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  • Brand : BIOFRON

  • Catalogue Number : BN-O1864

  • Specification : 98%(HPLC)

  • CAS number : 643-56-1

  • Formula : C17H14O3

  • Molecular Weight : 266.29

  • PUBCHEM ID : 69509

  • Volume : 20mg

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Catalogue Number


Analysis Method





Molecular Weight



Botanical Source

Structure Type











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

Flash Point


Boiling Point

564.7ºC 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#:643-56-1) 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.




Glucotoxicity or lipotoxicity leads to hyperglycemia and insulin secretion deficiency, which are important causes for the onset of type 2 diabetes mellitus (T2DM). Thus, the restoration of β-cell function is a long-sought goal in diabetes research. Previous studies have implicated pancreatic and duodenal homeobox 1 gene (Pdx1) in β-cell function and insulin secretion. In this study, we established a Pdx1 promoter-dependent luciferase system and identified the natural compound dracorhodin perchlorate (DP) as an effective promotor of Pdx1 expression. We further demonstrated that DP could significantly inhibit β-cell apoptosis induced by 33 mm glucose or 200 μm palmitate by interfering with endoplasmic reticulum stress and mitochondrial pathways and enhance insulin secretion as well. These effects were associated with enhanced activities of Erk1/2, which in turn promoted Pdx1 expression and increased the ratio of Bcl2/Bax, since inhibition of the Erk1/2 pathway abolished the DP-induced expression of Pdx1 and suppression of apoptosis. In addition, our in vivo results in diabetic mice indicated that DP treatment lowered blood glucose, raised insulin levels, enhanced Pdx1 expression and increased islet size and number in the pancreas of diabetic mice. Our findings suggest that Pdx1 is a potential target molecule of DP in the treatment of T2DM via the inhibition of glucotoxicity- or lipotoxicity- induced β-cell apoptosis and the attenuation of insulin secretion dysfunction.


Pdx1; dracorhodin perchlorate; glucotoxicity; insulin; lipotoxicity.


Dracorhodin perchlorate protects pancreatic β-cells against glucotoxicity- or lipotoxicity-induced dysfunction and apoptosis in vitro and in vivo


Lei Liu 1, Chen Liang 2, Pucheng Mei 2, Hong Zhu 2, Meiling Hou 1, Chunlei Yu 1, Zhenbo Song 2, Yongli Bao 2, Yanxin Huang 2, Jingwen Yi 1, Shuyue Wang 2, Yin Wu 2, Lihua Zheng 2, Ying Sun 1, Guannan Wang 2, Mingxin Huo 3, Shaonian Yang 2 4, Luguo Sun 2, Yuxin Li 1

Publish date

2019 Sep;




Dracorhodin perchlorate (DP), a synthetic analogue of the anthocyanin red pigment dracorhodin, has been shown to exert various pharmacological effects, including anticancer activity. However, its effects on human esophageal squamous cell carcinoma (ESCC) cells have not been previously investigated, and the molecular mechanisms underlying its anticancer activity remain unclear. In the present study, it was demonstrated that DP significantly reduced the viability of ESCC cells compared with that noted in normal human liver LO2 cells. Treatment with DP induced G2/M phase cell cycle arrest through upregulation of p21 and p27, and downregulation of cyclin B1 and Cdc2. Furthermore, DP treatment induced caspase‑dependent apoptosis, which could be reversed by exposure to Z‑VAD‑FMK, a caspase inhibitor. Western blotting demonstrated that DP induced apoptosis through extrinsic and intrinsic pathways by upregulating death receptor 4 (DR4), DR5, cleaved caspase‑3/‑7/‑9 and cleaved poly (ADP‑ribose) polymerase (PARP), and by decreasing total PARP, total caspase‑3/7, Bcl‑2 and caspase‑9/‑10. Moreover, DP treatment decreased the phosphorylation of Janus kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3), AKT, and forkhead box O3a (FOXO3a) in ESCC cells, indicating that the activity of the JAK2/STAT3 and AKT/FOXO3a signaling pathways was inhibited. Therefore, DP is a promising therapeutic agent for ESCC.


Dracorhodin perchlorate induces apoptosis and G2/M cell cycle arrest in human esophageal squamous cell carcinoma through inhibition of the JAK2/STAT3 and AKT/FOXO3a pathways


Zhengyang Lu 1, Chenyang Lu 2, Cheng Li 3, Yan Jiao 4, Yanqing Li 5, Guangxin Zhang 6

Publish date

2019 Sep




Dragon blood has been used in wound treatment for many years and can be obtained from several distinct plant species. Dracorhodin, the active substituent of dragon blood, is a characteristic compound of the palm tree, Daemonorops draco. At present, the only method to evaluate the quality of commercial dragon blood samples is a HPLC method which determines the amount of dracorhodin in a dragon blood sample. In this study, we used zebrafish embryos as a platform to demonstrate the in vivo pro-angiogenic activity of dracorhodin perchlorate, the chemically synthesized analog of dracorhodin. By using this platform, three different commercial dragon blood samples were also examined. Our results clearly show that even though the commercial dragon blood samples had similar amounts of dracorhodin, they showed highly variable biological activity, such as pro-angiogenic effects and toxicity. In short, an in vivo activity assay platform for rapidly examining the biological activity of commercial dragon blood samples was successfully established here, which complements the current HPLC-based assay method.


Angiogenesis; Dracorhodin chlorate; Dragon blood.


In vivo pro-angiogenic effects of dracorhodin perchlorate in zebrafish embryos: A novel bioactivity evaluation platform for commercial dragon blood samples


Preethi Krishnaraj 1, Yu Chang 2, Tsung-Jung Ho 3, Nai-Chen Lu 4, Ming-Der Lin 5, Hao-Ping Chen 6

Publish date

2019 Jan;

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