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    CAS No. 553-21-9 Price $40 / 20mg
    Catalog No.CFN98928Purity>=98%
    Molecular Weight232.3 Type of CompoundSesquiterpenoids
    FormulaC15H20O2Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Costunolide has antipyretic, anti-inflammatory, anti-oxidant, anti-carcinogenic and anti-fungal activities, it possesses normo-glycemic and hypolipidemic activity. Costunolide inhibits RANKL-induced osteoclast differentiation by suppressing RANKL-mediated c-Fos transcriptional activity; it inhibits IL-1beta gene expression by blocking the activation of MAPKs and DNA binding of AP-1; it also induces the ROS-mediated mitochondrial permeability transition and resultant cytochrome c release,
    Targets: NF-kB | p65 | ROS | AP-1 | IL Receptor | p38MAPK | JNK | LDL | Chk | c-Fos | AP-1
    In vitro:
    Phytother Res. 2014 Oct;28(10):1499-505.
    In vitro and in silico evaluation of NF-κB targeted costunolide action on estrogen receptor-negative breast cancer cells--a comparison with normal breast cells.[Pubmed: 24733523]
    Costunolide, a sesquiterpene lactone is a plant-derived secondary metabolite found to be present in most of the pharmacologically active herbs, being the cause for their medicinal values. The present study aims to evaluate the cytotoxic effect of Costunolide isolated from Costus speciosus rhizome extract on MDA-MB-231 cells and explore its targeted action in comparison with its action on the normal breast cells (MCF 10A).
    The effect of Costunolide on cell viability of the cells was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide viability assay. The targeted action of the compound was analyzed comparing the effectiveness of the compound to alter the protein expression levels of NF-κB subunits in the normal and the cancer cells using western blotting analysis. In silico studies were performed to predict the targeted interaction of Costunolide with the NF-κB subunit proteins. Costunolide inhibited the cell viability of MDA-MB-231 cells in a dose-dependent manner leaving no significant change in the viability of the normal breast cells. The over expressed NF-κB subunits - p65, 52 and 100 in the cancer cells were found to be downregulated when treated with Costunolide at an effective dose of 20 and 40 μM Costunolide. In silico results provided stable interactions between Costunolide and the target proteins, supporting the in vitro results in addition.
    Thus, Costunolide derived from C. speciosus plant source elevates a fresh conviction for its use in breast cancer therapy for its cytotoxic efficacy and non-toxic nature.
    Biochem Biophys Res Commun. 2004 Jan 2;313(1):171-7.
    Costunolide inhibits interleukin-1beta expression by down-regulation of AP-1 and MAPK activity in LPS-stimulated RAW 264.7 cells.[Pubmed: 14672714]
    Costunolide, a sesquiterpene lactone isolated from the root of Saussurea lappa Clarke, is known to have a variety of biological activities, including anti-carcinogenic and anti-fungal activities.
    Here, we demonstrated the inhibitory effect of Costunolide on the protein and mRNA expression of interleukin-1beta (IL-1beta) in LPS-stimulated RAW 264.7 cells. We also showed that Costunolide suppressed the transcriptional activity of the IL-1beta promoter. Moreover, Costunolide inhibited the activity of AP-1 transcription factor, and the phosphorylation of MAPKs, including SAPK/JNK and p38 MAP kinase. The inhibitory effect of Costunolide on AP-1 activity was also confirmed by an electrophoretic mobility shift assay. Additionally, specific inhibitors of SAPK/JNK and p38 MAP kinase, SP600125 and SB203580, also suppressed LPS-induced increase in IL-1beta gene expression and AP-1 DNA binding.
    Taken together, these results demonstrate that Costunolide inhibits IL-1beta gene expression by blocking the activation of MAPKs and DNA binding of AP-1 in LPS-stimulated RAW 264.7 cells.
    In vivo:
    J Ethnopharmacol. 2009 Jul 30;124(3):369-76.
