Product Name Cimicifugoside
CAS No.: 66176-93-0
Catalog No.: CFN90481
Molecular Formula: C37H54O11
Molecular Weight: 674.81 g/mol
Purity: >=98%
Type of Compound: Triterpenoids
Physical Desc.: Powder
Targets: AChR | Potassium Channel
Source: The roots of Saposhnikovia divaricata
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Price: $218/20mg
Cimicifugoside is a novel specific nucleoside transport inhibitor that displays synergistic potentiation of methotrexate cytotoxicity. Cimicifugoside shows immunosuppressive activity, which is preferentially directed toward B-cell function with larger doses being required for suppression of T-cell function. Cimicifugoside is also a phytoestrogen, it can selectively inhibit nicotinic acetylcholine receptor (nAChR) -mediated response in bovine chromaffin cells.
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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.

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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.
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    Eur J Pharm Sci. 2009 Nov 5;38(4):355-61.
    Inhibition of nucleoside transport and synergistic potentiation of methotrexate cytotoxicity by cimicifugoside, a triterpenoid from Cimicifuga simplex.[Pubmed: 19748575]
    Cimicifugoside, a triterpenoid isolated from Cimicifuga simplex, which has been used as a traditional Chinese medicine due to its anti-inflammatory, analgesic or anti-pyretic action, was examined for inhibition of nucleoside transport and synergistic potentiation of methotrexate cytotoxicity.
    Cimicifugoside inhibited uptake of uridine, thymidine and adenosine in human leukemia U937 cells with the low nanomolar IC(50) values, but did not affect that of uracil, leucine or 2-deoxyglucose at Cimicifugoside analogs differentially inhibited uridine uptake in the order Cimicifugoside>cimicifugenin (aglycon of Cimicifugoside)>bugbanoside B>cimicifugenin A, O-methyl cimicifugenin and bugbanoside A. Cimicifugoside had less affinity for the binding site of nitrobenzylthioinosine (typical high-affinity inhibitor of equilibrative nucleoside transporter-1) in U937 cells, K562 cells and human erythrocyte membranes compared with the prototype nucleoside transport inhibitor dipyridamole. Cimicifugoside markedly potentiated methotrexate cytotoxicity in a culture of U937 cells and human carcinoma KB cells. Potentiation of methotrexate cytotoxicity by Cimicifugoside analogs in U937 cells was in proportion to their inhibitory activity against uridine uptake.
    The present study demonstrates that Cimicifugoside is a novel specific nucleoside transport inhibitor that displays synergistic potentiation of methotrexate cytotoxicity.
    Res Commun Chem Pathol Pharmacol. 1981 Jun;32(3):565-8.
    Differential cytotoxicity of cytosine arabinoside toward murine leukemia L1210 cells and murine bone marrow progenitor cells inhibited in nucleoside transport by cimicifugoside.[Pubmed: 6791252]

    Cytotoxicities of cytosine arabinoside (Ara C) and showdomycin to murine L1210 leukemia cells was prevented by a nucleoside transport inhibitor, Cimicifugoside. Ara C toxicity to bone marrow progenitor cells, however, was observed even in the presence of Cimicifugoside.
    The difference of Ara C toxicity toward L1210 cells and bone marrow cells pretreated with Cimicifugoside may be originated in the different characteristics of membrane transport site of nucleosides.
    J Pharmacobiodyn. 1980 Dec;3(12):643-8.
    The immune response of splenic lymphocytes after cimicifugoside treatment in vitro and pretreatment in vivo.[Pubmed: 7277179]

    Pretreatment of mouse splenocytes with Shigella lipopolysaccharide and concanavalin A followed by 50 ng/ml of Cimicifugoside resulted in a 69% and 31% inhibition of blastogenesis compared to controls. The plaque forming colony assay using sheep erythrocytes (SRBC) showed a decreased number of plaque forming colonies after exposure of the splenic cells to 1 microgram/ml of Cimicifugoside. Cimicifugoside, 0.1 mg/mouse i.p. suppressed the anti-SRBC response in the plaque forming assay. The major inhibition of the antibody response occurred when Cimicifugoside was administered 1 day before the primary immunization with SRBC. The delayed type hypersensitivity to picryl chloride was suppressed after i.v. administration of Cimicifugoside, 1.0-2.0 mg/mouse.
    The immunosuppressive activity of Cimicifugoside is preferentially directed toward B-cell function with larger doses being required for suppression of T-cell function.
    J Pharmacol Exp Ther. 2004 May;309(2):641-9.
    Phytoestrogen cimicifugoside-mediated inhibition of catecholamine secretion by blocking nicotinic acetylcholine receptor in bovine adrenal chromaffin cells.[Pubmed: 14757852 ]
    We investigated the effect of the phytoestrogen Cimicifugoside, one of the pharmacologically active ingredients of the medicinal plant Cimicifuga racemosa (black cohosh) that has been used to treat many kinds of neuronal and menopausal symptoms, such as arthritis, menopausal depression, and nerve pain.
    Cimicifugoside inhibited calcium increase induced by 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), a nicotinic acetylcholine receptor (nAChR) agonist in bovine adrenal chromaffin cells with a half-maximal inhibitory concentration (IC(50)) of 18 +/- 2 microM. In contrast, Cimicifugoside did not affect the calcium increases evoked by high K(+), veratridine, and bradykinin. The DMPP-induced sodium increase was also inhibited by Cimicifugoside with an IC(50) of 2 +/- 0.3 microM, suggesting that the activity of nAChRs is inhibited by Cimicifugoside. Cimicifugoside did not affect the KCl-induced secretion but markedly inhibited the DMPP-induced catecholamine secretion that was monitored by carbon-fiber amperometry in real time and high-performance liquid chromatography through electrochemical detection.
    The results suggest that Cimicifugoside selectively inhibits nAChR-mediated response in bovine chromaffin cells.

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