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  • Brand : BIOFRON

  • Catalogue Number : BF-E4010

  • Specification : 98%(HPLC)

  • CAS number : 95041-90-0

  • Formula : C18H22O5

  • Molecular Weight : 318.36

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



Botanical Source

Dendrobium officinale,Dendrobium chrysotoxum

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Flash Point

Boiling Point

Melting Point


InChl Key

WGK Germany


HS Code Reference

Personal Projective Equipment

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For Reference Standard and R&D, Not for Human Use Directly.

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provides coniferyl ferulate(CAS#:95041-90-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

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Description :

Erianin induces a JNK/SAPK-dependent metabolic inhibition in human umbilical vein endothelial cells. PUMID/DOI:15113050 In Vivo. 2004 Mar-Apr;18(2):223-8. BACKGROUND:Erianin is a natural product derived from Dendrobium chrysotoxum, with promising antitumor activity.MATERIALS AND METHODS:To evaluate the metabolic effect of Erianin, a cytosensor assay for acidification rate, MTT assay, measurement of lactate, glucose and ATP were performed in human umbilical vein endothelial cells (HUVECs) exposed to 1-100 nM Erianin. JNK/SAPK activity was detected by Western blot.RESULTS:welve- or 24- hour incubation with Erianin induced a dose-dependent metabolic inhibition, as indicated by reduced acidification rate and cell viability, with an endothelium-selectivity. Erianin caused decreases in lactate production, glucose consumption and intracellular ATP level. Pretreatment with the JNK/SAPK inhibitor SP600125 significantly abolished these inhibitory responses, and especially restored the Erianin-induced decreases in ATP and the Erianin-induced phosphorylation of JNK/SAPK with dose- and time- dependence.CONCLUSION:Erianin inhibited endothelial metabolism in a JNK/SAPK-dependent manner. This mechanism may be involved in the potential antitumnor and antiangiogenic actions of Erianin. Erianin induces apoptosis in human leukemia HL-60 cells. PUMID/DOI:11749794 Acta Pharmacol Sin. 2001 Nov;22(11):1018-22. AIM:To investigate the effect of Erianin on human HL-60 cell line and explore its mechanism of apoptosis in vitro.METHODS:Inhibition of proliferation was measured with colorimetric MTT assay. The morphologic changes were observed by fluorescence and electron microscopes. DNA fragmentation was visualized by agarose gel electrophoresis, and the DNA degradation was determined by flow cytometry. Immunohistochemical analysis was used to identify the expression of bcl-2 and bax genes.RESULTS:The growth of human HL-60 cells was significantly inhibited by Erianin 20-81.9 nmol/L during 72 h treatment (P < 0.01). The IC50 value was 38 nmol/L after a 24-h exposure to Erianin, while that of vincristine, the positive control, was 101 nmol/L. The typical morphologic changes were observed and the nuclear DNA fragmentation exhibited ""ladder"" pattern. The cell cycle of HL-60 cells was arrested in G2/M phase, and expression of bcl-2 gene was decreased while that of bax was increased.CONCLUSION:Erianin showed potent inhibitory activity on the proliferation of HL-60 cells. The inhibition might be relative to the apoptosis induced by Erianin and the altered expression of bcl-2 and bax genes in HL-60 cells. In vivo and in vitro evaluation of erianin, a novel anti-angiogenic agent. PUMID/DOI:15196540 Eur J Cancer. 2004 Jul;40(10):1554-65. This study evaluated the anti-angiogenic activities of Erianin in vivo and in vitro. Erianin, a natural product from Dendrobium chrysotoxum, caused moderate growth delay in xenografted human hepatoma Bel7402 and melanoma A375 and induced significant vascular shutdown within 4 h of administering 100 mg/kg of the drug. Erianin also displayed potent anti-angiogenic activities in vitro: it abrogated spontaneous or basic fibroblast growth factor-induced neovascularisation in chick embryo; it inhibited proliferation of human umbilical vein endothelial cells (EC(50) 34.1+/-12.7 nM), disrupted endothelial tube formation, and abolished migration across collagen and adhesion to fibronectin. Erianin also exerted selective inhibition toward endothelial cells, and quiescent endothelium showed more resistance than in proliferative and tumour conditions. In a cytoskeletal study, Erianin depolymerised both F-actin and beta-tubulin, more significantly in proliferating endothelial cells than in confluent cells. In conclusion, Erianin caused extensive tumour necrosis, growth delay and rapid vascular shutdown in hepatoma and melanoma models; it inhibited angiogenesis in vivo and in vitro and induced endothelial cytoskeletal disorganisation. These findings suggest that Erianin has the therapeutic potential to inhibit angiogenesis in vivo and in vitro.