Damnacanthal

Damnacanthal
Product Name Damnacanthal
CAS No.: 477-84-9
Catalog No.: CFN98723
Molecular Formula: C16H10O5
Molecular Weight: 282.3 g/mol
Purity: >=98%
Type of Compound: Anthraquinones
Physical Desc.: Yellow powder
Targets: Syk | Akt | IL Receptor | TNF-α | Caspase | NF-kB | p53 | p21 | p38MAPK | Bcl-2/Bax | Histamine Receptor
Source: The fruits of Morinda citrifolia Linn.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price:
Damnacanthal possesses anti-cancer, immunomodulatory, antinociceptive and anti-inflammatory actions, it can treat or prevent hepatocellular carcinoma through its inhibitory effects on the HGF/c-Met axis. Damnacanthal inhibits mast cell activation induced by different stimuli and open a new window for the use of this compound as a mast cell stabilizer. Damnacanthal can inhibit the NF-κB/receptor-interacting protein-2/caspase-1 signal pathway by inhibiting p56lck tyrosine kinase.
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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

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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    Mol Immunol. 2015 May;65(1):86-93.
    Damnacanthal inhibits IgE receptor-mediated activation of mast cells.[Pubmed: 25656801]
    Damnacanthal, an anthraquinone obtained from the noni fruit (Morinda citrifolia L.), has been described to possess anti-cancer and anti-inflammatory properties. Since mast cells are key players in various inflammatory conditions as well as in cancer, we considered the possibility that the biological actions of Damnacanthal, at least partly, could be due to effects on mast cells. Many of the biological activities of mast cells are mediated by IgE receptor cross-linking, which results in degranulation with release of preformed granule mediators, as well as de novo synthesis and release of additional compounds.
    METHODS AND RESULTS:
    Here we show that Damnacanthal has profound inhibitory activity on mast cell activation through this pathway. The release of the granule compounds beta-hexosaminidase and tryptase release was completely abrogated by Damnacanthal at doses that were non-toxic to mast cells. In addition, Damnacanthal inhibited activation-dependent pro-inflammatory gene induction, as well as cytokine/chemokine release in response to mast cell stimulation. The mechanism underlying Damnacanthal inhibition was linked to impaired phosphorylation of Syk and Akt. Furthermore, Damnacanthal inhibited mast cell activation in response to calcium ionophore A23187.
    CONCLUSIONS:
    Altogether, the data presented here demonstrate that Damnacanthal inhibits mast cell activation induced by different stimuli and open a new window for the use of this compound as a mast cell stabilizer.
    Sci Rep. 2015 Jan 26;5:8021.
    Damnacanthal, a noni anthraquinone, inhibits c-Met and is a potent antitumor compound against Hep G2 human hepatocellular carcinoma cells.Damnacanthal, a noni anthraquinone, inhibits c-Met and is a potent antitumor compound against Hep G2 human hepatocell[Pubmed: 25620570]
    Damnacanthal, an anthraquinone present in noni plants, targets several tyrosine kinases and has antitumoral effects. This study aims at getting additional insight on the potential of Damnacanthal as a natural antitumor compound.
    METHODS AND RESULTS:
    The direct effect of Damnacanthal on c-Met was tested by in vitro activity assays. Additionally, Western blots of c-Met phosphorylation in human hepatocellular carcinoma Hep G2 cells were performed. The antitumor effects of Damnacanthal were tested by using cell growth, soft agar clonogenic, migration and invasion assays. Their mechanisms were studied by Western blot, and cell cycle, apoptosis and zymographic assays. Results show that Damnacanthal targets c-Met both in vitro and in cell culture. On the other hand, Damnacanthal also decreases the phosphorylation levels of Akt and targets matrix metalloproteinase-2 secretion in Hep G2 cells. These molecular effects are accompanied by inhibition of the growth and clonogenic potential of Hep G2 hepatocellular carcinoma cells, as well as induction of Hep G2 apoptosis.
    CONCLUSIONS:
    Since c-Met has been identified as a new potential therapeutical target for personalized treatment of hepatocellular carcinoma, Damnacanthal and noni extract supplements containing it could be potentially interesting for the treatment and/or chemoprevention of hepatocellular carcinoma through its inhibitory effects on the HGF/c-Met axis.
    Pharm Biol. 2010 Apr;48(4):446-52.
    Immunomodulatory effects of damnacanthal isolated from roots of Morinda elliptica.[Pubmed: 20645725]
    Morinda elliptica Ridley (Rubiaceae) has been used traditionally as a medicine to treat various diseases in Malaysia and southeast Asia. In the present study we investigated the immunomodulatory effects of Damnacanthal isolated from the roots of Morinda elliptica.
