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    CAS No. 19309-14-9 Price $40 / 20mg
    Catalog No.CFN99890Purity>=98%
    Molecular Weight270.3 Type of CompoundChalcones
    FormulaC16H14O4Physical DescriptionYellow powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Cardamonin is a naturally occurring chalcone with strong anti-inflammatory , anticancer, anti-melanogenesis, and vascular activity. It is a novel TRPA1 antagonist with IC50 of 454 nM and also a NF-kB inhibitor. It ameliorates insulin resistance induced by high insulin and high glucose through the mTOR and signal pathway. It also may be a potential whitening agent for use in cosmetics and in the medical treatment of hyperpigmentation disorders.
    Targets: JNK | NOS | COX | Calcium Channel | Potassium Channel | NF-kB | MMP(e.g.TIMP) | IkB | ROS | p53 | GSK-3 | TGF-β/Smad | Wnt/β-catenin | NO | PGE | AMPK | IKK | hTRPA1
    In vitro:
    Biomol Ther (Seoul). 2015 Mar;23(2):141-8.
    Cardamonin Suppresses TGF-β1-Induced Epithelial Mesenchymal Transition via Restoring Protein Phosphatase 2A Expression.[Pubmed: 25767682]
    Epithelial mesenchymal transition (EMT) is the first step in metastasis and implicated in the phenotype of cancer stem cells. Therefore, understanding and controlling EMT, are essential to the prevention and cure of metastasis.
    In the present study, we examined, by Western blot, reverse transcription polymerase chain reaction (RT-PCR), and confocal microscopy, the effects of Cardamonin (CDN) on transforming growth factor-β1 (TGF-β1)-induced EMT of A549 lung adenocarcinoma cell lines. TGF-β1 induced expression of N-cadherin and decreased expression of E-cadherin. CDN suppressed N-cadherin expression and restored E-cadherin expression. Further, TGF-β1 induced migration and invasion of A549 cancer cells, which was suppressed by CDN. TGF-β1 induced c-Jun N-terminal kinase (JNK) activation during EMT, but CDN blocked it. Protein serine/threonine phosphatase 2A (PP2A) expression in A549 cancer cells was reduced by TGF-β1 but CDN restored it.
    The overall data suggested that CDN suppresses TGF-β1-induced EMT via PP2A restoration, making it a potential new drug candidate that controls metastasis.
    Mol Immunol. 2007 Feb;44(5):673-9.
    Cardamonin inhibits COX and iNOS expression via inhibition of p65NF-kappaB nuclear translocation and Ikappa-B phosphorylation in RAW 264.7 macrophage cells.[Pubmed: 16777230 ]
    Cardamonin, a chalcone isolated from the fruits of a local plant Alpinia rafflesiana, has Cardamonin, a chalcone isolated from the fruits of a local plant Alpinia rafflesiana, has demonstrated anti-inflammatory activity in cellular models of inflammation.
    In this report, we evaluated the ability of Cardamonin to suppress both NO and PGE2 synthesis, iNOS and COX-2 expression and enzymatic activity, and key molecules in the NF-kappaB pathway in order to determine its molecular target. Cardamonin suppressed the production of NO and PGE2 in interferon-gamma (IFN-gamma)- and lipopolysaccharide (LPS)-induced RAW 264.7 cells. This inhibition was demonstrated to be caused by a dose-dependent down-regulation of both inducible enzymes, iNOS and COX-2, without direct effect upon iNOS or COX-2 enzyme activity. Subsequently we determined that the inhibition of inducible enzyme expression was due to a dose-dependent inhibition of phosphorylation and degradation of I-kappaBalpha, which resulted in a reduction of p65NF-kappaB nuclear translocation.
    We conclude that Cardamonin is a potential anti-inflammatory drug lead that targets the NF-kappaB pathway.
    J Cardiovasc Pharmacol. 2001 May;37(5):596-606.
    Vasorelaxant effects of cardamonin and alpinetin from Alpinia henryi K. Schum.[Pubmed: 11336110]
    The vascular effects of Cardamonin and alpinetin from Alpinia henryi K. Schum. were examined in the rat isolated mesenteric arteries.
    1H and 13C nuclear magnetic resonance spectra showed that Cardamonin is present in trans-form, and single-crystal radiographic structure revealed that alpinetin is present in S configuration. Both Cardamonin and alpinetin produced a rightward shift in the concentration-response curve for phenylephrine in a noncompetitive manner, and they induced relaxation of phenylephrine-preconstricted arteries with respective mean inhibitory concentrations (IC50) of 9.3+/-0.6 microM and 27.5+/-2.8 microM. Both compounds also relaxed arteries preconstricted by endothelin I or U46619. Their relaxant effects were decreased in endothelium-removed rings. Pretreatment with N(G)-nitro-L-arginine methyl ester or methylene blue inhibited relaxation induced by both agents, and pretreatment with L-arginine reversed the effect of N(G)-nitro-L-arginine methyl ester on Cardamonin-induced endothelium-dependent relaxation. The relaxant effects of Cardamonin and alpinetin were unaffected by indomethacin (3 microM). Cardamonin and alpinetin inhibited 60 mM K+-induced contraction with respective IC50 of 11.5+/-0.3 microM and 37.9+/-3.6 microM. In addition, both agents inhibited the transient contraction induced by 3 microM phenylephrine or by 10 mM caffeine in Ca2+-free Krebs solution. Finally, these two agents also concentration dependently relax the arteries preconstricted by 1 microM phorbol 12,13-diacetate in Ca2+-free Krebs solution.
    These results indicate that purified Cardamonin and alpinetin from A. henryi K. Schum. relaxed rat mesenteric arteries through multiple mechanisms. They induced both endothelium-dependent and -independent relaxation; the former is likely mediated by nitric oxide whereas the latter is probably mediated through nonselective inhibition of Ca2+ influx and intracellular Ca2+ release and inhibition of the protein kinase C-dependent contractile mechanism.
    Cardamonin Description
    Source: The seeds of Alpinia katsumadai Hayata
    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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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.6996 mL 18.498 mL 36.9959 mL 73.9919 mL 92.4898 mL
    5 mM 0.7399 mL 3.6996 mL 7.3992 mL 14.7984 mL 18.498 mL
    10 mM 0.37 mL 1.8498 mL 3.6996 mL 7.3992 mL 9.249 mL
    50 mM 0.074 mL 0.37 mL 0.7399 mL 1.4798 mL 1.8498 mL
    100 mM 0.037 mL 0.185 mL 0.37 mL 0.7399 mL 0.9249 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:
    Planta Med. 2013 Apr;79(6):452-8.
    Cardamonin ameliorates insulin resistance induced by high insulin and high glucose through the mTOR and signal pathway.[Pubmed: 23512499]
    The aim of this study is to investigate the effects of Cardamonin, a potential inhibitor of the mammalian target of the rapamycin, on insulin-resistant vascular smooth muscle cells and the molecular mechanisms involved.
    Vascular smooth muscle cells were cultured with high glucose and high insulin to induce insulin resistance. The mammalian target of rapamycin was overstimulated in cells that were incubated with high glucose and high insulin, as reflected by the excessive activation of S6 kinase 1. Insulin-resistant vascular smooth muscle cells displayed hyperphosphorylation of insulin receptor substrate-1 at Ser residues 636/639, which decreased the activity of insulin receptor substrate-1. Also, the activation of protein kinase B and phosphorylation of glycogen synthesis kinase-3β were inhibited. Cardamonin increased the 2-deoxyglucose uptake and glycogen concentration, which was reduced by insulin resistance. As with rapamycin, Cardamonin inhibited the activity of the mammalian target of rapamycin and S6 kinase 1, decreased the Ser 636/639 phosphorylation of insulin receptor substrate-1 and increased the activation of protein kinase B. Both of them increased the Ser9 phosphorylation of glycogen synthesis kinase-3β and decreased the expression of glycogen synthesis kinase-3β. However, neither Cardamonin nor rapamycin increased the expression of glucose transport 4 which decreased in insulin-resistant vascular smooth muscle cells.
    This study suggests that Cardamonin inhibited the activity of the mammalian target of rapamycin and eliminated the negative feedback of the mammalian target of rapamycin and S6 kinase 1 on the insulin-signaling pathway.
    Life Sci. 2013 Feb 7;92(2):154-60.
    Novel suppressive effects of cardamonin on the activity and expression of transglutaminase-2 lead to blocking the migration and invasion of cancer cells.[Pubmed: 23201552 ]
    Alpinia katsumadai was recently found in our previous study to have anti-migratory and anti-invasion activities against HT-1080 cells. However, the study did not demonstrate the exact component of Alpinia katsumadai with anti-migratory and anti-invasive activities. We tested the effects and relevant mechanism of Cardamonin (CDN) on the migration and invasion of cancer cells.
    Migration and invasion of cancer cells were measured using multi-well chambers. Zymography and Western blots were used to examine the effects of CDN on the activities of matrix metalloproteinases (MMPs) and expression of transglutaminase-2 (Tgase-2). CDN, but not alpinetin, dose-dependently suppressed the migration and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced invasion of HT-1080 sarcoma cells. CDN suppressed the expression of Tgase-2, MMP-2, NF-κB and MMP-9 in HT-1080 cells, and suppressed MMP-2 and MMP-9 activities. Gene silencing of Tgase-2 suppressed the migration and invasion of HT-1080 cells and suppressed the activities of MMP-2 and MMP-9. Migration of various cancer cells having high levels of Tgase-2 were also inhibited by CDN. CDN and Alpinia katsumadai extracts also directly inhibited the activity of Tgase-2.
    CDN inhibits migration of several cancer cell lines expressing Tgase-2 via suppression of Tgase-2 expression and inhibition of Tgase-2 activity. The finding that CDN has Tgase-2 inhibitory activity will give us a new scaffold or clue of pharmacophore for the development of more effective Tgase-2 inhibitors.
    Cell Research:
    Br J Pharmacol. 2012 Feb;165(3):741-53.
    Cardamonin sensitizes tumour cells to TRAIL through ROS- and CHOP-mediated up-regulation of death receptors and down-regulation of survival proteins.[Pubmed: 21797841]
    TNF-related apoptosis-inducing ligand (TRAIL) is currently in clinical trials as a treatment for cancer, but development of resistance is a major drawback. Thus agents that can overcome resistance to TRAIL are urgently needed. Cardamonin (2',4'-dihydroxy-6'-methoxychalcone) has been shown to affect cell growth by modulating various cell signalling pathways. Hence, we investigated the effect of Cardamonin on the actions of TRAIL.
    The effect of Cardamonin on TRAIL was measured by plasma membrane integrity, phosphatidylserine exposure, mitochondrial activity, and activation of caspase-8, caspase-9, and caspase-3 in human colon cancer cells. Cardamonin potentiated TRAIL-induced apoptosis and this correlated with up-regulation of both the TRAIL death receptor (DR) 4, 5 at mRNA and protein levels. TRAIL-decoy receptor DcR1 was down-regulated by Cardamonin. Induction of DRs by Cardamonin occurred in a variety of cell types. Gene silencing of the DRs by small interfering RNA (siRNA) abolished the effect of Cardamonin on TRAIL-induced apoptosis, suggesting that sensitization was mediated through the DR. Induction of the DR by Cardamonin was p53-independent but required CCAAT/enhancer binding protein homologous protein (CHOP); Cardamonin induced CHOP, and its silencing by siRNA eliminated the induction of DR5. Cardamonin increased the production of reactive oxygen species (ROS) and quenching ROS abolished its induction of receptors and enhancement of TRAIL-induced apoptosis. Cardamonin also decreased the expression of various cell survival proteins.
    Cardamonin potentiates TRAIL-induced apoptosis through ROS-CHOP-mediated up-regulation of DRs, decreased expression of decoy receptor and cell survival proteins. Thus, Cardamonin has the potential to make TRAIL more effective as an anticancer therapy.
    Biochem Biophys Res Commun. 2009 Dec 18;390(3):500-5.
    Cardamonin suppresses melanogenesis by inhibition of Wnt/beta-catenin signaling.[Pubmed: 19800318 ]
    Wnt/beta-catenin signaling plays important roles in many developmental processes, including neural crest-derived melanocyte development.
    Here we show that Cardamonin, a calchone from Aplinia katsumadai Hayata, inhibited pigmentation in melanocytes through suppression of Wnt/beta-catenin signaling pathway. Cardamonin significantly suppressed the expression of microphthalmia-associated transcription factor (MITF) and tyrosinase, which are melanocyte differentiation-associated markers, in human normal melanocytes, thereby decreasing intracellular melanin production. In addition, Cardamonin promoted the degradation of intracellular beta-catenin that was accumulated by Wnt3a-conditioned medium (Wnt3a CM) or bromoindirubin-3'-oxime (BIO), a glycogen synthase kinase-3beta (GSK-3beta) inhibitor, in HEK293 reporter cells and human normal melanocytes.
    Our findings indicate that Cardamonin may be a potential whitening agent for use in cosmetics and in the medical treatment of hyperpigmentation disorders.