Bisindolylmaleimide VIII acetate (Ro 31-7549 acetate; 100 μg; IP; every other day for three doses) results in nearly complete tumor regression combined toTRA-8. The treatment with Bisindolylmaleimide VIII acetate alone does not induce significant tumor regression[2]. Animal Model: 6-8-week-old female NOD/SCID mice[2]. Dosage: 100 μg Administration: IP; every other day for three doses Result: Resulted in nearly complete tumor regression combined toTRA-8.
In Vitro
Bisindolylmaleimide VIII acetate (Ro 31-7549 acetate; 5 μM; 8, 12 hours) dramatically increases TRA-8-induced cell death in time-dependent and TRA-8 dose-dependent manners[2]. Bisindolylmaleimide VIII acetate (5 μM; 6 hours) significantly decreases procaspase-8 at 4 h and completely disappeares at 6 h after the combined treatment with TRA-8[2]. Apoptosis Analysis[2] Cell Line: 1321N1 cells Concentration: 5 μM Incubation Time: 8, 12 hours Result: Dramatically increased TRA-8-induced cell death in time-dependent and TRA-8 dose-dependent manners. Western Blot Analysis[2] Cell Line: 1321N1 cells Concentration: 5 μM Incubation Time: 6 hours Result: Significantly decreased procaspase-8 at 4 h and completely disappeared at 6 h.
Kinase Assay
Cell Assay
Animal Administration
References
[1]. Wilkinson SE, et al. Isoenzyme specificity of bisindolylmaleimides, selective inhibitors of protein kinase C. Biochem J. 1993 Sep 1;294 ( Pt 2):335-7.
[2]. Ohtsuka T, et al. Bisindolylmaleimide VIII enhances DR5-mediated apoptosis through the MKK4/JNK/p38 kinase and the mitochondrial pathways. J Biol Chem. 2002 Aug 9;277(32):29294-303.
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