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Catalogue Number : BF-F4002
Specification : 98%(HPLC)
CAS number : 24268-41-5
Formula : C15H18O2
Molecular Weight : 230.3
PUBCHEM ID : 179413
Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

Curcuma phaeocaulis

Structure Type



Standards;Natural Pytochemical;API




Furanodienon/Cyclodeca[b]furan-4(7H)-one, 8,11-dihydro-3,6,10-trimethyl-, (5Z)-/furanodien-6-one/(5Z)-3,6,10-Trimethyl-8,11-dihydrocyclodeca[b]furan-4(7H)-one/furanodiene-6-one/(1(10)E,4E)-8,12-epoxygermacra-1(10),4,7,11-tetraen-6-one/(5E,9E)-3,6,10-Trimethyl-8,11-dihydro-7H-cyclodeca[b]furan-4-one




1.0±0.1 g/cm3


Methanol; Chloroform; Ethyl Acetate

Flash Point

172.0±20.6 °C

Boiling Point

363.8±42.0 °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#:24268-41-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Estrogen receptor alpha (ERα) plays an important role in the development and progression of breast cancer and thus the attenuation of ERα activities is a promising treatment strategy. Furanodienone is one of the main bioactive chemical components of Rhizoma Curcumae which is commonly used in Chinese medicine for the treatment of cancer. In this study, we investigated the effects of furanodienone on human breast cancer MCF-7, T47D, and MDA-MB-231 cells. Our results showed that furanodienone could inhibit MCF-7, T47D, and MDA-MB-231 cells proliferation in a dose (10-160 µM) dependent manner. ERα-negative MDA-MB-231 cells were less sensitive to furanodienone than ERα-positive MCF-7 and T47D cells. Furanodienone could effectively block 17β-estradiol (E2)-stimulated MCF-7 cell proliferation and cell cycle progression and induce apoptosis evidenced by the flow cytometric detection of sub-G1 DNA content and the appearance of apoptotic nuclei after DAPI staining. Furanodienone specifically down-regulated ERα protein and mRNA expression levels without altering ERβ expression. Furanodienone treatment inhibited E2-stimulation of estrogen response element (ERE)-driven reporter plasmid activity and ablated E2-targeted gene (e.g., c-Myc, Bcl-2, and cyclin D1) expression which resulted in the inhibition of cell cycle progression and cell proliferation, and in the induction of apoptosis. Knockdown of ERα in MCF-7 cells by ERα-specific siRNA decreased the cell growth inhibitory effect of furanodienone. These findings suggest that effects of furanodienone on MCF-7 cells are mediated, at least in part, by inhibiting ERα signaling.


Furanodienone Inhibits Cell Proliferation and Survival by Suppressing ERα Signaling in Human Breast Cancer MCF-7 Cells


Ying-Wei Li 1 , Guo-Yuan Zhu, Xiao-Ling Shen, Jian-Hong Chu, Zhi-Ling Yu, Wang-Fun Fong

Publish date

2011 Jan




Purpose: Overexpression of EGFR and HER2 is seen in breast cancers and results in poor prognosis and decreased patient survival. Clinically, EGFR and HER2 are effective therapeutic targets. The objective of this study is to investigate the in vitro effects of furanodienone, an active chemical component isolated from Rhizoma Curcumae, on the activation of EGFR/HER2 signaling, cell cycle, and apoptosis in HER2-overexpressing BT474 and SKBR3 cells.
Methods: Cell growth was assessed by SRB protein assay. Cell cycle analysis was carried out by flow cytometry, and apoptosis was observed by Annexin V and DAPI staining. Effects of furanodienone on the activation of EGFR/HER2 signaling-related proteins were analyzed by western blotting.
Results: Furanodienone inhibited cell growth in BT474 and SKBR3 cells. Furanodienone caused G1 arrest in BT474 cells and induced apoptosis in SKBR3 cells. Furanodienone interfered with EGFR/HER2 signaling in treated cells as shown by decreases in phosphorylated EGFR, HER2, Akt, Gsk3β and an increase in p27(kip1) protein. Accordingly, furanodienone inhibited EGF-induced phosphorylation of EGFR, HER2, Akt, and Gsk3β. EGFR-specific siRNA knockdown did not affect the cell growth inhibitory effect of furanodienone. On the contrary, specific siRNA knockdown of HER2 increased cellular resistance to furanodienone toxicity. In HER-2-deficient MDA-MB-231 cells, the transfection and expression of HER2 increased the sensitivity of cells to furanodienone toxicity.
Conclusion: Furanodienone inhibited EGFR/HER2 signaling pathway in BT474 and SKBR3 cells. More importantly, the effect of furanodienone was specifically dependent on HER2, but not EGFR, expression.


Furanodienone Induces Cell Cycle Arrest and Apoptosis by Suppressing EGFR/HER2 Signaling in HER2-overexpressing Human Breast Cancer Cells


Ying-Wei Li 1 , Guo-Yuan Zhu, Xiao-Ling Shen, Jian-Hong Chu, Zhi-Ling Yu, Wang-Fun Fong

Publish date

2011 Nov




Furanodienone, a major bioactive constituents of sesquiterpene derived from Rhizoma Curcumae, has been proven to possess the potent anticancer efficacy on human breast cancer cells. Here, we investigated the cytotoxicity of furanodienone on human colorectal carcinoma cell lines in vitro and in vivo, as well as its underlying molecular mechanisms in the induction of apoptosis. In this study, we found that furanodienone significantly inhibited proliferation of RKO and HT-29 cells, induced mitochondrial dysfunction characterized by collapse of mitochondrial transmembrane potential and reduction of ATP level, and promoted the production of reactive oxygen species (ROS) that functions upstream of caspase-dependent apoptosis. The antioxidant N-acetyl cysteine, a ROS scavenger, abolished this apoptosis induced by furanodienone. In addition, furanodienone elevated the expression of p-p38, p-JNK, but decreased p-ERK, as a result of the produced ROS. The specific inhibitors U0126, SP600125 and SB202190 attenuated the expression of MAPKs, and regulated the expression of cleaved caspase-8, -9 and -3. Furthermore, the potential inhibitory effect of furanodienone on CRC cells was also corroborated in mouse xenograft model. In conclusion, the results demonstrated that furanodienone-triggered ROS plays a pivotal role in apoptosis as an upstream molecule-modulating activity of caspases in mitochondrial pathway via stimulating MAPKs signaling pathway. Our finding may provide a novel candidate for development of antitumor drugs targeting on colorectal cancer.


Furanodienone Induces G0/G1 Arrest and Causes Apoptosis via the ROS/MAPKs-mediated Caspase-Dependent Pathway in Human Colorectal Cancer Cells: A Study in Vitro and in Vivo


Ying Jiang 1 , Xiaoqin Wang 1 , Daode Hu 1

Publish date

2017 May 25