Fig. 5: Combination therapy of BTSA1.2 and Navitoclax shows potent efficacy in resistant colorectal tumor xenografts.
From: Co-targeting of BAX and BCL-XL proteins broadly overcomes resistance to apoptosis in cancer
a Schematic of SW480 xenograft efficacy study. b Body weight measurements of Nu/Nu mice at 0, 7, and last day of treatment with vehicle, 100 mg/kg Navitoclax, 200 mg/kg BTSA1.2 or the combination. c Tumor volume curves of vehicle, Navitoclax, BTSA1.2 or the combination cohorts. d Tumor weight after completing study. Data in b–d, represent from n = 5 mice (Vehicle, BTSA1.2 and Navitoclax) or n = 6 mice (Combination). Statistics were obtained using two-way Anova: *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. e Schematic of SW480 pharmacodynamic xenograft study. f Example of kinetic curve of mitochondria potential in tumors treated with vehicle or combination upon stimuli of BH3-BIM peptide, Puma2A, CCCP or Alamethicin. Data are mean ± SD from n = 3 g, Dynamic BH3-profiling of tumors from mice treated with vehicle or BTSA1.2 and Navitoclax combination. Bar graph represent % of mitochondria depolarization of tumor cells detected by JC-1 upon treatment with BH3-BIM derived peptide or DMSO. Each point corresponds to the mean of n = 3 technical replicates; ± SD from n = 2 independent vehicle mice or n = 3 independent combination mice. Statistics were obtained using two-way Anova: *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. h, i Detection of cleaved Caspase-3 and cleaved PARP apoptotic markers by western blot analysis from SW480 tumors. Relative protein levels were normalized to β-Actin loading control. Data are mean ± SD from n = 3 mice. Statistics were obtained using two-way Anova: *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. Source data are provided as a Source Data file.
