Fig. 6
From: A novel Mcl-1 inhibitor synergizes with venetoclax to induce apoptosis in cancer cells
The combination of MI-238 and venetoclax potently inhibited the development of AML in murine model. A Schematic diagram of the experimental design showing the timeline for the treatment and imaging. B Representative bioluminescent images of the Molm13 tumor burden in mice treated with vehicle, MI-238 (70 mg/kg), venetoclax (50 mg/kg) or their combination. C, D The percentage of human CD45 (hCD45) and human CD33 (hCD33) positive cells were analyzed by flow cytometry to measure the Molm13 tumor burden. The representative flow cytometry plots (C) and quantification of hCD45 and hCD33 double positive (hCD45+/hCD33+) cells (D) were shown. Data are represented as mean ± SD from three independent replicates. ***P < 0.001 and ****P < 0.0001 by two-tailed t-test. E, F Immunochemistry (IHC) analysis of hCD45 expression in bone marrow from experimental mice. Representative staining (E) and quantification (F) were shown. Data represent mean ± SD from three independent replicates, *P < 0.05 and ****P < 0.0001 by two-tailed t-test. G Kaplan–Meier analysis showed MI-238 in combination with venetoclax resulted in a survival benefit in Molm13 AML xenograft mice. **P < 0.01 by log-rank (Mantel–Cox) test (n = 5)