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  • Brand : BIOFRON

  • Catalogue Number : BF-O3001

  • Specification : 98%

  • CAS number : 23696-28-8

  • Formula : C12H13N3O4

  • Molecular Weight : 263.25

  • Volume : 100mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

Cyprinus carpio var. Jian

Structure Type








1.4±0.1 g/cm3


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

Flash Point


Boiling Point


Melting Point

209°C (dec.)



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#:23696-28-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




In this paper, an advanced molecularly imprinted electrochemical sensor (MIECS) based on electropolymerized olaquindox (OLA) surface molecularly imprinted polymer thin film on a modified glassy carbon electrode (GCE) was developed for the detection of OLA. It was fabricated by coating dopamine@graphene (DGr) on GCE, then electropolymerizing pyrrole (Py) and molecularly imprinted polymers (MIPs). Graphene (Gr) was introduced for improving conductivity and sensitivity. Dopamine (DA) was used for dispersion and adhesion of Gr. Polypyrrole (PPy) could fix DGr and enhance the current response evidently. The established sensor could selectively recognize OLA but not the analogs of OLA. Some essential parameters controlling the performance of the developed sensor were investigated and optimized. Under optimal conditions, the linear relationship between the current intensity and OLA concentration was obtained from 50 nmol L-1 to 500 nmol L-1 with a limit of detection (LOD) of 7.5 nmol L-1. Analytical results of OLA based on the developed MIECS for fish and feedstuffs showed a good agreement with the results based on high performance liquid chromatography (HPLC).


Dopamine@graphene; Molecularly imprinted electrochemical sensor; Olaquindox; Polypyrrole; Thin film.


Molecularly imprinted electrochemical sensor based on polypyrrole/dopamine@graphene incorporated with surface molecularly imprinted polymers thin film for recognition of olaquindox


Xiaoyun Bai 1, Bo Zhang 1, Miao Liu 1, Xuelian Hu 1, Guozhen Fang 2, Shuo Wang 3

Publish date

2020 Apr




A hybrid nanocomposite consisting of hydroxylated multi-walled carbon nanotubes (MWCNTs-OH) and cube mesoporous carbon (CMK-8) was applied in this study to construct an MWCNT-OH/CMK-8/gold electrode (GE) electrochemical sensor and simultaneously perform the electro-reduction of olaquindox (OLA) and carbadox (CBX). The respective peak currents of CBX and OLA on the modified electrode increased by 720- and 595-fold relative to the peak current of GE. The performances of the modified electrode were investigated with electrochemical impedance spectroscopy, cyclic voltammetry, and differential pulse voltammetry. Then, the modified electrodes were used for the individual and simultaneous determination of OLA and CBX. The fabricated sensor demonstrated a linear response at 0.2-500 nmol/L in optimum experimental conditions, and the detection limits were 104.1 and 62.9 pmol/L for the simultaneous determination of OLA and CBX, respectively. As for individual determination, wide linear relationships were obtained for the detected OLA with levels of 0.05-500 nmol/L with LOD of 20.7 pmol/L and the detected CBX with levels of 0.10-500 nmol/L with LOD of 50.2 pmol/L. The fabricated sensor was successfully used in the independent and simultaneous determination of OLA and CBX in spiked pork samples.


CMK−8; MWCNTs−OH; carbadox; differential pulse voltammetry; electrochemical sensor; olaquindox; simultaneous determination.


Novel Electrochemical Sensor Fabricated for Individual and Simultaneous Ultrasensitive Determination of Olaquindox and Carbadox Based on MWCNT-OH/CMK-8 Hybrid Nanocomposite Film


Yanqing Liu 1 2, Gengxin Hu 1 3, Hongwu Wang 4 5, Su Yao 1 2, Yinjian Ye 1 2

Publish date

2019 Aug 22




To monitor the illegal use of olaquindox in animals, a monoclonal antibody-based surface plasmon resonance (SPR) biosensor method has been developed to detect 3-methyl-quinoxaline-2-carboxylic acid, the marker residues of olaquindox, in swine tissues. The limit of detection was 1.4 µg kg-1 in swine muscle and 2.7 µg kg-1 in swine liver, which are lower than the EU recommended concentration (10 µg kg-1). The recoveries were from 82% to 104.6%, with coefficients of variation of less than 12.2%. Good correlations between SPR and HPLC results (r = 0.9806, muscle; r = 0.9698, liver) and between SPR and ic-ELISA results (r = 0.9918, muscle; r = 0.9873, liver) were observed in the affected tissues, which demonstrated the reliability of the SPR method. This method would be a rapid and reliable tool for the screening of the residues of olaquindox in the edible tissues of animals.




