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Catalogue Number : BD-P0139
Specification : 98.0%(HPLC)
CAS number : 33458-82-1
Formula : C38H47NO18
Molecular Weight : 805.8
PUBCHEM ID : 477607
Volume : 10mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

Structure Type







[(1S,3R,13S,14S,17S,18R,19R,20R,21S,22R,23R,24R)-18,19,21,22,24-pentaacetyloxy-25-hydroxy-3,13,14,25-tetramethyl-6,15-dioxo-2,5,16-trioxa-11-azapentacyclo[,20.03,23.07,12]pentacosa-7(12),8,10-trien-20-yl]methyl acetate


1.4±0.1 g/cm3


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

Flash Point

437.4±32.9 °C

Boiling Point

799.6±60.0 °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#:33458-82-1) 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.




Covering: up to 2018

With contributions from the global natural product (NP) research community, and continuing the Raw Data Initiative, this review collects a comprehensive demonstration of the immense scientific value of disseminating raw nuclear magnetic resonance (NMR) data, independently of, and in parallel with, classical publishing outlets. A comprehensive compilation of historic to present-day cases as well as contemporary and future applications show that addressing the urgent need for a repository of publicly accessible raw NMR data has the potential to transform natural products (NPs) and associated fields of chemical and biomedical research. The call for advancing open sharing mechanisms for raw data is intended to enhance the transparency of experimental protocols, augment the reproducibility of reported outcomes, including biological studies, become a regular component of responsible research, and thereby enrich the integrity of NP research and related fields.


The value of universally available raw NMR data for transparency, reproducibility, and integrity in natural product research†


James B. McAlpine,corresponding authora,* Shao-Nong Chen,a Andrei Kutateladze,b John B. MacMillan,c Giovanni Appendino,d Andersson Barison,e Mehdi A. Beniddir,f Maique W. Biavatti,g Stefan Bluml,h Asmaa Boufridi,i Mark S. Butler,j Robert J. Capon,j Young H. Choi,k David Coppage,c Phillip Crews,c Michael T. Crimmins,l Marie Csete,m Pradeep Dewapriya,j Joseph M. Egan,n Mary J. Garson,o Gregory Genta-Jouve,p William H. Gerwick,q,r Harald Gross,s Mary Kay Harper,t Precilia Hermanto,u James M. Hook,u Luke Hunter,u Damien Jeannerat,v Nai-Yun Ji,w Tyler A. Johnson,c David G. I. Kingston,x Hiroyuki Koshino,y Hsiau-Wei Lee,c Guy Lewin,f Jie Li,r Roger G. Linington,n Miaomiao Liu,i Kerry L. McPhail,z Tadeusz F. Molinski,aa Bradley S. Moore,q,r Joo-Won Nam,ab Ram P. Neupane,ac Matthias Niemitz,ad Jean-Marc Nuzillard,ae Nicholas H. Oberlies,af Fernanda M. M. Ocampos,e Guohui Pan,ag Ronald J. Quinn,i D. Sai Reddy,b Jean-Hugues Renault,ae Jose Rivera-Chavez,ah Wolfgang Robien,ai Carla M. Saunders,aj Thomas J. Schmidt,ak Christoph Seger,al Ben Shen,ag Christoph Steinbeck,am Hermann Stuppner,al Sonja Sturm,al Orazio Taglialatela-Scafati,an Dean J. Tantillo,aj Robert Verpoorte,k Bin-Gui Wang,w,ao Craig M. Williams,o Philip G. Williams,ac Julien Wist,ap Jian-Min Yue,aq Chen Zhang,ar Zhengren Xu,ag Charlotte Simmler,a David C. Lankin,a Jonathan Bisson,a and Guido F. Paulicorresponding authora,*

Publish date

2019 Jan 1;




The limited neurobiological understanding of PTSD has been partially attributed to the need for improved animal models. Stress-enhanced fear learning (SEFL) in rodents recapitulates many PTSD-associated behaviors, including stress-susceptible (SS) and -resilient (SR) subgroups in outbred rats. Identification of subgroups requires additional behavioral phenotyping, a confound to mechanistic studies.

