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  • Brand : BIOFRON

  • Catalogue Number : BN-O1597

  • Specification : 98%(HPLC)

  • CAS number : 549-84-8

  • Formula : C21H26N2O3

  • Molecular Weight : 354.5

  • PUBCHEM ID : 3058605

  • Volume : 5mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

This product is isolated and purified from the peel of Corynante yohimbe

Structure Type



Standards;Natural Pytochemical;API




Methyl (16α,17β)-17-hydroxyyohimban-16-carboxylate/Yohimban-16α-carboxylic acid, 17β-hydroxy-, methyl ester/Yohimban-16-α-carboxylic acid, 17-β-hydroxy-, methyl ester/.beta.-Yohimbine/Amsonin/Yohimban-16α-carboxylic acid, 17β-hydroxy-, methyl ester (8CI)/Yohimban-16-carboxylic acid, 17-hydroxy-, methyl ester, (16α,17β)-/Amsonine/b-Yohimbine/β-Yohimbine


methyl (1S,15R,18R,19R,20S)-18-hydroxy-1,3,11,12,14,15,16,17,18,19,20,21-dodecahydroyohimban-19-carboxylate


1.3±0.1 g/cm3


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

Flash Point

282.2±30.1 °C

Boiling Point

543.0±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#:549-84-8) 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.


Abstracts from the 3rd Conference on Aneuploidy and Cancer: Clinical and Experimental Aspects Berkeley, CA, USA. 26 - 29 January 2017


Athel Cornish-Bowden,corresponding author1 Athel Cornish-Bowden,corresponding author2 David Rasnick,corresponding author3 Henry H. Heng,corresponding author4 Steven Horne,4 Batoul Abdallah,4 Guo Liu,4 Christine J. Ye,5 Mathew Bloomfield,corresponding author6,7 Mark D. Vincent,corresponding author8 C. Marcelo Aldaz,corresponding author9 Jenny Karlsson,10 Anders Valind,10 Caroline Jansson,10 David Gisselsson,corresponding author10,11,12 Jennifer A. Marshall Graves,corresponding author13 Aleksei A. Stepanenko,corresponding author14 Svitlana V. Andreieva,14 Kateryna V. Korets,14 Dmytro O. Mykytenko,14 Nataliya L. Huleyuk,15 Vladimir P. Baklaushev,16 Oksana A. Kovaleva,17 Vladimir P. Chekhonin,18,19 Yegor S. Vassetzky,20 Stanislav S. Avdieiev,14 Bjorn Bakker,21 Aaron S. Taudt,21 Mirjam E. Belderbos,21,23 David Porubsky,21 Diana C. J. Spierings,21 Tristan V. de Jong,21 Nancy Halsema,21 Hinke G. Kazemier,21 Karina Hoekstra-Wakker,21 Allan Bradley,22 Eveline S. J. M. de Bont,23 Anke van den Berg,24 Victor Guryev,21 Peter M. Lansdorp,21,25,26 Maria Colome Tatche,21,25,27 Floris Foijer,corresponding author21 Thomas Liehr,corresponding author28 Nicolaas C. Baudoin,29 Joshua M. Nicholson,29 Kimberly Soto,29 Isabel Quintanilla,30 Jordi Camps,30 Daniela Cimini,corresponding author29 M. Durrbaum,corresponding author31,32 N. Donnelly,31 V. Passerini,31 C. Kruse,31 B. Habermann,32 Z. Storchova,31,33 Daniele Mandrioli,corresponding author34 Fiorella Belpoggi,34 Ellen K Silbergeld,35 Melissa J Perry,36 Rolf I. Skotheim,corresponding author37,38 Marthe Løvf,37,38 Bjarne Johannessen,37,38 Andreas M. Hoff,37,38 Sen Zhao,37,38 Jonas M. SveeStrømme,37,38 Anita Sveen,37,38 Ragnhild A. Lothe,37,38 R. Hehlmann,corresponding author39 A. Voskanyan,39 A. Fabarius,39 Alfred Bocking,corresponding author40 Stefan Biesterfeld,41 Leonid Berynskyy,42 Christof Borgermann,43 Rainer Engers,44 Josef Dietz,45 A. Fritz,corresponding author46 N. Sehgal,47 J. Vecerova,48 B. Stojkovicz,49 H. Ding,49 N. Page,46 C. Tye,46 S. Bhattacharya,50 J. Xu,49 G. Stein,46 J. Stein,46 R. Berezney,47 Xue Gong,51,52 Sarah Grasedieck,51,52 Julian Swoboda,51,52 Frank G. Rucker,52 Lars Bullinger,52 Jonathan R. Pollack,corresponding author51 Fani-Marlen Roumelioti,53 Maria Chiourea,53 Christina Raftopoulou,53 Sarantis Gagos,corresponding author53 Peter Duesberg,corresponding author54 Mat Bloomfield,54,55 Sunyoung Hwang,56 Hans Tobias Gustafsson,56 Ciara O’Sullivan,56 Aracelli Acevedo-Colina,56 Xinhe Huang,57 Christian Klose,58 Andrej Schevchenko,58 Robert C. Dickson,57 Paola Cavaliere,59 Noah Dephoure,59 Eduardo M. Torres,corresponding author56 Martha R. Stampfer,corresponding author60,61 Lukas Vrba,61 Mark A. LaBarge,60,62 Bernard Futscher,61 James C. Garbe,60 Yi-Hong Zhou,corresponding author63 Andrew L. Trinh,64 Yi-Hong Zhou,65 and Michelle Digmancorresponding author64

