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  • Brand : BIOFRON

  • Catalogue Number : BF-C1017

  • Specification : 98%

  • CAS number : 553-21-9

  • Formula : C15H20O2

  • Molecular Weight : 232.32

  • PUBCHEM ID : 5281437

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Aucklandia costus,Dolomiaea souliei

Structure Type



Standards;Natural Pytochemical;API




Cyclodeca[b]furan-2(3H)-one, 3a,4,5,8,9,11a-hexahydro-6,10-dimethyl-3-methylene-, (3aS,6E,10E,11aR)-/Costunlide/(3aS,6Z,10Z,11aR)-6,10-Dimethyl-3-methylene-3a,4,5,8,9,11a-hexahydrocyclodeca[b]furan-2(3H)-one/costunolid/Cyclodeca[b]furan-2(3H)-one, 3a,4,5,8,9,11a-hexahydro-6,10-dimethyl-3-methylene-, (3aS,6Z,10Z,11aR)-/Costulide/Costunolide/COSTUNDIDE/(3aS,6E,10E,11aR)-6,10-dimethyl-3-methylidene-3a,4,5,8,9,11a-hexahydrocyclodeca[b]furan-2(3H)-one/CUSTUNOLIDE/(3aS,6E,10E,11aR)-6,10-Dimethyl-3-methylene-3a,4,5,8,9,11a-hexahydrocyclodeca[b]furan-2(3H)-one/(3aS,6Z,10Z,11aR)-6,10-dimethyl-3-methylidene-3a,4,5,8,9,11a-hexahydrocyclodeca[b]furan-2(3H)-one




1.0±0.1 g/cm3


Methanol; Ethyl Acetate

Flash Point

162.0±25.3 °C

Boiling Point

385.4±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#:553-21-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Costunolide, a sesquiterpene lactone extracted from Radix Aucklandiae, has the activity against multiple cancers. However, the effect of costunolide on gastric cancer (GC) have remained to be ambiguous. In this study, we investigated the underlying mechanisms of apoptosis induced by costunolide in human gastric adenocarcinoma BGC-823 cells in vitro and in vivo.

The viability of BGC-823 cells was detected by MTT assay. The apoptosis and mitochondrial membrane potential (ΔΨm) of BGC-823 cells induced by costunolide were analyzed by flow cytometry. The inhibiton of costunolide on human gastric adenocarcinoma was estimated in xenografts in nude mice. Apoptosis related proteins and genes were detected by Western blot and Q-PCR.

Costunolide inhibited the viability of BGC-823 cells in a time and concentration dependent manner. Costunolide induced the apoptosis and lowered the ΔΨm of BGC-823 cells significantly. Costunolide increased the expression of Bax, cleaved caspase 9, cleaved caspase 7, cleaved caspase 3 and cleaved poly ADP ribose polymerase (PARP) proteins and decreased the expression of Bcl-2, pro-caspase 9, pro-caspase 7, pro-caspase 3 and PARP proteins. Costunolide upregulated the expression of puma, Bak1 and Bax mRNA and downregulated the expression of Bcl-2 mRNA. In addition, we demonstrated that costunolide inhibited the growth and induced apoptosis of BGC-823 cells xenografted in athymic nude mice. Costunolide increased the expression of cleaved caspase 9, cleaved caspase 3 and Bax proteins and decreased the expression of Bcl-2 protein in xenografted tumor. Costunolide upregulated the expression of puma and Bax mRNA and decreased the expression of Bcl-2 mRNA in xenografted tumor.

Collectively, our results suggested that costunolide induced mitochondria-mediated apoptosis in human gastric adenocarcinoma BGC-823 cells and could be the candidate drug against GC in clinical practice.


Apoptosis; Costunolide; Gastric cancer; Xenografted nude mice


Costunolide induces mitochondria-mediated apoptosis in human gastric adenocarcinoma BGC-823 cells.


Yan Z1,2, Xu T1,2, An Z1, Hu Y1, Chen W1, Ma J1, Shao C1, Zhu F3,4.

