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  • Brand : BIOFRON

  • Catalogue Number : BD-P0047

  • Specification : 98.0%(HPLC)

  • CAS number : 37239-48-8

  • Formula : C41H47NO20

  • Molecular Weight : 873.81

  • PUBCHEM ID : 73321

  • Volume : 10mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

Structure Type







[(1S,3R,18S,19R,20R,21R,22S,23R,24R,25R)-20,22,23,25-tetraacetyloxy-21-(acetyloxymethyl)-15,26-dihydroxy-3,15,26-trimethyl-6,16-dioxo-2,5,17-trioxa-11-azapentacyclo[,21.03,24.07,12]hexacosa-7(12),8,10-trien-19-yl] furan-3-carboxylate


1.5±0.1 g/cm3


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

Flash Point

488.6±34.3 °C

Boiling Point

884.4±65.0 °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#:37239-48-8) 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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Background: Liver cancer is a common malignant tumor with high mortality. Currently, effective medicines against liver cancer are still lacking. Paclitaxel is a wide-spectrum anti-tumor agent, while wilfortrine has been shown to have an inhibitory effect on the proliferation of liver cancer cells. This study thus investigated the potential effect of paclitaxel combined with wilfortrine on cultured liver cancer cells and related mechanisms, in order to provide evidence for pathogenesis and treatment of liver cancer.

Material/methods: Liver cancer cell line HpeG2 was divided into control, paclitaxel, wilfortrine, and combined treatment groups. Cell proliferation was tested by MTT, while invasion was detected in Transwell chamber assay. Apoptotic protein Bcl-2 and Bax expression levels were further quantified using real-time PCR and Western blotting.

Results: Both of those 2 drugs can effectively inhibit cancer cell proliferation, depress invasion ability, increase Bcl-2 expression, and elevate Bax expression levels (p<0.05 in all cases). The combined therapy had better treatment efficacy compared to either of those drugs alone (p<0.05). Conclusions: The combined treatment using wilfortrine and paclitaxel can inhibit proliferation and invasion of liver cancer cells via down-regulating Bcl-2 and up-regulating Bax, with better efficacy than single use of either drug.


Effect of Combined Treatment Using Wilfortrine and Paclitaxel in Liver Cancer and Related Mechanism


Shuzhen Li 1, Lei Zheng 1

Publish date

2016 Apr 4




Liver cancers are characterized by high morbidity and mortality owing to few effective drugs for its treatment. Wilfortrine has several pharmacological effects, including an inhibitory effect on liver cancer cell proliferation. However, whether wilfortrine can induce liver cancer cell apoptosis has not been elucidated. We investigated the role of wilfortrine on liver cancer cell HepG2 apoptosis and analyzed its possible mechanisms to provide a theoretical basis for clinical analysis of liver cancer pathogenesis. The liver cancer cell line HepG2 was treated with 40 mM wilfortrine for 48 h. Flow cytometry was applied to detect HepG2 cell apoptosis and cell cycle changes. Western blot was used to analyze Bcl-2 and Bax expression. The HepG2 cell apoptosis rate increased significantly after treatment with wilfortrine, especially the early apoptosis rate (P < 0.05). However, wilfortrine did not change the cell cycle of HepG2 cells. After wilfortrine treatment, Bcl- 2 expression decreased significantly (P < 0.05); on the contrary, Bax expression increased noticeably compared with the control group (P < 0.05). Wilfortrine can induce liver cancer cell HepG2 apoptosis, but with no effect on the cell cycle, mainly by promoting Bax expression and inhibiting anti-apoptotic protein Bcl-2 expression.