Publish date





Multi-targeting of oncoproteins by a single molecule represents an effectual, rational, and an alternative approach to target therapy. We carried out a systematic study to reveal the mechanisms of action of newly synthesized Cu2+ compounds of 2-naphthalenol and 1-(((2-pyridinylmethyl)imino)methyl)- (C1 and C2). The antiproliferative activity of the as-synthesized complexes in three human cancer cell lines indicates their potential as multi-targeted antitumor agents. Relatively, C1 and C2 showed better efficacy in vitro relative to Cisplatin and presented promising levels of toxicity against A-549 cells. On the whole, the Cu2+ complexes exhibited chemotherapeutic effects by generating reactive oxygen species (ROS) and arresting the cell cycle in the G0/G1 phase by competent regulation of cyclin and cyclin-dependent kinases. Fascinatingly, the Cu2+ complexes were shown to activate the apoptotic and autophagic pathways in A-549 cells. These complexes effectively induced endoplasmic reticulum stress-mediated apoptosis, inhibited topoisomerase-1, and damaged cancer DNA through a ROS-mediated mechanism. The synthesized Cu2+ complexes established ROS-mediated targeting of multiple cell signaling pathways as a fabulous route for the inhibition of cancer cell growth.


Cu(II) complex, 2-hydroxy-1-naphthaldehyde, cytotoxicity, anticancer mechanism


Anticancer Function and ROS-Mediated Multi-Targeting Anticancer Mechanisms of Copper (II) 2-hydroxy-1-naphthaldehyde Complexes


Muhammad Hamid Khan, Meiling Cai, Jungang Deng, Ping Yu, Hong Liang,* and Feng Yang*

Publish date

2019 Jul;




Lung cancer is one of the most commonly diagnosed cancers with survival much lower in patients diagnosed with distal metastases. It is therefore imperative to identify pathways involved in lung cancer invasion and metastasis and to consider the therapeutic potential of agents that can interfere with these molecular pathways. This study examines nWASP expression in human lung cancer tissues and explores the effect of nWASP inhibition and knockdown on lung cancer cell behaviour.

QPCR has been used to measure nWASP transcript expression in human lung cancer tissues. The effect of wiskostatin, an nWASP inhibitor, on A-549 and SK-MES-1 lung carcinoma cell growth, adhesion, migration and invasion was also examined using several in vitro functional assays, including ECIS, and immunofluorescence staining. The effect of nWASP knockdown using siRNA on particular behaviours of lung cancer cells was also examined.

Patients with high levels of nWASP expression in tumour tissues have significantly lower survival rates. nWASP transcript levels were found to correlate with lymph node involvement (p = 0.042). nWASP inhibition and knockdown was shown to significantly impair lung cancer cell growth. nWASP inhibition also affected other cell behaviours, in SK-MES-1 invasion and A-549 cell motility, adhesion and migration. Paxillin and FAK activity are reduced in lung cancer cell lines following wiskostatin and nWASP knockdown as shown by immunofluorescence and western blot.

These findings highlight nWASP as an important potential therapeutic target in lung cancer invasion and demonstrate that inhibiting nWASP activity using the inhibitor wiskostatin can significantly alter cell behaviour in vitro.


nWASP, Lung, Cancer, Invasion, Wiskostatin


Neural Wiskott-Aldrich syndrome protein (nWASP) is implicated in human lung cancer invasion


Bethan A. Frugtniet,1 Tracey A. Martin,corresponding author1 Lijian Zhang,2 and Wen G. Jiang1

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