Surface plasmon resonance biosensor for the determination of 3-methyl-quinoxaline-2-carboxylic acid, the marker residue of olaquindox, in swine tissues


Dapeng Peng 1, Owen Kavanagh 2, Haijiao Gao 1, Xiya Zhang 1, Sijun Deng 3, Dongmei Chen 1, Zhenli Liu 1, Changqing Xie 1, Chen Situ 4, Zonghui Yuan 5

Publish date

2020 Jan 1

Description :

Reactive oxygen species-dependent JNK downregulated olaquindox-induced autophagy in HepG2 cells. PUMID/DOI:25042557 J Appl Toxicol. 2015 Jul;35(7):709-16. Autophagy plays an important role in response to intracellular and extracellula:r stress to sustain cell survival. However, dysregulated or excessive autophagy may lead to cell death, known as ""type II programmed cell death,"" and it is closely associated with apoptosis. In our previous study, we proposed that Olaquindox induced apoptosis of HepG2 cells through a caspase-9 dependent mitochondrial pathway. In this study, we investigated autophagy induced by Olaquindox and explored the crosstalk between apoptosis and autophagy in Olaquindox-treated HepG2 cells. Olaquindox-induced autophagy was demonstrated by the accumulation of monodansylcadervarine, as well as elevated expression of autophagy-related MAP-LC3 and Beclin 1 proteins. The autophagy inhibitor 3-methyladenine significantly increased the apoptotic rate induced by Olaquindox, which was correlated with increased ratio of Bax/Bcl-2. The further studies showed that Olaquindox increased the levels of reactive oxygen species (ROS), and antioxidant N-acetyl-L-cysteine (NAC) effectively blocked the accumulation of ROS but failed to block autophagy. Moreover, Olaquindox induced the activation of c-Jun N-terminal protein kinase (JNK), and JNK inhibitor SP600125 failed to block autophagy. Instead, Olaquindox-induced autophagy was enhanced by NAC or SP600125. Meanwhile, JNK activation was remarkably blocked by NAC, indicating that ROS may be the upstream signaling molecules of JNK activation and involved in the negative regulation of Olaquindox-induced autophagy. These results suggest that Olaquindox induces autophagy in HepG2 cells and that Olaquindox-induced apoptosis can be enhanced by 3-methyladenine. Olaquindox-induced autophagy in HepG2 cells is upregulated by Beclin 1 but downregulated by ROS-dependent JNK. Olaquindox-induced apoptosis is suppressed through p38 MAPK and ROS-mediated JNK pathways in HepG2 cells. PUMID/DOI:23812630 Cell Biol Toxicol. 2013 Aug;29(4):229-38. We investigated mitogen-activated protein kinase (MAPK) pathways as well as reactive oxygen species (ROS) in Olaquindox-induced apoptosis. Exposure of HepG2 cells to Olaquindox resulted in the phosphorylation of p38 MAPK and c-Jun N-terminal kinases (JNK). To confirm the role of p38 MAPK and JNK, HepG2 cells were pretreated with MAPKs-specific inhibitors prior to Olaquindox treatment. Olaquindox-induced apoptosis was significantly potentiated by the JNK inhibitor (SP600125) or the p38 MAPK inhibitor (SB203580). Furthermore, we observed that Olaquindox treatment led to ROS generation and that Olaquindox-induced apoptosis and ROS generation were both significantly reduced by the antioxidants, superoxide dismutase and catalase. In addition, the levels of phosphorylation of JNK, but not p38 MAPK, were significantly suppressed after pretreatment of the antioxidants, while inhibition of the activations of JNK or p38 MAPK had no effect on ROS generation. This result suggested that ROS may be the upstream mediator for the activation of JNK. Conclusively, our results suggested that apoptosis in response to Olaquindox treatment in HepG2 cells might be suppressed through p38 MAPK and ROS-JNK pathways.