CAS No. : 1001600-56-1

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For research use only. Not Intended for Therapeutic Use!
Cat No:I000074
Molecular Formula:C70H96N10O8
Molecular Weight:1205.57
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Cat No:I000074
Cas No:1001600-56-1

BV6(cas 1001600-56-1) is a small-molecule Smac mimetic, which antagonizes IAP and induces autoubiquitination and subsequent proteasomal degradation of cIAP1 and cIAP2. BV6 treatment had no effect on necrotic cell death induced by poly(I:C)+IFNβ, anti-Fas+zVAD-fmk, or H2O2, but greatly sensitized cells to TNF-induced necrosis. As observed in L929 cells, BV6 treatment of FADD-deficient Jurkat cells led to a rapid loss of cIAP1 and cIAP2 and greatly sensitized these cells to TNF-induced necrosis. BV6 significantly enhances the radiosensitization of HCC193 and H460 cells in vitro. Four-hour pre-incubation with 2.5μMol BV6 moderately enhanced CIK cell-mediated lysis of hematological (H9, THP-1, and Tanoue) and solid malignancies (RH1, RH30, and TE671). However, BV6 also increased apoptosis of non-malignant cells like peripheral blood mononuclear cells and most notably had an inhibitory effect on immune cells potentially limiting their cytotoxic potential.

1. J Thorac Oncol. 2011 Nov;6(11):1801-9. doi: 10.1097/JTO.0b013e318226b4a6.
BV6, an IAP antagonist, activates apoptosis and enhances radiosensitization of non-small cell lung carcinoma in vitro.
Li W(1), Li B, Giacalone NJ, Torossian A, Sun Y, Niu K, Lin-Tsai O, Lu B.
Author information:
(1)Department of Radiation Oncology, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
INTRODUCTION: Defects in the apoptosis pathway limit the effectiveness of radiation in non-small cell lung cancer (NSCLC) therapy. BV6 is an antagonist of cIAP1 and XIAP, members of the inhibitors of apoptosis (IAP) family. We investigated the potential of BV6 to sensitize NSCLC cell lines to radiation. METHODS: HCC193 and H460 lung cancer cell lines were treated with BV6 to investigate the effects of drug administration on cell proliferation, apoptosis, inhibition of XIAP and cIAP1, and radiosensitivity. Subsequent immunoblotting and Hoechst staining were used to determine the role of apoptosis in radiosensitization. Finally, the pathway of apoptosis was characterized by Western blot analysis for cleaved caspase-8 and cleaved caspase-9 and enzyme-linked immunosorbent assays for TNF-α. RESULTS: HCC193 was found to be more sensitive than H460 to BV6-induced apoptosis in a concentration-dependent and time-dependent manner. BV6 significantly sensitized both cell lines to radiation (HCC193-DER = 1.38, p < 0.05 at 1 μM BV6; H460-DER = 1.42, p < 0.05 at 5 μM BV6), but a higher concentration of and longer incubation time with BV6 was necessary for H460 cells. The BV6-induced radiosensitization of HCC193 favored the extrinsic pathway of apoptosis, whereas that of H460 favored the intrinsic pathway. CONCLUSIONS: BV6, an IAP antagonist, significantly enhanced the radiosensitization of HCC193 and H460 cells in vitro. More research is warranted to test the mechanism of action of BV6 and to assess its potential in vivo and in the clinical setting.
2. Scand J Immunol. 2000 Jun;51(6):543-7.
Human T-cell receptor BV6 gene polymorphism in relation to expression level and CD4/CD8 skewness.
Obata F(1), Shiiba R, Iizuka M, Kashiwagi N, Kurosu F, Shimada N, Nishijima M, Tozawa H.
Author information:
(1)Department of Immunology, Kitasato University School of Allied Health Sciences, Sagamihara, Kanagawa, Japan.
Using 50 samples of umbilical cord blood lymphocytes from Japanese donors, we analysed two human T-cell receptor beta variable (TCRBV) genes, BV6S4 and BV6S5, for their polymorphism, usage frequencies and CD4/CD8 skewness. They showed contrasting CD4/CD8 skewness, BV6S4 to CD8+ T cells and BV6S5 to CD4+ T cells. Genotyping of the BV6S4 alleles (A1, A2 and A3) revealed two of the six possible BV6S4 genotypes, A1/A2 and A2/A2. Among the two BV6S4 genotypes, no significant difference was detected in usage frequency or CD4/CD8 skewness. On the other hand, genotyping of the BV6S5 alleles (A1 and A2) revealed all three possible BV6S5 genotypes, A1/A1, A1/A2 and A2/A2, and the gene usage frequency was high, in the order A1/A1 > A1/A2 > A2/A2. These results indicate that the amino acid substitutions in BV6S5 (S36R and G70E) are in some way associated with the expression level of this gene. In the analysis of CD4/CD8 skewness, the three BV6S5 genotypes had similar skewness, indicating that A1 alleles are expressed more frequently than A2 alleles in both CD4+ and CD8+ T-cell populations. Although BV6S5 exhibits marked skewness to CD4+ T cells, our results indicate that the higher expression of A1 alleles is not associated with the increased ratio of CD4+ T cells.
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