Catalog No.S8061 Synonyms: BI-97C1
Molecular Weight(MW): 700.78
Sabutoclax(BI-97C1) is a pan-Bcl-2 inhibitor, including Bcl-xL, Bcl-2, Mcl-1 and Bfl-1 with IC50 of 0.31 μM, 0.32 μM, 0.20 μM and 0.62 μM, respectively.
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(e) Abs (490 nm) was measured by MTS assay in siControl or siPTBP1 treated PC3 cells with DMSO, 1000 nM ABT737, or 100 nM Sabutoclax for 48 h, showing no significant change in cell viability following siPTBP1 treatment in DMSO control, ABT737, or Sabutoclax treated cells. (f) PC3 cells transfected with siControl or a mixture of two siPTBP1 were treated with 1000 nM ABT737 or 100 nM Sabutoclax combined with various doses of docetaxel for 48 h and cell viability was assessed by MTS assay. The viability of cells with 1000 nM ABT737 or 100 nM Sabutoclax alone was set as 100%. All data are presented as mean±S.E.M., n=3. The statistical significance was determined by unpaired student t-test where *P<0.05; **P<0.01; ***P<0.001.
Cell Death Differ, 2016, 23(10):1681-90.. Sabutoclax purchased from Selleck.
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|Description||Sabutoclax(BI-97C1) is a pan-Bcl-2 inhibitor, including Bcl-xL, Bcl-2, Mcl-1 and Bfl-1 with IC50 of 0.31 μM, 0.32 μM, 0.20 μM and 0.62 μM, respectively.|
BI-97C1 potently inhibits cell growth of human prostate cancer, lung cancer, and lymphoma cell lines with EC50 values of 0.13, 0.56, and 0.049 μM, respectively, and shows little cytotoxicity against bax-/-bak-/- cells. It is suggest that treatment with the combination regimen of mda-7/IL-24 and BI-97C1 induces autophagy that facilitates apoptosis in association with up-regulation of NOXA, accumulation of Bim, and activation of Bax and Bak.
|In vivo||BI-97C1 displays in vivo efficacy in transgenic mice in which Bcl-2 is overexpressed in splenic B-cells and also demonstrates superior single-agent antitumor efficacy in a prostate cancer mouse xenograft model that depends on Mcl-1 for survival. Treatment with Ad.5/3-mda-7 and BI-97C1 significantly inhibits the growth of human PC xenografts in nude mice and spontaneously induced PC in Hi-myc transgenic mice. Tumor growth inhibition correlats with increased TUNEL staining and decreased Ki-67 expression in both PC xenografts and prostates of Hi-myc mice.|
Competitive fluorescence polarization assays (FPA) :A Bak BH3 peptide (F-BakBH3) (GQVGRQLAIIGDDINR) is labeled at the N-terminus with fluorescein isothiocyanate (FITC) and purified by HPLC. For competitive binding assays, 100 nM GST-Bcl-XL ΔTM protein is preincubated with the tested compound at varying concentrations in 47.5 μL PBS (pH = 7.4) in 96-well black plates at room temperature for 10 min, and then 2.5 μL of 100 nM FITC-labeled Bak BH3 peptide is added to produce a final volume of 50 μL. The wild-type and mutant Bak BH3 peptides are included in each assay plate as positive and negative controls, respectively. After 30 min incubation at room temperature, the polarization values in millipolarization units are measured at excitation/emission wavelengths of 480/535 nm with a multilabel plate reader. IC50 is determined by fitting the experimental data to a sigmoidal dose-response nonlinear regression model. Data reported are mean of three independent experiments. Performance of Bcl-2 and Mcl-1FPA are similar. Briefly, 50 nM of GST-Bcl-2 or -Mcl-1are incubatedwith various concentrations of compound (4 and 11-14) for 2 min, and then 15 nM FITC-conjugated-Bim BH3 peptide is added in PBS buffer. Fluorescence polarization is measured after 10 min.
|In vitro||DMSO||100 mg/mL warmed (142.69 mM)|
|Ethanol||54 mg/mL warmed (77.05 mM)|
|Water||slightly soluble or insoluble|
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