We employed a SEFL paradigm in inbred male and female C57BL/6 that combines acute stress with fear conditioning to precipitate “traumatic” memories. Extinction and long-term retention of extinction were examined after SEFL. Further characterization of SEFL effects on male mice was performed with additional behavioral tests, determination of regional activation by Fos immunofluorescence and RNA-sequencing of the basolateral amygdala (BLA).

Stressed animals displayed persistently elevated freezing during extinction. While more uniform in females, SEFL produced male subgroups with differential susceptibility that were identified without post-training phenotyping. Additional phenotyping of males revealed PTSD-associated behaviors, including extinction-resistant fear memory, hyperarousal, generalization and dysregulated corticosterone in SS males. Altered Fos activation was also seen in the infralimbic cortex and BLA of SS males after remote memory retrieval. Key behavioral outcomes, including susceptibility, were replicated by two independent laboratories. RNA-sequencing of the BLA revealed transcriptional divergence between the male subgroups, including genes with reported polymorphic association to PTSD patients.

This SEFL model provides a tool for development of PTSD therapeutics that is compatible with the growing number of mouse-specific resources. Furthermore, use of an inbred strain allows for investigation into epigenetic mechanisms that are expected to critically regulate susceptibility and resilience.


memory, stress, learning, traumatic, extinction, resilience


Susceptibility and resilience to PTSD-like behaviors in inbred mice


Stephanie E. Sillivan,1,2 Nadine F. Joseph,1,2 Sarah Jamieson,1,2 Michelle L. King,3 Itzamarie Chevere-Torres,4 Illeana Fuentes,4 Gleb P. Shumyatsky,4 Alicia F. Brantley,3 Gavin Rumbaugh,2 and Courtney A. Miller1,2,*

Publish date

2018 Dec 15.




Lysyl-tRNA synthetase (KRS), a protein synthesis enzyme in the cytosol, relocates to the plasma membrane after a laminin signal and stabilizes a 67-kDa laminin receptor (67LR) that is implicated in cancer metastasis; however, its potential as an antimetastatic therapeutic target has not been explored. We found that the small compound BC-K-YH16899, which binds to KRS, impinged on interaction of KRS with 67LR and suppressed metastasis in 3 different mouse models. The compound inhibited KRS-67LR interaction in two ways. First, it directly blocked the association between KRS and 67LR. Second, it suppressed the dynamic movement of the N-terminal extension of KRS and reduced membrane localization of KRS. However, it did not affect the catalytic activity of KRS. Our results suggest that specific modulation of a cancer-related KRS-67LR interaction may offer a way to control metastasis while avoiding the toxicities associated with inhibition of the normal functions of KRS.


Chemical inhibition of prometastatic lysyl-tRNA synthetase-laminin receptor interaction


Dae Gyu Kim,1,2,15 Jin Young Lee,1,2,15 Nam Hoon Kwon,1,2 Pengfei Fang,3 Qian Zhang,4 Jing Wang,3 Nicolas L. Young,5 Min Guo,3 Hye Young Cho,6 AmeeqUl Mushtaq,6 Young Ho Jeon,6 Jin Woo Choi,1,7 Jung Min Han,1,2 Ho Woong Kang,8 Jae Eun Joo,8 Youn Hur,8 Wonyoung Kang,9 Heekyoung Yang,9 Do-Hyun Nam,9 Mi-Sook Lee,2 Jung Weon Lee,2 Eun-Sook Kim,10 Aree Moon,10 Kibom Kim,1,2 Doyeun Kim,1,2 Eun Joo Kang,1 Youngji Moon,1 Kyung Hee Rhee,2 Byung Woo Han,2 Jee Sun Yang,11 Gyoonhee Han,11 Won Suk Yang,1,2 Cheolju Lee,12 Ming-Wei Wang,13 and Sunghoon Kim1,2,14,*

Publish date

2014 May 15