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  • Brand : BIOFRON

  • Catalogue Number : BF-I3004

  • Specification : 98%

  • CAS number : 470-17-7

  • Formula : C15H20O2

  • Molecular Weight : 232.32

  • PUBCHEM ID : 73285

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystal

Botanical Source

Dendrobium officinale,Atalantia buxifolia,Dicliptera chinensis,Inula helenium

Structure Type



Standards;Natural Pytochemical;API




iso-Alantolactone/ISOHELENIN/Naphtho[2,3-b]furan-2(3H)-one, decahydro-8a-methyl-3,5-bis(methylene)-, (3aR,4aS,8aR,9aR)-/ISOALANTOACTONE/(3aR,4aS,8aR,9aR)-8a-Methyl-3,5-bis(methylene)decahydronaphtho[2,3-b]furan-2(3H)-one/isolantolactone/Isoalantolactone/(3aR,4aS,8aR,9aR)-8a-methyl-3,5-dimethylidenedecahydronaphtho[2,3-b]furan-2(3H)-one




1.1±0.1 g/cm3


Methanol; Ethyl Acetate

Flash Point

152.7±25.3 °C

Boiling Point

364.9±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#:470-17-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Esophageal cancer is the eighth most prevalent cancer and has high mortality in our society. Isoalantolactone, extracted from Inula helenium L, has shown potent anticancer effects on a variety of cancers. However, its effect on human esophageal cancer, and the underlying molecular mechanism, remain to be investigated. In the present study, we demonstrated that isoalantolactone induced apoptosis in esophageal cancer cells. Treatment with isoalantolactone activated caspases-3, -7, and -10, and upregulated death receptor (DR)5. Furthermore, DR5 knockdown partially reversed the effect of isoalantolactone. These results indicated the extrinsic apoptosis was induced by isoalantolactone. In addition, intracellular reactive oxygen species (ROS) were significantly elevated after treatment with isoalantolactone. N-Acetylcysteine, an ROS scavenger, blocked both the apoptosis and decreased cell viability caused by isoalantolactone. In vivo, significant suppression of tumor growth by isoalantolactone was observed in an ECA109 cell xenograft mouse model. Isoalantolactone showed no obvious adverse effects on mouse weight and histology of heart, liver, spleen, lung, and kidney. In conclusion, our results revealed that isoalantolactone induced apoptosis through the extrinsic pathway via upregulation of DR5 and elevation of ROS in human esophageal cancer cells. Isoalantolactone, therefore, could be a potential candidate in developing anticancer agents for esophageal cancer patients.


Apoptosis; Death receptor 5; Esophageal cancer; Isoalantolactone; ROS.


Isoalantolactone Induces Apoptosis Through Reactive Oxygen Species-Dependent Upregulation of Death Receptor 5 in Human Esophageal Cancer Cells


Zhengyang Lu 1 , Guangxin Zhang 2 , Yifan Zhang 3 , Peiyan Hua 2 , Meidan Fang 2 , Meiliang Wu 3 , Tongjun Liu 4

Publish date

2018 Aug 1




Background: This study was designed to explore the anticancer potential of isoalantolactone, a sesquiterpene lactone, on esophageal squamous cell carcinoma (ESCC) cells and associated molecular mechanisms.
Methods: ESCC cell lines were treated with isoalantolactone or vehicle and tested for viability, proliferation, cell cycle distribution, and apoptosis. Xenograft tumor studies in nude mice were done to examine the in vivo anticancer effect of isoalantolactone.
Results: Isoalantolactone treatment reduced ESCC cell viability and proliferation in vitro, which was coupled with induction of G0/G1 cell cycle arrest and apoptosis. In vivo studies confirmed the growth-suppressive effect of isoalantolactone on ESCC cells. Mechanistically, isoalantolactone reversed microRNA-21-mediated repression of programmed cell death 4 (PDCD4). Overexpression of microRNA-21 and knockdown of PDCD4 blocked the growth suppression and apoptosis induction by isoalantolactone in ESCC cells.
Conclusions: Isoalantolactone shows growth-suppressive activity against ESCC cells, which is ascribed to upregulation of PDCD4 via downregulation of microRNA-21.


Apoptosis; Death receptor 5; Esophageal cancer; Isoalantolactone; ROS.


Isoalantolactone Inhibits Esophageal Squamous Cell Carcinoma Growth Through Downregulation of MicroRNA-21 and Derepression of PDCD4


Shi-Wang Wen 1 , Yue-Feng Zhang 1 , Yong Li 1 , Yan-Zhao Xu 1 , Zhen-Hua Li 1 , Huilai Lu 1 , Yong-Gang Zhu 1 , Zhen-Xu Liu 1 , Zi-Qiang Tian 2

Publish date

2018 Sep




Background: Prostate cancer is one of the most commonly diagnosed cancers in men worldwide. Currently available therapies for metastatic prostate cancer are only marginally effective. Therefore, new therapeutic agents are urgently needed to improve patient outcome. Isoalantolactone (IATL), an active sesquiterpene naturally present in many vegetables and medicinal plants, is known to induce cell death and apoptosis in various cancer cell lines. Nevertheless, antitumor mechanisms initiated by IATL in cancer cells have not been fully defined.
Methods: Cell apoptosis and cellular ROS levels were analyzed by flow cytometry. Western blot and qRT-PCR were used to analyze the protein and mRNA levels of indicated molecules, respectively. Nude mice xenograft model was used to test the effects of IATL on prostate cancer cell growth in vivo.
Results: In this study, we found that IATL dose-dependently inhibited cancer cell growth and induced apoptosis in PC-3 and DU145 cells. Mechanistically, our data found that IATL induced reactive oxygen species (ROS) production, resulting in the activation of endoplasmic reticulum stress pathway and eventually cell apoptosis in prostate cancer cells. IATL also decreased the protein expression levels of p-STAT3 and STAT3, and the effects of IATL were reversed by pretreatment with N-acetyl-L-cysteine (NAC). In vivo, we found that IATL inhibited the growth of prostate cancer xenografts without exhibiting toxicity. Treatment of mice bearing human prostate cancer xenografts with IATL was also associated with induction of ER stress and inhibtion of STAT3.
Conclusion: In summary, our results unveil a previously unrecognized mechanism underlying the biological activity of IATL, and provide a novel anti-cancer candidate for the treatment of prostate cancer.


ER stress; Isoalantolactone; Prostate cancer; Reactive oxygen species; STAT3.


Isoalantolactone Induces Apoptosis Through ROS-mediated ER Stress and Inhibition of STAT3 in Prostate Cancer Cells


Wei Chen 1 , Ping Li 1 , Yi Liu 2 , Yu Yang 1 , Xueting Ye 1 , Fangyi Zhang 1 , Hang Huang 3

Publish date

2018 Dec 12

Description :

Isoalantolactone is an apoptosis inducer, which also acts as an alkylating agent.