Effect of wilfortrine on human hepatic cancer HepG2 cell proliferation potential in vitro


M Yue 1, X J Shen 1, Y X Liu 2, X Y Lin 3, S Q Zhou 1, Y H Song 4

Publish date

2015 Nov 30




A novel liquid chromatography-atmospheric-pressure chemical ionization-mass spectrometry (LC-APCI/MS) method was developed and validated for the simultaneous determination of four sesquiterpene pyridine alkaloids (wilfortrine, wilfordine, wilforgine and wilforine) in human plasma. The chromatographic separation was performed on a Shim-pack XR-ODS column using an ammonium acetate buffer solution-acetonitrile in a gradient program. The detection was achieved by an ion trap mass spectrometry in the positive selected ion monitoring (SIM) mode. The method utilized acetonitrile as protein precipitation solvent and followed by solid-phase extraction (SPE). Calibration curves were linear for the four alkaloids over the range of 0.5-100.0 μg/L with the limits of quantification of 0.5 μg/L, while the method exhibited the recovery of 86.5-98.6%, intra- and inter-day RSDs of less than 8.2% and 12.8%, respectively. Methodology was validated in line with the EU requirements (Commission Decision 2002/657/EC). Results of incurred samples demonstrated excellent reproducibility. To our knowledge, this is the first analytical method for simultaneous determination of the four sesquiterpene pyridine alkaloids in plasma. The method was applicable to clinical pharmaceutical research of alkaloids in rheumatoid arthritis volunteer patients after oral administrations.


Determination of four pyridine alkaloids from Tripterygium wilfordii Hook. f. in human plasma by high-performance liquid chromatography coupled with mass spectrometry


Mei-qiang Cai 1, Xiao-hong Chen, Shi-wei He, Xiao-kun OuYang, Mi-cong Jin

Publish date

2011 Nov 15

Description :

Various monomers of Tripterygium wilfordii effecting adenosine deaminase activity and inducing HL-60 cell apopotosis PUMID/DOI: Li W, Long Z T, Hua F H, et al. Various monomers of Tripterygium wilfordii effecting adenosine deaminase activity and inducing HL-60 cell apopotosis[J]. Fudan University Journal of Medical Sciences, 2007, 34(1):107-110. Purpose To investigate the effect of various monomers of Tripterygium wilfordii on adenosine deaminase(ADA) activity in HL-60 cell and their function of inducing cellular apoptosis. Methods HL-60 cell was incubated with different monomers of Tripterygium wilfordii at different concentrations(10 mg/L, 1 mg/L, 0.1 mg/L) for 24 hours to detect the ADA activity. Wilforlide A, which was the most potent inhibitor to ADA activity, was selected out for future investigation. HL-60 cell was cultured with different concentrations of Wilforlide A(10 mg/L, 1 mg/L, 0.1 mg/L), or with 0.1 mg/L Wilforlide A plus 0.5 mmol/L adenosine, or 0.5 mmol/L adenosine alone for 24 h to test their effect on apoptotic rate. Results 1 Both Celafurine and Wilforlide A could obviously inhibit ADA activity in HL-60 cell(P<0.01), moreover, their inhibitory ability was in direct proportion to their concentrations. While the inhibitory function of Wilfortrine could only be detected at the concentration of 10 mg/L(P<0.01). 3-epikatonic acid, Wilfordine and Tripdiolide showed no obvious inhibitory function on ADA activity in HL-60 cell(P>0.05). 3 The obvious apoptosis of HL-60 cell could be detected after incubated with Wilforlide A at 10 mg/L or 1 mg/L. It showed no marked difference in HL-60 cell apoptosis when incubated only with 0.1 mg/L of Wilforlide A or only with adenosine compared to control groups. But the higher apoptosis could be observed when both Wilforlide A and adenosine were added to HL-60 cell. So, Wilforlide A and adenosine probably had synergistic effect on cellular apoptosis. Conclusions Some monomers of Tripterygium Wilfordii, including Wilforlide A, Celafurine and Wilfortrine, could inhibit the activity of ADA at certain concentrations. They were probably one kind of inhibitors to ADA. Meanwhile, Wilforlide A could reduce obvious cellular apoptosis while inhibited ADA activity in HL-60 cell.