Discontinued Product

Silibinin (Cat. No. 0637) has been withdrawn from sale for commercial reasons.
Description: Induces G1 arrest
Chemical Name: [2R-[2a,3b,6(2R*,3R*)]]-2-[2,3-Dihydro-3-(4-hydroxy-3-methoxyphenyl)-2-(hydroxymethyl)-1,4-benzodioxin-6-yl]-2,3-dihydro-3,5,7-trihydroxy-4H-1-benzopyran-4-one
Literature (2)

Biological Activity for Silibinin

The active principle from Silybum marianum. Used for treatment of liver damage.

Technical Data for Silibinin

M. Wt 482.44
Storage Store at RT
CAS Number 22888-70-6

The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.

Tocris products are intended for laboratory research use only, unless stated otherwise.

Product Datasheets for Silibinin

Certificate of Analysis is currently unavailable on-line.
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References for Silibinin

References are publications that support the biological activity of the product.

Sonnenbichler et al (1986) Stimulatory effect of silbinin on the DNA synthesis in partially hepatectomized rat livers: non-response in hematoma and other malign cell lines. Biochem.Pharmacol. 35 538 PMID: 3004503

Sonnenbichler et al (1999) Stimulatory effects of silibinin and silicristin from the milk thistle silybum marianum on kidney cells. J.Pharmacol.Exp.Ther. 290 1375 PMID: 10454517

Zi and Agarwal (1999) Silibinin decreases prostate-specific antigen with cell growth inhibition via G1 arrest, leading to differentiation of prostate carcinoma cells: implication for prostate cancer intervention. Proc.Natl.Acad.Sci.U.S.A. 96 7490 PMID: 10377442

Martindale 29th Ed. 1613

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Keywords: Silibinin, Silibinin supplier, Cell, Cycle, Inhibitors, 0637, Tocris Bioscience

Citations for Silibinin

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Literature in this Area

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Cell Cycle and DNA Damage Research Product Guide

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In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. This poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.