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    Procyanidin C1
    Information
    CAS No. 37064-30-5 Price $418 / 5mg
    Catalog No.CFN99560Purity>=98%
    Molecular Weight866.77Type of CompoundFlavonoids
    FormulaC45H38O18Physical DescriptionPowder
    Download Manual    COA    MSDS    SDFSimilar structuralComparison (Web)
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    Procyanidin C1 Description
    Source: The fruits of Vitis vinifera L.
    Biological Activity or Inhibitors: 1. In vitro, Procyanidin C1 (PC1) can dose-dependently decrease Fc epsilon RI-mediated degranulation and cytokine production of mast cells, inhibit tyrosine phosphorylation of Syk and linker for activation of T cells, and the ROS generation in stimulated mast cells.
    2. Procyanidin C1-induced vasorelaxation is associated with the activation of the calcium-dependent NO/cGMP pathway, involving potassium channel activation, thus, it may represent a novel and potentially therapeutically relevant compound for the treatment of cardiovascular diseases.
    3. Procyanidin C1 is the main active compound in the CC extract responsible for EMT inhibition and that procyanidin C1 could be useful as a lead compound to develop inhibitors of cancer metastasis and other diseases related to EMT.
    4. Procyanidin C1 has anti-inflammatory effects, can inhibit IKKb activity in vitro and reduce the LPS-induced production of ROS, thus, it exerts the anti-inflammatory effects by inhibiting ERK1/2 and IKKb activity.
    Solvent: Pyridine, Methanol, Ethanol, 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.
    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.1537 mL 5.7685 mL 11.5371 mL 23.0742 mL 28.8427 mL
    5 mM 0.2307 mL 1.1537 mL 2.3074 mL 4.6148 mL 5.7685 mL
    10 mM 0.1154 mL 0.5769 mL 1.1537 mL 2.3074 mL 2.8843 mL
    50 mM 0.0231 mL 0.1154 mL 0.2307 mL 0.4615 mL 0.5769 mL
    100 mM 0.0115 mL 0.0577 mL 0.1154 mL 0.2307 mL 0.2884 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.
    Procyanidin C1 References Information
    Citation [1]

    J Med Food. 2014 Jul;17(7):742-8.

    Procyanidin C1 causes vasorelaxation through activation of the endothelial NO/cGMP pathway in thoracic aortic rings.[Pubmed: 24971771 ]
    The aim of this study was to clarify the efficacy of Procyanidin C1 (Pro C1) for modulating vascular tone. Procyanidin C1 induced a potent vasorelaxant effect on phenylephrine-constricted endothelium-intact thoracic aortic rings, but had no effect on denuded thoracic aortic rings. Moreover, Procyanidin C1 caused a significant increase in nitric oxide (NO) production in endothelial cells. Procyanidin C1-induced vasorelaxation and Procyanidin C1-induced NO production were significantly decreased in the presence of a nonspecific potassium channel blocker (tetraethylammonium chloride [TEA]), an endothelial NO synthase inhibitor (N(G)-monomethyl-L-arginine [L-NMMA]), and a store-operated calcium entry inhibitor (2-aminoethyl diphenylborinate [2-APB]). Procyanidin C1-induced vasorelaxation was also completely abolished by an inhibitor of soluble guanyl cyclase, which suggests that the Procyanidin C1 effects observed involved cyclic guanosine monophosphate (cGMP) production. Interestingly, Procyanidin C1 significantly enhanced basal cGMP levels. Taken together, these results indicate that Procyanidin C1-induced vasorelaxation is associated with the activation of the calcium-dependent NO/cGMP pathway, involving potassium channel activation. Thus, Procyanidin C1 may represent a novel and potentially therapeutically relevant compound for the treatment of cardiovascular diseases.
    Citation [2]

    Int J Oncol. 2013 Dec;43(6):1901-6.

