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    Calycosin
    Information
    CAS No. 20575-57-9 Price $100 / 20mg
    Catalog No.CFN99140Purity>=98%
    Molecular Weight284.26Type of CompoundFlavonoids
    FormulaC16H12O5Physical DescriptionYellow powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Calycosin, a selective estrogen receptor modulator, is also a vasorelaxant and a noncompetitive Ca(2+) channel blocker. It has anti-oxidative, anti-inflammatory, hepatoprotective,antineoplastic, and effective skin-lightening activities. Calycosin exhibited tyrosinase inhibitory activity with an IC(50) value of 38.4 microM, it suppressed breast cancer cell growth via ERβ-dependent regulation of IGF-1R, p38 MAPK and PI3K/Akt pathways.
    Targets: Bcl-2/Bax | Caspase | Akt | FXR | STAT | p38MAPK | ERK | JNK | PI3K | IGF-1R | Calcium Channel
    In vitro:
    Cell Physiol Biochem. 2015;35(2):722-8.
    Calycosin and Genistein Induce Apoptosis by Inactivation of HOTAIR/p-Akt Signaling Pathway in Human Breast Cancer MCF-7 Cells.[Pubmed: 25613518]
    Calycosin and genistein are the two main components of isoflavones. Previously, we reported that these compounds display antitumor activities in the breast cancer cell lines MCF-7 and T47D. In the present study, we investigated the mechanism of action of Calycosin and genistein, and their respective efficacies as potential therapies for the treatment of breast carcinoma in the clinic.
    METHODS AND RESULTS:
    MCF-7 cells were treated with Calycosin or genistein. Cell proliferation and apoptosis were measured using CCK8 assay and Hoechst 33258. The expression level of phosphorylated Akt protein was determined by western blotting. Expression level of HOTAIR was quantified by real-time PCR. Both Calycosin and genistein inhibited proliferation and induced apoptosis in MCF-7 breast cancer cells, especially after treatment with Calycosin. Treatment of MCF-7 cells with Calycosin or genistein resulted in decreased phosphorylation of Akt, and decreased expression of its downstream target, HOTAIR.
    CONCLUSIONS:
    Calycosin is more effective in inhibiting breast cancer growth in comparison with genistein, through its regulation of Akt signaling pathways and HOTAIR expression.
    PLoS One. 2014 Mar 11;9(3):e91245.
    Calycosin suppresses breast cancer cell growth via ERβ-dependent regulation of IGF-1R, p38 MAPK and PI3K/Akt pathways.[Pubmed: 24618835]
    We previously reported that Calycosin, a natural phytoestrogen structurally similar to estrogen, successfully triggered apoptosis of estrogen receptor (ER)-positive breast cancer cell line, MCF-7.
    METHODS AND RESULTS:
    To better understand the antitumor activities of Calycosin against breast cancer, besides MCF-7 cells, another ER-positive cell line T-47D was analyzed here, with ER-negative cell lines (MDA-231, MDA-435) as control. Notably, Calycosin led to inhibited cell proliferation and apoptosis only in ER-positive cells, particularly in MCF-7 cells, whereas no such effect was observed in ER-negative cells. Then we investigated whether regulation of ERβ, a subtype of ER, contributed to Calycosin-induced apoptosis in breast cancer cells. The results showed that incubation of Calycosin resulted in enhanced expression ERβ in MCF-7 and T-47D cells, rather than MDA-231 and MDA-435 cells. Moreover, with the upregulation of ERβ, successive changes in downstream signaling pathways were found, including inactivation of insulin-like growth factor 1 receptor (IGF-1R), then stimulation of p38 MAPK and suppression of the serine/threonine kinase (Akt), and finally poly(ADP-ribose) polymerase 1 (PARP-1) cleavage. However, the other two members of the mitogen-activated protein kinase (MAPK) family, extracellular signal-regulated kinase (ERK) 1/2 and c-Jun N-terminal kinase (JNK), were not consequently regulated by downregulated IGF-1R, indicating ERK 1/2 and JNK pathways were not necessary to allow proliferation inhibition by Calycosin.
