Cyanidin Chloride

Cyanidin Chloride
Product Name Cyanidin Chloride
CAS No.: 528-58-5
Catalog No.: CFN99741
Molecular Formula: C15H11O6Cl
Molecular Weight: 322.70 g/mol
Purity: >=98%
Type of Compound: Flavonoids
Physical Desc.: Powder
Targets: HbA1c glycation | LXR-β | NFATc1 | c-Fos | Mitf
Source: The peels of Glycinemax (L.) merr
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Price: $198/20mg
Cyanidin Chloride, the main phenolic antioxidant in the grape (Vitis vinifera), in particular in the liposomal forms, could be used for treatment of diabetes mellitus complications. It has a dual effect on RANKL-induced osteoclastogenesis, exhibits therapeutic potential in prevention of osteoclasts related bone disorders.
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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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    Biochem Pharmacol. 1996 Oct 11;52(7):1033-9.
    Inhibition of lipid peroxidation and the active oxygen radical scavenging effect of anthocyanin pigments isolated from Phaseolus vulgaris L.[Pubmed: 8831722]

    METHODS AND RESULTS:
    No attention has been paid to anthocyanin pigments from the viewpoint of inhibitors of lipid peroxidation and scavengers of active oxygen radicals; therefore, we investigated the antioxidative, radical scavenging, and inhibitory effects on lipid peroxidation by UV light irradiation of three anthocyanin pigments, pelargonidin 3-O-beta-D-glucoside (P3G), cyanidin 3-O-beta-D-glucoside (C3G), and delphinidin 3-O-beta-D-glucoside (D3G), isolated from the Phaseolus vulgaris L. seed coat, and their aglycons, pelargonidin chloride (Pel), Cyanidin Chloride (Cy), and delphinidin chloride (Del).
    CONCLUSIONS:
    All pigments had strong antioxidative activity in a liposomal system and reduced the formation of malondialdehyde by UVB irradiation. On the other hand, the extent of antioxidative activity in a rat liver microsomal system and the scavenging effect of hydroxyl radicals (-OH) and superoxide anion radicals (O2-) were influenced by their own structures.
    J Cell Physiol . 2018 Mar;233(3):2502-2512.
    Cyanidin Chloride inhibits ovariectomy-induced osteoporosis by suppressing RANKL-mediated osteoclastogenesis and associated signaling pathways[Pubmed: 28771720]
    Abstract Over-production and activation of osteoclasts is a common feature of osteolytic conditions such as osteoporosis, tumor-associated osteolysis, and inflammatory bone erosion. Cyanidin Chloride, a subclass of anthocyanin, displays antioxidant and anti-carcinogenesis properties, but its role in osteoclastic bone resorption and osteoporosis is not well understood. In this study, we showed that Cyanidin Chloride inhibits osteoclast formation, hydroxyapatite resorption, and receptor activator of NF-κB ligand (RANKL)-induced osteoclast marker gene expression; including ctr, ctsk, and trap. Further investigation revealed that Cyanidin Chloride inhibits RANKL-induced NF-κB activation, suppresses the degradation of IκB-α and attenuates the phosphorylation of extracellular signal-regulated kinases (ERK). In addition, Cyanidin Chloride abrogated RANKL-induced calcium oscillations, the activation of nuclear factor of activated T cells calcineurin-dependent 1 (NFATc1), and the expression of c-Fos. Further, we showed that Cyanidin Chloride protects against ovariectomy-induced bone loss in vivo. Together our findings suggest that Cyanidin Chloride is capable of inhibiting osteoclast formation, hydroxyapatite resorption and RANKL-induced signal pathways in vitro and OVX-induced bone loss in vivo, and thus might have therapeutic potential for osteolytic diseases. Keywords: Cyanidin Chloride; RANKL; bone resorption; osteoclast; osteolysis.
    Planta Med. 2013 Nov;79(17):1599-604.
    Treatment of diabetes in the mouse model by delphinidin and cyanidin hydrochloride in free and liposomal forms.[Pubmed: 24108435]
    Cyanidin Chloride and delphinidin are the main phenolic antioxidants in the grape (Vitis vinifera). The aim of this study was to investigate the in vitro and in vivo inhibitory effects of delphinidin and Cyanidin Chloride in the free and liposomal forms on the albumin glycation reaction.
    METHODS AND RESULTS:
    Delphinidin and Cyanidin Chlorides were encapsulated in the liposomes using an extrusion method. The rate of albumin glycation was evaluated using the ELISA method. Finally, in vivo anti-glycation of delphinidin and Cyanidin Chloride in the free and liposomal forms in diabetic mice was investigated. The encapsulation efficacies of delphinidin and Cyanidin Chloride in the liposomes were 89.05 % ± 0.18 and 85.00 % ± 0.15, respectively. In vitro treatment with 100 mg/mL delphinidin and Cyanidin Chloride in free forms could reduce the rate of albumin glycation to 30.50 ± 3.46 and 46.00 ± 2.50 %, respectively. Under identical conditions, the delphinidin and Cyanidin Chloride-loaded liposomes could reduce the rate of albumin glycation to 8.50 ± 2.10 and 14.60 ± 3.60 %, respectively. In vivo testing showed that anti-glycation activity of delphinidin and cyanidin in loaded forms was higher than in free forms. The daily administration of 100 mg/kg delphinidin chloride-loaded liposomes to diabetic mice at eight weeks could decrease the rate of albumin and HbA1c glycation to 46.35 ± 1.20 and 3.60 ± 0.25 %, respectively. Moreover, under identical conditions, the loaded liposomes with Cyanidin Chloride could decrease the rate of albumin and HbA1c glycation to 55.56 ± 1.32 and 4.95 ± 0.20 %, respectively.
    CONCLUSIONS:
    The findings showed that delphinidin and Cyanidin Chloride, in particular in the liposomal forms, could be used for treatment of diabetes mellitus complications.
    J Cell Physiol. 2014 Dec 24.
    Dual Effect of Cyanidin on RANKL-Induced Differentiation and Fusion of Osteoclasts.[Pubmed: 25545964]
    Bone homeostasis is maintained by the balance between osteoblastic bone formation and osteoclastic bone resorption. Osteoclasts are multinucleated cells derived from hematopoietic stem cells (HSCs) or monocyte/macrophage progenitor cells and formed by osteoclasts precursors (OCPs) fusion. Cyanidin Chloride is an anthocyanin widely distributed in food diet with novel antioxidant activity. However, the effect of Cyanidin Chloride on osteoclasts is still unknown.
    METHODS AND RESULTS:
    We investigated the effect of Cyanidin Chloride on RANKL-induced osteoclasts differentiation and cell fusion. The results showed that Cyanidin Chloride had a dual effect on RANKL-induced osteoclastogenesis. Lower dosage of cyanidin (< 1μg/ml) has a promoting effect on osteoclastogenesis while higher dosage of Cyanidin Chloride (> 10μg/ml) has an inhibitory effect. Fusogenic genes like CD9, ATP6v0d2, DC-STAMP, OC-STAMP and osteoclasts related genes like NFATc1, mitf and c-fos were all regulated by Cyanidin Chloride consistent to its dual effect. Further exploration showed that low concentration of Cyanidin Chloride could increase osteoclasts fusion whereas higher dosage of cyanidin lead to the increase of LXR-β expression and activation which is suppressive to osteoclasts differentiaton.
    CONCLUSIONS:
    All these results showed that Cyanidin Chloride exhibits therapeutic potential in prevention of osteoclasts related bone disorders.
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