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  • Brand : BIOFRON

  • Catalogue Number : BF-D1004

  • Specification : 98%

  • CAS number : 474-58-8

  • Formula : C35H60O6

  • Molecular Weight : 576.85

  • PUBCHEM ID : 5742590

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



White powder

Botanical Source

Cynomorium songaricum,Melia azedarach,Bupleurum marginatum,Aloe vera,Dioscorea nipponica

Structure Type



Standards;Natural Pytochemical;API




β-D-Glucopyranoside, (3β)-stigmast-5-en-3-yl/Daucosterin/lyoniside/Coriandrinol/(3b)-Stigmast-5-en-3-yl b-D-Glucopyranoside/Sitogluside/β-Sitosterol β-D-glucoside/β-sitosterol-D-glucoside/b-Daucosterol/b-Sitosteryl glucoside/Alexandrin/Eleutheroside A/β-sitosterol 3-O-β-D-glucopyranoside/1513DMIa/Sterolin/β-sitosteryl-β-D-glucopyranoside/3b-(b-D-glucopyranosyloxy)stigmast-5-ene/Doursterol/(3β)-Stigmast-5-en-3-yl β-D-glucopyranoside/3β-(β-D-Glucopyranosyloxy)stigmast-5-ene/Stigmast-5-ene, 3-β-(β-D-glucopyranosyloxy)-/BSSG/β-Sitosteryl glucoside/3-β-D-glucosylsitosterol/3-β-(β-D-Glucopyranosyloxy)stigmast-5-ene




1.1±0.1 g/cm3


Methanol and methylene chloride mixture

Flash Point

361.2±31.5 °C

Boiling Point

673.6±55.0 °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#:474-58-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Daucosterol (DS) is a plant phytosterol which is shown to induce oxidative stress mediated apoptosis in various cancer cell lines. However, the molecular mechanism underlying its cellular action has not been documented against Non- Small Cell Lung Cancer (NSCLC). Therefore, we attempted to decipher the mechanisms responsible for DS-induced anti-proliferation on human NSCLC cells. The present study showed, DS strongly inhibits the growth of A549 cells after 72 h time point with an IC50 value of ∼20.9 μM. Further DS elicits increased reactive oxygen species level and promote intrinsic apoptotic cell death on A549 cells as evidenced by increased expression of caspase-3, caspase-9, Bax, PARP inactivation, cytochrome-c release, and diminished expression of bcl-2 protein. DS failed to display its apoptotic actions upon pretreatment with the reactive oxygen species inhibitor NAC (N-acetyl cysteine). Indeed, apoptotic signal which was enhanced through p53/p21 activation and knockdown of p53 expression also moderately affected the DS induced apoptosis. In addition, DS preferentially inhibited the cell growth of p53 wild-type NSCLC cell lines than the mutant p53 models. Further, we show that inhibition of Thioredoxin (TrxR) redox system is principally associated with DS induced oxidative stress mediated apoptotic cell death on A549 cells. Moreover, we also demonstrated that DS stably interacted with serine residues in TrxR active sites. The obtained results confirmed that the anti-proliferative mechanism and increased reactive oxygen species level of DS was associated with down-regulation of TrxR1 pathway which triggers the p53 mediated intrinsic apoptotic mode of cell death in NSCLC cells.

Copyright © 2019. Published by Elsevier B.V.


Apoptosis; Daucosterol; Lung cancer; Reactive oxygen species; Thioredoxin redox system


Daucosterol disturbs redox homeostasis and elicits oxidative-stress mediated apoptosis in A549 cells via targeting thioredoxin reductase by a p53 dependent mechanism.


Rajavel T1, Banu Priya G1, Suryanarayanan V2, Singh SK2, Pandima Devi K3.

