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  • Brand : BIOFRON

  • Catalogue Number : BN-O0995

  • Specification : 99%(HPLC)

  • CAS number : 33815-57-5

  • Formula : C16H20O9

  • Molecular Weight : 356.32

  • PUBCHEM ID : 11360257

  • Volume : 5mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

This product is isolated and purified from the herbs of Saxifraga stolonifera Curt.

Structure Type



Standards;Natural Pytochemical;API




2.3-Dihydroxy-2-cyclopenten-1-on/2-hydroxytetronic acid/8,10-di-O-methylbergenin/N-{[(2-Methyl-2-propanyl)oxy]carbonyl}-3-(4-pyridinyl)alanine/3,4-Dihydroxy-5H-furan-2-on/dimethylbergenin/3-Pyridin-4-yl-D-alanine,N-BOC protected/Pyrano[3,2-c][2]benzopyran-6(2H)-one, 3,4,4a,10b-tetrahydro-3,4-dihydroxy-2-(hydroxymethyl)-8,9,10-trimethoxy-, (2R,3S,4S,4aR,10bS)-/3,4-dihydroxy-5H-furan-2-one/Boc-3-(4-Pyridyl)-DL-alanine/tri-O-methylnorbergenin/Boc-4-Pyridyl-Ala-OH/(2R,3S,4S,4aR,10bS)-3,4-Dihydroxy-2-(hydroxymethyl)-8,9,10-trimethoxy-3,4,4a,10b-tetrahydropyrano[3,2-c]isochromen-6(2H)-one/4-Pyridinepropanoic acid, α-[[(1,1-dimethylethoxy)carbonyl]amino]-




1.2±0.1 g/cm3


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

Flash Point

228.5±27.3 °C

Boiling Point

454.3±40.0 °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#:33815-57-5) 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.




The phosphobase methylation pathway catalyzed by the phosphoethanolamine methyltransferase in Plasmodium falciparum (PfPMT), the malaria parasite, offers an attractive target for anti-parasitic drug development. PfPMT methylates phosphoethanolamine (pEA) to phosphocholine for use in membrane biogenesis. Quantum mechanics and molecular mechanics (QM/MM) calculations tested the proposed reaction mechanism for methylation of pEA involving the previously identified Tyr-19-His-132 dyad, which indicated an energetically unfavorable mechanism. Instead, the QM/MM calculations suggested an alternative mechanism involving Asp-128. The reaction coordinate involves the stepwise transfer of a proton to Asp-128 via a bridging water molecule followed by a typical Sn2-type methyl transfer from S-adenosylmethionine to pEA. Functional analysis of the D128A, D128E, D128Q, and D128N PfPMT mutants shows a loss of activity with pEA but not with the final substrate of the methylation pathway. X-ray crystal structures of the PfPMT-D128A mutant in complex with S-adenosylhomocysteine and either pEA or phosphocholine reveal how mutation of Asp-128 disrupts a hydrogen bond network in the active site. The combined QM/MM, biochemical, and structural studies identify a key role for Asp-128 in the initial step of the phosphobase methylation pathway in Plasmodium and provide molecular insight on the evolution of multiple activities in the active site of the PMT.


Computer Modeling, Crystallography, Enzyme Mechanism, Mutagenesis, Protein Structure


An Alternative Mechanism for the Methylation of Phosphoethanolamine Catalyzed by Plasmodium falciparum Phosphoethanolamine Methyltransferase*♦


Suwipa Saen-oon,‡,1 Soon Goo Lee,§,1 Joseph M. Jez,§,2 and Victor Guallar‡¶,3

Publish date

2014 Dec 5;




AT-rich interactive domain 1A (ARID1A) is a subunit of the Switch/Sucrose non-fermentable (SWI/SNF) chromatin remodeling complex. Recently, genome-wide whole exome sequencing revealed frequent mutations of ARID1A in hepatocellular carcinoma, but clinicopathological significance of ARID1A alteration has not been clarified yet. In this study, expression of ARID1A was investigated immunohistochemically in 290 cases of hepatocellular carcinomas. In the evaluation of tissue microarrays, cases of ARID1A alteration (63 total cases, 21.7%) consisted of 11 (3.8%) cases showing loss of expression and 52 (17.9%) with weak expression. Alteration of ARID1A was correlated with larger tumor size (P = 0.034) and well or moderate differentiation of tumor histology (P = 0.035). There was no significant correlation with age, sex, cirrhosis, TNM stage, tumor size, number of tumors, vascular invasion, patient survival, HBV infection, HCV infection, heavy use of alcohol, nor diabetes mellitus. EBER in situ hybridization was negative in all 11 cases with loss of ARID1A. Altered expression of ARID1A was inversely correlated with nuclear expression of p53 (P = 0.018) or beta-catenin (P = 0.025). There was some heterogeneity of ARID1A alteration within each case, and immunohistochemistry of the whole sections demonstrated that four of 11 cases with loss of ARID1A in TMA analysis showed localized positive area within the tumor. Alteration of ARID1A may accelerate tumor growth in a subset of hepatocellular carcinoma, and this pathway may be distinct from p53 and beta-catenin pathways.


ARID1A, hepatocellular carcinoma, p53, beta-catenin, immunohistochemistry


Altered expression of AT-rich interactive domain 1A in hepatocellular carcinoma


Hiroyuki Abe,1,* Akimasa Hayashi,1,* Akiko Kunita,1 Yoshihiro Sakamoto,2 Kiyoshi Hasegawa,2 Junji Shibahara,1 Norihiro Kokudo,2 Masashi Fukayama1

Publish date





To examine if an underlying diagnosis of rheumatoid arthritis (RA) or osteoarthritis (OA) impacts the 90-day readmission rates after total hip or knee arthroplasty (THA or TKA).

Prospectively collected data from an integrated healthcare system Total Joint Replacement Registry of adults with RA or OA undergoing unilateral primary THA or TKA during 2009-2011 were analyzed. Adjusted logistic regression models for 90-day readmission were fit. Odds ratios with 95% confidence intervals (CI) were calculated. Study year was an effect modifier for the outcome, therefore separate analyses were conducted for each of the three study years.

Of the 34,311 patients, 496 had RA and 33,815 had OA. Comparing RA and OA, there were: 73% and 61% women; 45% and 70% Caucasians; and the mean age was lower, 61 vs. 67 years (p<0.001). Respective crude 90-day readmission rates were 8.5% and 6.7%. The adjusted odds of 90-day readmission increased from year to year for RA compared to OA patients, from 0.89 (95% CI, 0.46-1.71) in 2009 to 1.34 (95% CI, 0.69-2.61) in 2010 to 1.74 (95% CI, 1.16-2.60) in 2011. The two most common readmission reasons were: joint prosthesis infection (10.2%) and septicemia (10.2%) in RA; joint prosthesis infection (5.7%) and other postoperative infection (5.1%) in OA. Conclusions RA is a risk factor for 90-day readmission after primary TKA or THA. An increasing risk of readmissions noted in RA in 2011 is concerning and indicates further studies should examine the reasons for this increasing trend.


Total hip replacement, total knee replacement, readmission, osteoarthritis, rheumatoid arthritis, arthroplasty, joint replacement, diagnosis, risk factor


Rheumatoid arthritis is associated with higher 90-day Hospital Readmission Rates Compared to Osteoarthritis after Hip or Knee arthroplasty: A cohort study


Jasvinder A. Singh, MBBS, MPH,1,2,3 Maria C.S. Inacio, PhD,4 Robert S. Namba, MD,5 and Elizabeth W. Paxton, MA4

Publish date

2015 May 1.

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