    Antipyretic and anti-inflammatory properties of the ethanolic extract, dichloromethane fraction and costunolide from Magnolia ovata (Magnoliaceae).[Pubmed: 19524658 ]
    Magnolia ovata (A.St.-Hil.) Spreng (formerly Talauma ovata), known as "pinha-do-brejo" or "baguaçu", is a large tree widely distributed in Brazil. Its trunk bark has been used in folk medicine against fever. However, no data have been published to support the antipyretic ethnopharmacological use. This study investigated the antipyretic and anti-inflammatory effects of the ethanolic extract (EEMO), dichloromethane fraction (DCM), and the isolated compound Costunolide.
    The antipyretic and anti-inflammatory activities were evaluated in experimental models of fever and inflammation in mice. The oral administration of EEMO, DCM and Costunolide inhibited carrageenan (Cg)-induced paw oedema (ID(50) 72.35 (38.64-135.46) mg/kg, 5.8 (2.41-14.04) mg/kg and 0.18 (0.12-0.27) mg/kg, respectively) and was effective in abolishing lipopolysaccharide (LPS)-induced fever (30 mg/kg, 4.5 mg/kg and 0.15 mg/kg, respectively). EEMO was also effective in reducing cell migration in the pleurisy model. Intraplantar injection of Costunolide also reduced the paw oedema, myeloperoxidase and N-acetyl-glucosaminidase activity induced by Cg in mice.
    Collectively, these results show, for the first time, that extracts obtained from Magnolia ovata possess antipyretic and anti-inflammatory properties, and Costunolide appears to be the compound responsible for these effects.
    Costunolide Description
    Source: The roots of Inula helenium L.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 4.3048 mL 21.5239 mL 43.0478 mL 86.0956 mL 107.6195 mL
    5 mM 0.861 mL 4.3048 mL 8.6096 mL 17.2191 mL 21.5239 mL
    10 mM 0.4305 mL 2.1524 mL 4.3048 mL 8.6096 mL 10.7619 mL
    50 mM 0.0861 mL 0.4305 mL 0.861 mL 1.7219 mL 2.1524 mL
    100 mM 0.043 mL 0.2152 mL 0.4305 mL 0.861 mL 1.0762 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Kinase Assay:
    Phytother Res. 2014 Apr;28(4):586-92.
    Costunolide inhibits osteoclast differentiation by suppressing c-Fos transcriptional activity.[Pubmed: 23832494]
    Costunolide, a sesquiterpene lactone, exhibits anti-inflammatory and anti-oxidant properties and mediates apoptosis. However, its effects and mechanism of action in osteoclasts remain unknown. Herein, we found that 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 of Costunolide were rescued by overexpression of constitutively active (CA)-NFATc1.
    Taken together, our results suggest that Costunolide inhibited RANKL-induced osteoclast differentiation by suppressing RANKL-mediated c-Fos transcriptional activity.
    Biol Pharm Bull. 2001 Mar;24(3):303-6.
    Costunolide induces apoptosis by ROS-mediated mitochondrial permeability transition and cytochrome C release.[Pubmed: 11256490]
    Costunolide is an active compound isolated from the root of Saussurea lappa Clarks, a Chinese medicinal herb, and is considered a therapeutic candidate for various types of cancers. Nevertheless, the pharmacological pathways of Costunolide are still unknown. In this study, we investigate the effects of Costunolide on the induction of apoptosis in HL-60 human leukemia cells and its putative pathways of action.
    Using apoptosis analysis, measurement of reactive oxygen species (ROS), and assessment of mitochondrial membrane potentials, we show that Costunolide is a potent inducer of apoptosis, and facilitates its activity via ROS generation, thereby inducing mitochondrial permeability transition (MPT) and cytochrome c release to the cytosol. ROS production, mitochondrial alteration, and subsequent apoptotic cell death in Costunolide-treated cells were blocked by the antioxidant N-acetylcystein (NAC). Cyclosporin A, a permeability transition inhibitor, also inhibited mitochondrial permeability transition and apoptosis.