Publish date

2019 Jul 15




The effects of daucosterol have been identified in cancer therapy and neuronal diseases. However, the regulatory function of daucosterol in DSS-induced colitis has not yet been investigated. In this study, we evaluated the immunological and therapeutic effects of daucosterol in a mouse model of dextran sulfate sodium (DSS)-induced colitis. Unlike vehicle mice, mice pre- or post-treated with daucosterol showed inhibition of body weight loss and the decrease in the disease activity index (DAI). In addition, daucosterol treatment rescued the DSS-induced decrease in colon length and disruption of the epithelial lining. Furthermore, it reduced DSS-induced production of reactive oxygen species (ROS), infiltration of macrophages, and expression of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β. Mice with colitis showed a decreased population of Foxp3+ cells, which was upregulated by daucosterol treatment. Furthermore, daucosterol increased natural killer (NK) cell activity and inhibited excessive IgA levels in mice with DSS-induced colitis. Collectively, our findings demonstrated that daucosterol significantly alleviated DSS-induced colitis, indicating the possibility of daucosterol as a therapeutic option for colitis.

Copyright © 2019. Published by Elsevier B.V.


Daucosterol; Dextran sulphate sodium-induced colitis; Foxp3; Immune response; Natural killer cell


Daucosterol suppresses dextran sulfate sodium (DSS)-induced colitis in mice.


Jang J1, Kim SM1, Yee SM1, Kim EM2, Lee EH3, Choi HR4, Lee YS5, Yang WK6, Kim HY7, Kim KH7, Kang HS8, Kim SH9.

Publish date

2019 Jul




Plant sterols (phytosterols) have been widely accepted as a natural anti-cancer agent in multiple malignant tumors. This study was designed to investigate the functions of daucosterol in prostate cancer progression and its possible molecular mechanisms. Our results showed that daucosterol inhibited cell proliferation and induced cell cycle arrest. Moreover, daucosterol treatment obviously promoted apoptosis and autophagy. An autophagy inhibitor, 3-methyladenine (3-MA) was proved to counteract daucosterol-triggered autophagy, growth inhibition, and apoptosis, indicating that daucosterol-induced apoptotic response was dependent on autophagy. Additionally, treatment with daucosterol resulted in increased phosphorylation of c-Jun N-terminal kinase (JNK). Furthermore, pre-treatment with a JNK-specific inhibitor SP600125 abated daucosterol-elicited autophagy and apoptotic cell death. Taken together, our findings demonstrated that daucosterol blocked prostate cancer growth at least partly through inducing autophagic-dependent apoptosis via activating JNK signaling, providing a promising candidate for the development of antitumor drugs in prostate cancer treatment.


JNK; Prostate cancer; apoptosis; autophagy; cell cycle; daucosterol


Daucosterol induces autophagic-dependent apoptosis in prostate cancer via JNK activation.


Gao P1,2, Huang X2, Liao T3, Li G2, Yu X4, You Y2, Huang Y5.

Publish date

2019 May 12

Description :

Daucosterol is a natural sterolin. IC50 value:Target:In vitro: In the study of the effects of daucosterol on the survival of cultured cortical neurons after neurons were subjected to oxygen and glucose deprivation and simulated reperfusion (OGD/R)(2), the results showed that post-treatment of daucosterol significantly reduced neuronal loss, as well as apoptotic rate and caspase-3 activity, displaying the neuroprotective activity. We also found that daucosterol increased the expression level of IGF1 protein, diminished the down-regulation of p-AKT(3) and p-GSK-3β(4), thus activating the AKT(5) signal pathway [1]. Cell counting kit-8 (CCK-8) assay showed that daucosterol significantly increased the quantity of viable cells and the effectiveness of daucosterol was similar to that of basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF) [2]. Daucosterol inhibits the proliferation of human breast cancer cell line MCF-7 and gastric cancer cell lines MGC803, BGC823 and AGS in a dose-dependent manner. Furthermore, daucosterol inhibits murine hepatoma H22 cell growth in ICR mice. Daucosterol treatment induces intracellular ROS generation and autophagy, but not apoptotic cell death. Treatment with ROS scavenger GSH (reduced glutathione), NAC (N-acetyl-l-cysteine) or autophagy inhibitor 3-Methyladenine (3-MA) counteracted daucosterol-induced autophagy and growth inhibition in BGC823 and MCF-7 cancer cells [3].In vivo: