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||The heartwood of Caesalpinia sappan Linn
|1. 3-Deoxysappanchalcone is an effective HO-1 inducer at the translational level.
2. 3-Deoxysappanchalcone has anti-inflammatory effects, is a valuable compound for modulating inflammatory conditions.
3. 3-Deoxysappanchalcone has anti-influenza virus activity, the mechanism involved anti-apoptosis and anti-inflammation activities in vitro.
4. 3-Deoxysappanchalcone has inhibitory activity on MMP-9 expression and production in TNF-α-treated cells, is mediated by the suppression of AP-1 and NF-κB activation.
||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
||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).
Whenever 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.
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||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.
Calculate Dilution Ratios(Only for Reference)
* 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.
3-Deoxysappanchalcone References Information
Int Immunopharmacol. 2014 Oct;22(2):420-6.
|The anti-inflammatory effect of 3-deoxysappanchalcone is mediated by inducing heme oxygenase-1 via activating the AKT/mTOR pathway in murine macrophages.[Pubmed: 25091623]|
|3-Deoxysappanchalcone (3-DSC), isolated from Caesalpinia sappan (Leguminosae), is a chalcone that exerts a variety of pharmacological activities. In the present study, we demonstrated that 3-Deoxysappanchalcone exerts anti-inflammatory activity in murine macrophages by inducing heme oxygenase-1 (HO-1) expression at the translational level. Treatment of RAW264.7 cells with 3-Deoxysappanchalcone induced HO-1 protein expression in a dose- and time-dependent manner without affecting HO-1 mRNA expression. Mitogen-activated protein kinase inhibitors or actinomycin D, a transcriptional inhibitor, did not block 3-Deoxysappanchalcone-mediated HO-1 induction. However, 3-Deoxysappanchalcone-mediated HO-1 induction was completely blocked by treatment with cycloheximide, a translational inhibitor, or rapamycin, an inhibitor of the mammalian target of rapamycin (mTOR). Strikingly, 3-Deoxysappanchalcone increased the phosphorylation level of mTOR downstream target molecules such as eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) and S6 kinase 1 (S6K1), as well as AKT in a dose- and time-dependent manner, suggesting that the 3-Deoxysappanchalcone induces HO-1 expression by activating the AKT/mTOR pathway. Consistent with the notion that HO-1 has anti-inflammatory properties, 3-Deoxysappanchalcone inhibited the production of nitric oxide (NO) and interleukin (IL)-6 in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Inhibition of HO-1 activity by treatment with tin protoporphyrin IX, a specific HO-1 inhibitor, abrogated the inhibitory effects of 3-Deoxysappanchalcone on the production of NO and IL-6 in LPS-stimulated RAW264.7 cells. Taken together, 3-Deoxysappanchalcone may be an effective HO-1 inducer at the translational level that has anti-inflammatory effects, and a valuable compound for modulating inflammatory conditions.
Planta Med. 2012 Jun;78(10):968-73.
|The protective effect of 3-deoxysappanchalcone on in vitro influenza virus-induced apoptosis and inflammation.[Pubmed: 22648377]|
| We previously reported that 3-Deoxysappanchalcone (3-DSC), a compound that is isolated from Caesalpinia sappan, exhibited in vitro anti-influenza activity. In the present study, we further identified that 3-Deoxysappanchalcone inhibited viral genomic replication and transcription only at a relatively high concentration. We then evaluated the effect of 3-Deoxysappanchalcone on the regulation of virus-induced cellular apoptosis. 3-Deoxysappanchalcone ameliorated virus-induced DNA fragmentation in a concentration-dependent manner, which tends to be a consequence of its inhibition of upstream caspase activation. 3-Deoxysappanchalcone also protected host cells against influenza-induced inflammation by suppressing CCL5 and CXCL10 secretions in endothelial cells and reducing the production of IL-6 and IL-1β in monocytes/macrophages. In conclusion, our results demonstrate that anti-influenza virus mechanisms of 3-Deoxysappanchalcone involved anti-apoptosis and anti-inflammation activities in vitro. Moreover, 3-Deoxysappanchalcone could be a promising drug candidate for influenza treatment.
Biol Pharm Bull. 2011;34(6):890-3.
|3-Deoxysappanchalcone inhibits tumor necrosis factor-α-induced matrix metalloproteinase-9 expression in human keratinocytes through activated protein-1 inhibition and nuclear factor-kappa B DNA binding activity.[Pubmed: 21628889]|
|Tumor necrosis factor α (TNF-α), which is a primary cytokine responsible for inflammatory responses in skin, induces the synthesis of matrix metalloproteinase-9 (MMP-9), which causes skin aging. The protective effects of 3-Deoxysappanchalcone against TNF-α-induced damage was investigated using human skin keratinocytes. The results showed that 3-Deoxysappanchalcone inhibited MMP-9 expression at the protein and mRNA level, by blocking the activation of activator protein-1 (AP-1) and nuclear factor kappa B (NF-κB). Taken together, the inhibitory activity of 3-Deoxysappanchalcone on MMP-9 expression and production in TNF-α-treated cells was found to be mediated by the suppression of AP-1 and NF-κB activation.