    METHODS AND RESULTS:
    The immunomodulatory effect of this compound was evaluated by using the lymphocyte proliferation assay with mouse thymocytes and human peripheral blood mononuclear cells (PBMC). In addition, the effect of the compound on PBMC cell cycle progression was studied by using flow cytometry. The production of human interleukin-2 and human inteleukin-12 cytokines was also assessed using the enzyme linked immunosorbent assay (ELISA) technique. The lymphocyte proliferation assay showed that Damnacanthal was able to activate mouse thymocytes and PBMC at a low concentration (0.468 microg/mL). Moreover, the production of human interleukin-2 and human interleukin-12 cytokines in the culture supernatant from Damnacanthal activated lymphocytes was markedly up-regulated at 24 h and sustained until 72 h with a slight decrease with time. A positive correlation was found between the level of these two cytokines and the MTT-based proliferation assay.
    CONCLUSIONS:
    Based on the above results, Damnacanthal can act as an immunomodulatory agent which may be very useful for maintaining a healthy immune system.
    Immunopharmacol Immunotoxicol. 2014 Oct;36(5):355-63.
    Damnacanthal inhibits the NF-κB/RIP-2/caspase-1 signal pathway by inhibiting p56lck tyrosine kinase.[Pubmed: 25139491]
    Damnacanthal is a major constituent of Morinda citrifolia L. (noni) and exhibits anti-cancer and anti-inflammatory activities. However, the effects of Damnacanthal on allergic diseases have not been determined.
    METHODS AND RESULTS:
    In this study, we investigated the effect of Damnacanthal on mast cell-mediated allergic inflammatory responses. Damnacanthal significantly and dose-dependently inhibited compound 48/80-induced systemic anaphylactic shock, histamine release and intracellular calcium levels. In particular, IgE-mediated passive cutaneous anaphylaxis was significantly inhibited by the oral administration of Damnacanthal. In addition, we report for the first time that p56lck tyrosine kinase was expressed in phorbol 12-myristate 13-acetate and calcium ionophore A23187 (PMACI)-stimulated mast cells. Furthermore, Damnacanthal inhibited the up-regulation of p56lck tyrosine kinase activity by PMACI and repressed PMACI-induced histidine decarboxylase expression and activity. Damnacanthal also inhibited PMACI-induced interleukin (IL)-1β, IL-6 and tumor necrosis factor-α expressions by suppressing nuclear factor-kappa B (NF-κB) activation and suppressed the activation of caspase-1 and the expression of receptor interacting protein-2.
    CONCLUSIONS:
    This study shows Damnacanthal inhibits the NF-κB/receptor-interacting protein-2/caspase-1 signal pathway by inhibiting p56lck tyrosine kinase and suggests that Damnacanthal has potential for the treatment of mast cell-mediated allergic disorders.
    Biol Pharm Bull. 2011;34(1):103-7.
    The antinociceptive and anti-inflammatory action of the CHCl3-soluble phase and its main active component, damnacanthal, isolated from the root of Morinda citrifolia.[Pubmed: 21212526]
    Morinda citrifolia (Rubiaceae, Noni) is a traditional medicine with various pharmacological activities.
    METHODS AND RESULTS:
    We investigated if the MeOH-, CHCl(3)- and BuOH-soluble phase and its main active component, Damnacanthal, isolated from the Noni root, have antinociceptive and anti-inflammatory actions in mice. The CHCl(3)-soluble phase (3 g/kg, per os (p.o.)) significantly reduced pain-related behavior observed in the formalin test. These effects were not suppressed by pretreatment with naloxone (1 mg/kg, intraperitoneally (i.p.)), an opioid receptor antagonist. The CHCl(3)-soluble phase (3 g/kg, p.o.) significantly reduced histamine-induced paw edema. The MeOH- and BuOH-soluble phase had no effect in either test. Furthermore, Damnacanthal (10-100 mg/kg, p.o.) exerted an antinociceptive effect on chemical nociceptive stimuli, and decreased histamine-induced paw edema. Damnacanthal was weakly bound to the histamine H(1) receptor.
    CONCLUSIONS:
    These data suggest that the CHCl(3)-soluble phase of the Noni root has antinociceptive and anti-inflammatory effects. Furthermore, these effects of Damnacanthal isolated from the Noni root is mediated in part by the histamine H(1) receptor.
    Oncol Lett. 2014 May;7(5):1479-1484.
    Damnacanthal is a potent inducer of apoptosis with anticancer activity by stimulating p53 and p21 genes in MCF-7 breast cancer cells.[Pubmed: 24765160]
    Damnacanthal, an anthraquinone compound, is isolated from the roots of Morinda citrifolia L. (noni), which has been used for traditional therapy in several chronic diseases, including cancer. Although noni has long been consumed in Asian and Polynesian countries, the molecular mechanisms by which it exerts several benefits are starting to emerge.
    METHODS AND RESULTS:
    In the present study, the effect of Damnacanthal on MCF-7 cell growth regulation was investigated. Treatment of MCF-7 cells with Damnacanthal for 72 h indicated an antiproliferative activity. The MTT method confirmed that Damnacanthal inhibited the growth of MCF-7 cells at the concentration of 8.2 μg/ml for 72 h. In addition, the drug was found to induce cell cycle arrest at the G1 checkpoint in MCF-7 cells by cell cycle analysis. Damnacanthal induced apoptosis, determined by Annexin V-fluorescein isothiocyanate/propidium iodide (PI) dual-labeling, acridine-orange/PI dyeing and caspase-7 expression. Furthermore, Damnacanthal-mediated apoptosis involves the sustained activation of p21, leading to the transcription of p53 and the Bax gene.
    CONCLUSIONS:
    Overall, the present study provided significant evidence demonstrating that p53-mediated Damnacanthal induced apoptosis through the activation of p21 and caspase-7.
    Mol Biol Cell. 2014 Mar;25(6):828-40.
    Damnacanthal, an effective inhibitor of LIM-kinase, inhibits cell migration and invasion.[Pubmed: 24478456]
    LIM-kinases (LIMKs) play crucial roles in various cell activities, including migration, division, and morphogenesis, by phosphorylating and inactivating cofilin.
    METHODS AND RESULTS:
    Using a bimolecular fluorescence complementation assay to detect the actin-cofilin interaction, we screened LIMK1 inhibitors and identified two effective inhibitors, Damnacanthal (Dam) and MO-26 (a pyrazolopyrimidine derivative). These compounds have already been shown to inhibit Lck, a Src family tyrosine kinase. However, in vitro kinase assays revealed that Dam inhibited LIMK1 more effectively than Lck. Dam suppressed LIMK1-induced cofilin phosphorylation and deceleration of actin retrograde flow in lamellipodia in N1E-115 cells. Dam impaired CXCL12-induced chemotactic migration of Jurkat T lymphocytes and Jurkat-derived, Lck-deficient JCaM1.6 cells and also inhibited serum-induced migration and invasion of MDA-MB-231 breast carcinoma cells.
    CONCLUSIONS:
    These results suggest that Dam has the potential to suppress cell migration and invasion primarily through the inhibition of LIMK kinase activity. Topical application of Dam also suppressed hapten-induced migration of epidermal Langerhans cells in mouse ears. Dam provides a useful tool for investigating cellular and physiological functions of LIMKs and holds promise for the development of agents against LIMK-related diseases. The bimolecular fluorescence complementation assay system used in this study will provide a useful method to screen for inhibitors of various protein kinases.
    Eur J Pharmacol. 2011 Jan 10;650(1):120-9.
    Activation of p38 MAPK by damnacanthal mediates apoptosis in SKHep 1 cells through the DR5/TRAIL and TNFR1/TNF-α and p53 pathways.[Pubmed: 20951126 ]
    The effect of the natural compound Damnacanthal from Morinda citrifolia on SKHep 1 cell growth regulation was investigated.
    METHODS AND RESULTS:
    Treatment of SKHep 1 cells with Damnacanthal for 24h indicated a dose-dependent antiproliferative activity. Damnacanthal seems to be selective for tumor cell lines, since there is only minimal toxicity against normal hepatocyte cells (FL83B). This is first demonstration that Damnacanthal-mediated apoptosis involves the sustained activation of the p38 MAPK pathway, leading to the transcription of the death receptor family genes encoding DR5/TRAIL and TNF-R1/TNF-α genes as well as the p53-regulated Bax gene. The Damnacanthal-mediated expression of DR5/TRAIL and TNF-R1/TNF-α results in caspase 8 activation, leading to Bid cleavage. In turn, activated Bid, acting with p53-regulated Bax, leads to cytochrome c released from mitochondria into the cytoplasm. Combined activation of the death receptors and mitochondrial pathways results in activation of the downstream effecter caspase 3, leading to cleavage of PARP. TRAIL- and TNF-α-mediated Damnacanthal-induced apoptosis could be suppressed by treatment with caspase inhibitors as well as soluble death receptors Fc:DR5 and Fc:TNF-R1 chimera.
    CONCLUSIONS:
    Taken together, this study provided first evidence demonstrating that TRAIL-, TNF-α-, and p53-mediated Damnacanthal-induced apoptosis require the activation of p38 MAPK and mitochondrion-mediated caspase-dependent pathways.
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