    Procyanidin C1 from Cinnamomi Cortex inhibits TGF-β-induced epithelial-to-mesenchymal transition in the A549 lung cancer cell line.[Pubmed: 24141365]
    Cancer metastasis is one of the most critical events in cancer patients, and the median overall survival of stage IIIb or IV patients with metastatic lung cancer in the TNM classification is only 8 or 5 months, respectively. We previously demonstrated that Juzentaihoto, a Japanese traditional medicine, can inhibit cancer metastasis through the activation of macrophages and T cells in mouse cancer metastatic models; however, the mechanism(s) through which Juzentaihoto directly affects tumor cells during the metastasis process and which herbal components from Juzentaihoto inhibit the metastatic potential have not been elucidated. In this study, we focused on the epithelial-to-mesenchymal transition (EMT), which plays an important role in the formation of cancer metastasis. We newly determined that only the Cinnamomi Cortex (CC) extract, one of 10 herbal components of Juzentaihoto, inhibits TGF-β-induced EMT. Moreover, the contents of catechin trimer in CC extracts were significantly correlated with the efficacy of inhibiting TGF-β-induced EMT. Finally, the structure of the catechin trimer from CC extract was chemically identified as Procyanidin C1 and the compound showed inhibitory activity against TGF-β-induced EMT. This illustrates that Procyanidin C1 is the main active compound in the CC extract responsible for EMT inhibition and that Procyanidin C1 could be useful as a lead compound to develop inhibitors of cancer metastasis and other diseases related to EMT.
    Citation [3]

    Int Arch Allergy Immunol. 2008;147(3):213-21.

    Procyanidin C1 from apple extracts inhibits Fc epsilon RI-mediated mast cell activation.[Pubmed: 18594151]
    BACKGROUND: Polyphenol-enriched fractions, which are extracted from unripe apples (Rosaceae, Malus spp.), consisting of procyanidins (polymers of catechins) are known to have an anti-allergenic effect on patients with various allergic diseases. Although it has been reported that apple extracts inhibit histamine release from mast cells, the molecular mechanisms for this anti-allergenic effect are not well understood. To elucidate the molecular mechanisms by which apple extracts induce their anti-allergenic effects, the effects of purified apple extract components on high-affinity receptors for IgE (Fc epsilon RI)-mediated mast cell activation were investigated. METHODS: The anti-allergic effect of oral administration of apple procyanidin extracts on passive cutaneous anaphylactic responses of BALB/c mice was assessed. We evaluated the effects of Procyanidin C1 (PC1) [epicatechin-(4beta-->8)-epicatechin-(4beta-->8)-epicatechin], a component of the procyanidin fraction, on mouse bone-marrow-derived mast cell degranulation, cytokine production, protein tyrosine phosphorylation and on the generation of intracellular reactive oxygen species (ROS) of cells stimulated by Fc epsilon RI cross-linking in vitro. RESULTS: In an in vivo study, oral administration of the procyanidin fraction suppressed the mast-cell-dependent allergic reaction. In in vitro studies, Procyanidin C1 dose-dependently decreased Fc epsilon RI-mediated degranulation and cytokine production of mast cells. Furthermore, Procyanidin C1 inhibited tyrosine phosphorylation of Syk and linker for activation of T cells, and the ROS generation in stimulated mast cells. CONCLUSIONS: Procyanidin C1 suppresses Fc epsilon RI-mediated mast cell activation by inhibiting intracellular signaling pathways. These observations provide evidence for the anti-allergenic effects of the procyanidin-enriched apple extract.
    Citation [4]

    Evid Based Complement Alternat Med. 2014;2014:365258.

    Immunosuppressive Effects of A-Type Procyanidin Oligomers from Cinnamomum tamala.[Pubmed: 25530780]
    Cinnamon barks extracts have been reported to regulate immune function; however, the component(s) in cinnamon barks responsible for this effect is/are not yet clear. The aim of this study is to find out the possible component(s) that can be used as therapeutic agents for immune-related diseases from cinnamon bark. In this study, the immunosuppressive effects of fraction (named CT-F) and five procyanidin oligomers compounds, cinnamtannin B1, cinnamtannin D1 (CTD-1), parameritannin A1, procyanidin B2, and Procyanidin C1, from Cinnamomum tamala or Cinnamomum cassia bark were examined on splenocytes proliferation model induced by ConA or LPS. Then, the effects of activated compound CTD-1 on cytokine production and 2,4-dinitrofluorobenzene (DNFB) induced delayed-type hypersensitivity (DTH) response were detected to evaluate the immunosuppressive activity of CTD-1. It was found that CT-F and CTD-1 significantly inhibited the splenocyte proliferation induced by ConA or LPS. CTD-1 dose-dependently reduced the level of IFN-γ and IL-2 and intensively suppressed DNFB-induced DTH responses. These findings suggest that the immunosuppressive activities of cinnamon bark are in part due to procyanidin oligomers. CTD-1 may be a potential therapeutic agent for immune-related diseases.