    CONCLUSIONS:
    Taken together, our results indicate that Calycosin tends to inhibit growth and induce apoptosis in ER-positive breast cancer cells, which is mediated by ERβ-induced inhibition of IGF-1R, along with the selective regulation of MAPK and phosphatidylinositol 3-kinase (PI3K)/Akt pathways.
    In vivo:
    J Neurol Sci. 2014 Apr 15;339(1-2):144-8.
    Downregulated RASD1 and upregulated miR-375 are involved in protective effects of calycosin on cerebral ischemia/reperfusion rats.[Pubmed: 24548484 ]
    Isoflavone Calycosin is a typical phytoestrogen extracted from Chinese medical herb Radix Astragali. It has been reported that estrogens could provide neuroprotective effects, and dietary intake of phytoestrogens could reduce stroke injury in cerebral ischemia/reperfusion (I/R) animal models.
    METHODS AND RESULTS:
    In the present study, we investigate the molecular mechanisms underlying the neuroprotective effects of Calycosin on middle cerebral artery occlusion (MCAO) rats. Focal cerebral ischemia was induced in male rats by MCAO, neurological deficits and brain edema was evaluated after 24h of reperfusion. The results shown Calycosin significantly reduced the infarcted volume and the brain water content, and improved the neurological deficit. To provide insight into the functions of estrogen receptor (ER)-mediated signaling pathway in neuroprotection by Calycosin, the expression of miR-375, ER-α, RASD1 (Dexamethasone-induced Ras-related protein 1) and Bcl-2 was determined by RT-PCR or western blot assay. Calycosin exhibited a downregulation of RASD1, and an upregulation of ER-α, miR-375 and Bcl-2.
    CONCLUSIONS:
    Our finding illustrated that Calycosin had been shown neuroprotective effects in cerebral ischemia/reperfusion rats, and the molecular mechanisms may correlate with the positive feedback between ER-α and miR-375, along with the regulation of downstream targets.
    Acta Pharmacol. Sin., 2006, 27(8):1007–12.
    Calcium channel blocking activity of calycosin, a major active component of Astragali Radix, on rat aorta.[Pubmed: 16867251]
    To investigate the vasoactivity of Calycosin, a major active component of Astragali Radix.
    METHODS AND RESULTS:
    Experiments were performed on isolated rat thoracic aortic rings pre-contracted with phenylephrine (PHE) or KCl. Calycosin produced a concentration-dependent relaxation on the tissue pre-contracted using PHE with 4.46+/-0.13 of pD(2) and 95.85%+/-2.67% of E(max); or using KCl with 4.27+/-0.05 of pD2 and 99.06%+/-2.15% of Emax, and displaced downwards the concentration-response curves of aortic rings to PHE or KCl. The relaxant effect of Calycosin on denuded endothelium aortic rings was the same as on intact endothelium aortic rings, and its vasorelaxant effect was not influenced by L-NAME or indomethacin. In Ca(2+)-free solution, Calycosin (30 micromol/L) did not have an effect on PHE (1 micromol/L)-induced aortic ring contraction. The effects of Calycosin and nifedipine where somewhat different; Calycosin decreased aortic ring contractions induced by the two agonists, but nifedipine displayed a more potent inhibitory effect on KCl-induced contractions than on PHE-induced contractions, and the vascular relaxing effects of Calycosin and nifidipine were additive on PHE-induced contraction but not KCl-induced.
    CONCLUSIONS:
    Calycosin is a vasorelaxant. Its action is endothelium-independent and is unrelated to intracellular Ca(2+) release. It is a noncompetitive Ca(2+) channel blocker. The effect of Calycosin on Ca(2+) channel blockade may be different from that of dihydropyridines. This study demonstrated a novel pharmacological activity of Calycosin, and supplied a theoretic foundation for Astragali Radix application.