Publish date

2019 Jun 26




Osteoarthritis (OA) is a chronic joint disease involving cartilage erosion and matrix degradation. Costunolide is a sesquiterpene lactone that has been demonstrated to exert anti‑inflammatory activities in a wide variety of cells. The aim of the present study was to investigate the effect of costunolide in OA treatment, using rat chondrocytes and an OA rat model, in which animals were subjected to destabilization of the medial meniscus. The results revealed that costunolide (2‑6 µM) had no effect on chondrocyte viability or phenotype maintenance. Costunolide decreased the interleukin (IL)‑1β‑induced upregulation of matrix metalloproteinases (MMPs), inducible nitric oxide synthase, cyclooxygenase‑2 and IL‑6, and increased the expression of collagen II and transcription factor SOX‑9, which were inhibited by IL‑1β. Costunolide significantly decreased p65 phosphorylation induced by IL‑1β and the translocation of p65 into the nucleus of rat chondrocytes, as observed by western blot analysis and immunofluorescence staining. In addition, activation of the Wnt/β‑catenin signaling pathway was inhibited by costunolide, as demonstrated by the level of activation of β‑catenin and the transfer of β‑catenin into the nucleus induced by IL‑1β. In vivo, cartilage treated with costunolide exhibited attenuated degeneration and lower Mankin scores compared with the OA group. The present study investigated the anti‑osteoarthritic effects of costunolide, which exerted anti‑inflammatory activities and inhibited MMPs expression. Taken together, these results indicate that costunolide may have a potential value in the treatment of OA.


Costunolide inhibits matrix metalloproteinases expression and osteoarthritis via the NF‑κB and Wnt/β‑catenin signaling pathways.


He Y1, Moqbel SAA1, Xu L1, Ran J1, Ma C1, Xu K1, Bao J1, Jiang L1, Chen W1, Xiong Y1, Wu L1.

Publish date

2019 Jul




Costunolide being a sesquiterpene lactone, is known to have anticancer properties. The present study investigated the anticancer effects of costunolide against the H1299 human non‑small‑cell lung cancer (NSCLC) cell line. Inhibition of cell viability by costunolide was assessed via a MTT assay. Furthermore, the apoptotic rate was detected using Annexin V/propidium iodide labeling. A colony forming cell assay was performed to investigate the antiproliferative effects of costunolide. Wound healing and Transwell assays were performed to determine the inhibitory effects of costunolide on migration and invasion, respectively. Western blot analysis was undertaken to determine protein expression, and reverse transcription‑quantitative PCR was performed to assess mRNA expression levels. The results demonstrated that costunolide inhibited the viability of H1299 cells, with a half maximal inhibitory concentration value of 23.93±1.67 µM and induced cellular apoptosis in a dose‑dependent manner. Furthermore, the colony formation, migrative and invasive abilities of the H1299 cells were inhibited in a dose‑ or time‑dependent manner. The protein expression levels of E‑cadherin increased and those of N‑cadherin decreased following treatment with costunolide, which suggested that costunolide inhibited epithelial‑to‑mesenchymal transition. The mRNA levels of B‑Raf, E‑cadherin, N‑cadherin, integrins α2 and β1, as well as matrix metalloproteinases 2 were also found to be regulated costunolide. These findings indicate the potential of costunolide in the treatment of NSCLC.


Costunolide induces apoptosis and inhibits migration and invasion in H1299 lung cancer cells.


Wei M1, Li J1, Qiu J1, Yan Y2, Wang H3, Wu Z4, Liu Y1, Shen X1, Su C1, Guo Q1, Pan Y1, Zhang P1, Zhang J1.

Publish date

2020 Mar 26

Description :

Costunolide, a sesquiterpene lactone, exhibits anti-inflammatory and anti-oxidant properties and mediates apoptosis.IC50 Value: 6.2 - 9.8 ug/mL(sarcoma cells viability)[3]Target: Apoptosis inducerin vitro: Costunolide significantly inhibited RANKL-induced BMM differentiation into osteoclasts in a dose-dependent manner without affecting cytotoxicity. Costunolide did not regulate the early signaling pathways of RANKL, including the mitogen-activated protein kinase and NF-κB pathways. However, costunolide suppressed nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1) expression via inhibition of c-Fos transcriptional activity without affecting RANKL-induced c-Fos expression. The inhibitory effects ofcostunolide were rescued by overexpression of constitutively active (CA)-NFATc1 [1]. Exposure of T24 cells to costunolide was also associated with increased expression of Bax, down-regulation of Bcl-2, survivin and significant activation of caspase-3, and its downstream target PARP [2]. Both costunolide and dehydrocostus lactone inhibited cell viability dose- and time-dependently. IC50 values ranged from 6.2 ug/mL to 9.8 ug/mL. Cells treated with costunolide showed no changes in cell cycle, little in caspase 3/7 activity, and low levels of cleaved caspase-3 after 24 and 48 h [3].in vivo: Neither costunolide nor alpha-MGBL affected the blood-ethanol elevation in pylorus-ligated rats or that induced by intraperitoneal and intraduodenal ethanol administration [4]. Costunolide and alpha-MGBL suppressed gastric emptying in rats given 20% ethanol and 1% sodium carboxymethyl cellulose.Clinical trial: