Sennidin A CAS NO.641-12-3

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General tips：For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
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Chemical Properties of Sennidin A

Source of Sennidin A

1 Rheum sp.

Biological Activity of Sennidin A

Preparing Stock Solutions of Sennidin A

References on Sennidin A

Necrosis targeted combinational theragnostic approach using radioiodinated Sennidin A in rodent tumor models.[Pubmed:24931286]

Oncotarget. 2014 May 30;5(10):2934-46.

Residual cancer cells and subsequent tumor relapse is an obstacle for curative cancer treatment. Tumor necrosis therapy (TNT) has recently been developed to cause residual tumor regression or destruction. Here, we exploited the avidity of the Sennidin A (SA) tracer and radioiodinated SA ((1)(3)(1)I-SA) to necrotic tumors in order to further empower TNT. We showed high uptake and prolonged retention of SA in necrotic tumors and a quick clearance in other non-targeted tissues including the liver. On SPECT-CT images, tumor mass appeared persistently as a hotspot. Based on the prominent targetability of (1)(3)(1)I-SA to the tumor necrosis, we designed a combinational theragnostic modality. The vascular disrupting agent (VDA) combretastatin A4 phosphate (CA4P) was used to cause massive tumor necrosis, which formed the target of (1)(3)(1)I-SA that subsequently killed the residual tumor cells by cross-fire irradiation of beta particles. Consequently, (1)(3)(1)I-SA combined with CA4P significantly inhibited tumor growth, extended tumor doubling time and prolonged mean animal survival. In conclusion, (1)(3)(1)I-SA in combination with necrosis inducing drugs/therapies may generate synergetic tumoricidal effects on solid malignancies by means of primary debulking and secondary cleansing process.

Sennidin stimulates glucose incorporation in rat adipocytes.[Pubmed:16603199]

Life Sci. 2006 Aug 8;79(11):1027-33.

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.

Isolation of a human intestinal anaerobe, Bifidobacterium sp. strain SEN, capable of hydrolyzing sennosides to sennidins.[Pubmed:8161172]

Appl Environ Microbiol. 1994 Mar;60(3):1041-3.

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 B to sennidins A and B via Sennidin A and 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.

Identification of Hydroxyanthraquinones as Novel Inhibitors of Hepatitis C Virus NS3 Helicase.[Pubmed:26262613]

Int J Mol Sci. 2015 Aug 7;16(8):18439-53.

Hepatitis C virus (HCV) is an important etiological agent of severe liver diseases, including cirrhosis and hepatocellular carcinoma. The HCV genome encodes nonstructural protein 3 (NS3) helicase, which is a potential anti-HCV drug target because its enzymatic activity is essential for viral replication. Some anthracyclines are known to be NS3 helicase inhibitors and have a hydroxyanthraquinone moiety in their structures; mitoxantrone, a hydroxyanthraquinone analogue, is also known to inhibit NS3 helicase. Therefore, we hypothesized that the hydroxyanthraquinone moiety alone could also inhibit NS3 helicase. Here, we performed a structure-activity relationship study on a series of hydroxyanthraquinones by using a fluorescence-based helicase assay. Hydroxyanthraquinones inhibited NS3 helicase with IC50 values in the micromolar range. The inhibitory activity varied depending on the number and position of the phenolic hydroxyl groups, and among different hydroxyanthraquinones examined, 1,4,5,8-tetrahydroxyanthraquinone strongly inhibited NS3 helicase with an IC50 value of 6 microM. Furthermore, hypericin and Sennidin A, which both have two hydroxyanthraquinone-like moieties, were found to exert even stronger inhibition with IC50 values of 3 and 0.8 microM, respectively. These results indicate that the hydroxyanthraquinone moiety can inhibit NS3 helicase and suggest that several key chemical structures are important for the inhibition.

Description

Sennidin A, isolated from the leaves of Cassia angustifolia, inhibits HCV NS3 helicase, with an IC50 of 0.8 μM. Sennidin A induces phosphorylation of Akt and glucose transporter 4 (GLUT4) translocation. Sennidin A stimulates the glucose incorporation.

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