketamine on the electroencephalogram (EEG) is markedly changed in the presence of propofol: on its own ketamine increases θ (4-8 Hz) and decreases α (8-13 Hz) oscillations, whereas ketamine induces a significant shift to beta band frequencies (13-30 Hz) in the presence of propofol. Second, both ketamine and propofol cause inhibition of the inward pacemaker current Ih, by binding to the corresponding hyperpolarization-activated cyclic nucleotide-gated potassium channel 1 (HCN1) subunit. The resulting effect is a hyperpolarization of the neuron’s resting membrane potential. Third, the ability of both ketamine and propofol to induce hypnosis is reduced in HCN1-knockout mice. Here we show that one can theoretically understand the observed spectral changes of the EEG based on HCN1-mediated hyperpolarizations alone, without involving the supposed main mechanisms of action of these drugs through NMDA and GABAA, respectively. On the basis of our successful EEG model we conclude that ketamine and propofol should be antagonistic to each other in their interaction at HCN1 subunits. Such a prediction is in accord with the results of clinical experiment in which it is found that ketamine and propofol interact in an infra-additive manner with respect to the endpoints of hypnosis and immobility.


ketamine, propofol, EEG, HCN1, neural field theory, drug interaction, anesthesia, infra-additivity


Ketamine, Propofol, and the EEG: A Neural Field Analysis of HCN1-Mediated Interactions


Ingo Bojak,1,2,* Harry C. Day,1 and David T. J. Liley3,4

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