| Description | Isosilybin B is a flavonolignan extracted from silymarin that exhibits anti-prostate cancer (PCA) activity, inhibits cancer cell proliferation, and contributes to G1-phase blockade and apoptosis.Isosilybin B induces degradation of the androgen receptor. |
| In vitro | Isosilybin B also inhibited the microvessel sprouting from mouse dorsal aortas ex vivo, and the VEGF-induced cell proliferation, capillary-like tube formation, and invasiveness of human umbilical vein endothelial cells (HUVEC) in vitro. Further studies in HUVEC showed that these diastereoisomers target cell cycle, apoptosis, and VEGF-induced signaling cascade. Three-dimensional growth assay as well as co-culture invasion and in vitro angiogenesis studies (with HUVEC and DU145 cells) suggested the differential effectiveness of the diastereoisomers toward PCA and endothelial cells.[3] |
| In vivo | Isosilybin B (50 and 100 mg/kg body weight; oral) effectively inhibits the growth of advanced human PCA DU145 xenografts. Immunohistochemical analyses revealed that Isosilybin B inhibit tumor angiogenesis biomarkers (CD31 and nestin) and signaling molecules regulating angiogenesis (VEGF, VEGFR1, VEGFR2, phospho-Akt, and HIF-1α±) without adversely affecting the vessel-count in normal tissues (liver, lung, and kidney) of tumor-bearing mice.[3] |
| molecular weight | 482.44 |
| Molecular formula | C25H22O10 |
| CAS | 142796-22-3 |
| Storage | store at low temperature,keep away from direct sunlight | Powder: -20°C for 3 years | In solvent: -80°C for 1 year |
| References | 1. Deep G, et al. Isosilybin B and isosilybin A inhibit growth, induce G1 arrest and cause apoptosis in human prostate cancer LNCaP and 22Rv1 cells. Carcinogenesis. 2007 Jul;28(7):1533-42. 2. Deep G, et al. Isosilybin B causes androgen receptor degradation in human prostate carcinoma cells via PI3K-Akt-Mdm2-mediated pathway. Oncogene. 2008 Jun 26;27(28):3986-98. 3. Deep G, et al. Angiopreventive efficacy of pure flavonolignans from milk thistle extract against prostate cancer: targeting VEGF-VEGFR signaling. PLoS One. 2012;7(4):e34630. |