    Calycosin Description
    Source: The herbs of Astragalus membranaceus Bge. var. mongholicus.
    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 3.5179 mL 17.5895 mL 35.1791 mL 70.3581 mL 87.9477 mL
    5 mM 0.7036 mL 3.5179 mL 7.0358 mL 14.0716 mL 17.5895 mL
    10 mM 0.3518 mL 1.759 mL 3.5179 mL 7.0358 mL 8.7948 mL
    50 mM 0.0704 mL 0.3518 mL 0.7036 mL 1.4072 mL 1.759 mL
    100 mM 0.0352 mL 0.1759 mL 0.3518 mL 0.7036 mL 0.8795 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.
    Protocol
    Cell Research:
    Tumour Biol. 2015 Feb 12.
    Calycosin induces apoptosis in human ovarian cancer SKOV3 cells by activating caspases and Bcl-2 family proteins.[Pubmed: 25672608]
    Calycosin is widely used as a natural active compound for its anti-oxidative and anti-inflammation activity. Recently, several studies have shown that Calycosin can inhibit growth and induce apoptosis in human cancer cell lines; however, the mechanisms are not completely clarified yet.
    METHODS AND RESULTS:
    In this study, we investigated the effects of Calycosin on human ovarian carcinoma SKOV3 cells, as well as the mechanisms. SKOV3 cells were treated with Calycosin at a series of concentrations for different times. In vitro, the MTT assay showed that Calycosin had obvious anti-proliferation effects on SKOV3 cells in a dose- and time-dependent manner. Cell morphological changes which expressed by Hoechst 33258 staining were compared with apoptotic changes detected by fluorescence microscope. Compared with control group, the group treated with Calycosin showed a significant increase in apoptosis rate. Expression of apoptosis related Bax/Bcl-2 and caspases proteins were detected by Western blotting. The results demonstrated that Calycosin up-regulated the Bax/Bcl-2 ratio and cleaved caspase-3, cleaved caspase-9 expression in a dose-dependent manner.
    CONCLUSIONS:
    In summary, Calycosin might exert anti-growth and induce-apoptosis activity against ovarian cancer SKOV3 cells through activating caspases and Bcl-2 family proteins, therefore presenting as a promising therapeutic agent for the treatment of ovarian cancer.
    Animal Research:
    Pharm Res. 2015 Feb;32(2):538-48.
    Protective effects of calycosin against CCl4-induced liver injury with activation of FXR and STAT3 in mice.[Pubmed: 25143196]
    Investigating the hepatoprotective effect of Calycosin against acute liver injury in association with FXR activation and STAT3 phosphorylation.
    METHODS AND RESULTS:
    The acute liver injury model was established by intraperitoneal injection of CCl4 in C57BL/6 mice. Serum alanine aminotransferase, aspartate aminotransferase, HE staining and TUNEL assay were used to identify the amelioration of the liver histopathological changes and hepatocytes apoptosis after Calycosin treatment. ELISA kit and 5-bromo-2-deoxyuridine immunohistochemistry were used to measure the liver bile acid concentration and hepatocyte mitotic rate in vivo. The relation between Calycosin and activation of FXR and STAT3 was comfirmed using the Luciferase assay, Molecular docking, Real-time PCR and Western Blot in vitro. The liver histopathological changes, hepatocytes apoptosis, liver bile acid overload and hepatocyte mitosis showed significant changes after Calycosin treatment. Calycosin promoted the expression of FXR target genes such as FoxM1B and SHP but the effect was reversed by FXR suppressor guggulsterone. Molecular docking results indicated that Calycosin could be embedded into the binding pocket of FXR, thereby increasing the expressions of STAT3 tyrosine phosphorylation and its target genes, Bcl-xl and SOCS3.
    CONCLUSIONS:
    Calycosin plays a critical role in hepatoprotection against liver injury in association with FXR activation and STAT3 phosphorylation.