Sennidin B

Sennidin B
Product Name Sennidin B
CAS No.: 517-44-2
Catalog No.: CFN99598
Molecular Formula: C30H18O10
Molecular Weight: 538.46 g/mol
Purity: >=98%
Type of Compound: Anthraquinones
Physical Desc.: Yellow powder
Targets: Akt | GLUT | PI3K
Source: The leaves of Cassia angustifolia.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Sennidin B stimulates glucose incorporation in rat adipocytes.
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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:

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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    Appl Environ Microbiol. 1994 Mar;60(3):1041-3.
    Isolation of a human intestinal anaerobe, Bifidobacterium sp. strain SEN, capable of hydrolyzing sennosides to sennidins.[Pubmed: 8161172]
    A strictly anaerobic bacterium capable of metabolizing sennosides was isolated from human feces and identified as Bifidobacterium sp., named strain SEN.
    The bacterium hydrolyzed sennosides A and Sennidin B to sennidin A and Sennidin B via sennidin A and Sennidin B 8-monoglucosides, respectively. Among nine species of Bifidobacterium having beta-glucosidase activity, only Bifidobacterium dentium and B. adolescentis metabolized sennoside B to Sennidin B, suggesting that the sennoside-metabolizing bacteria produce a novel type of beta-glucosidase capable of hydrolyzing sennosides to sennidins.
    Phytomedicine. 2008 May;15(5):373-7.
    Transport of sennosides and sennidines from Cassia angustifolia and Cassia senna across Caco-2 monolayers--an in vitro model for intestinal absorption.[Pubmed: 17481875]
    Laxative effects of Senna preparations are mainly mediated by rheinanthrone, a metabolite formed in the intestinal flora from dianthrones. Nevertheless, it was not clear whether dianthrones are bioavailable at all and contribute to the overall effects of this important medicinal plant.
    Using the Caco-2 human colonic cell line as an in vitro model of the human intestinal mucosal barrier, the bioavailability of dianthrones was studied in apical to basolateral (absorptive) and basolateral to apical (secretive) direction. Permeability coefficients (P(c)) and percent transport were calculated based on quantitations by HPLC. From the data obtained it was concluded that sennoside A and sennoside B, as well as their aglycones sennidin A and Sennidin B are transported through the Caco-2 monolayers in a concentration-dependent manner and their transport was linear with time. The absorption in apical to basolateral direction was poor and P(c) values were comparable to mannitol. The transport was higher in the secretory direction, indicating a significant efflux (e.g. by efflux pumps) of the (poorly) absorbed compounds in the intestinal lumen again.
    Our findings support the general understanding that the laxative effects of Senna are explainable mainly by metabolites and not by the natively present dianthrones.
    Life Sci. 2006 Aug 8;79(11):1027-33.
    Sennidin stimulates glucose incorporation in rat adipocytes.[Pubmed: 16603199]
    A novel small molecule compound which exerts insulin mimetic is desirable.
    Dozens of natural products that have quinone, naphthoquinone, or anthraquinone structure, were tested by a glucose incorporation assay. We found that sennidin A, anthraquinone derivative, stimulated glucose incorporation to near level of maximal insulin-stimulated and Sennidin B, a stereoisomer of sennidin A, also stimulated, but the activity of Sennidin B was lower than sennidin A. Sennidin A-stimulated glucose incorporation was completely inhibited by wortmannin. Sennidin A did not induce tyrosine phosphorylation of insulin receptor (IR) and insulin receptor substrate-1 (IRS-1), but induced phosphorylation of Akt and glucose transporter 4 (GLUT4) translocation.
    Our results suggest that in rat adipocytes, sennidin A stimulates glucose incorporation in the phosphatidylinositol 3-kinase (PI3K)- and Akt-dependent, but in the IR/IRS1-independent manner.
    Pharmacology. 1988;36 Suppl 1:129-37.
    Instability of rhein-9-anthrone as a problem in pharmacological and analytical use.[Pubmed: 3368511]
    The stability of rhein-9-anthrone, one of the main and most active metabolites of the sennoside A +sennoside B, was studied under physiological conditions.
    A high-pressure liquid chromatographic method for the determination of rhein-9-anthrone and its oxidation products, rhein and sennidin A + Sennidin B, was developed. Rhein-9-anthrone, dissolved in Tyrode buffer at pH 6.5 or 7.5 at a concentration of 10(-4) mol/l, completely disappeared from a solution warmed to 37 degrees C within 30 min. More than 90% were transformed into rhein and sennidin A +Sennidin B. Pharmacological experiments in rats showed that net water absorption in the small intestine was reversed to net secretion by rhein-9-anthrone, whereas rhein and sennidins in corresponding concentrations were ineffective.
    As at least rhein is known to stimulate secretion under different experimental conditions, all pharmacological results with rhein-9-anthrone must be interpreted with caution and should be checked whether they essentially differ from those of its main oxidation products.
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