    Our data indicate that Costunolide induces the ROS-mediated mitochondrial permeability transition and resultant cytochrome c release. This is the first report on the mechanism of the anticancer effect of Costunolide.
    Cell Research:
    Radiat Oncol. 2011 May 30;6:56.
    Costunolide causes mitotic arrest and enhances radiosensitivity in human hepatocellular carcinoma cells.[Pubmed: 21624128]
    This work aimed to investigate the effect of Costunolide, a sesquiterpene lactone isolated from Michelia compressa, on cell cycle distribution and radiosensitivity of human hepatocellular carcinoma (HCC) cells.
    The assessment used in this study included: cell viability assay, cell cycle analysis by DNA histogram, expression of phosphorylated histone H3 (Ser 10) by flow cytometer, mitotic index by Liu's stain and morphological observation, mitotic spindle alignment by immunofluorescence of alpha-tubulin, expression of cell cycle-related proteins by Western blotting, and radiation survival by clonogenic assay. Our results show that Costunolide reduced the viability of HA22T/VGH cells. It caused a rapid G2/M arrest at 4 hours shown by DNA histogram. The increase in phosphorylated histone H3 (Ser 10)-positive cells and mitotic index indicates Costunolide-treated cells are arrested at mitosis, not G2, phase. Immunofluorescence of alpha-tubulin for spindle formation further demonstrated these cells are halted at metaphase. Costunolide up-regulated the expression of phosphorylated Chk2 (Thr 68), phosphorylated Cdc25c (Ser 216), phosphorylated Cdk1 (Tyr 15) and cyclin B1 in HA22T/VGH cells. At optimal condition causing mitotic arrest, Costunolide sensitized HA22T/VGH HCC cells to ionizing radiation with sensitizer enhancement ratio up to 1.9.
    Costunolide could reduce the viability and arrest cell cycling at mitosis in hepatoma cells. Logical exploration of this mitosis-arresting activity for cancer therapeutics shows Costunolide enhanced the killing effect of radiotherapy against human HCC cells.
    Animal Research:
    Chem Biol Interact. 2009 May 15;179(2-3):329-34.
    Normo-glycemic and hypolipidemic effect of costunolide isolated from Costus speciosus (Koen ex. Retz.)Sm. in streptozotocin-induced diabetic rats.[Pubmed: 19007766 ]
    Diabetes mellitus is the most common and serious metabolic disorder among people all over the world. Many plants have successfully been used to overcome this problem. Costus speciosus is widely used in Indian medicine to treat various diseases including diabetes. Bioassay guided fractionation was followed to isolate Costunolide from the hexane extract of C. speciosus root.
    The structure was elucidated using X-ray crystallography. Costunolide was administered to streptozotocin (STZ) (50 mg/kg bw)-induced diabetic male wistar rats at different doses (5, 10, 20 mg/kg bw) for 30 days to assess its effect on fasting plasma glucose and cholesterol levels. It was found that plasma glucose was significantly (p<0.05) reduced in a dose-dependent manner when compared to the control. In addition, oral administration of Costunolide (20 mg/kg bw) significantly decreased glycosylated hemoglobin (HbA(1c)), serum total cholesterol, triglyceride, LDL cholesterol and at the same time markedly increased plasma insulin, tissue glycogen, HDL cholesterol and serum protein. Also Costunolide restored the altered plasma enzyme (aspartate aminotransferase, alanine aminotrasferase, lactate dehydrogenase, alkaline phosphatase and acid phosphatase) levels to near normal. Costunolide might have stimulated the beta islets to secrete insulin by inhibiting the expression of nitric oxide synthase.
    The results of this experimental study indicated that Costunolide possessed normo-glycemic and hypolipidemic activity and hence it could be used as a drug for treating diabetes.