Fig. 9: Cotreatment with HPA-12 and Creno is effective in FLT3-ITD+ and FLT3-TKD+ AML patient-derived cells.
From: Targeting ceramide transfer protein sensitizes AML to FLT3 inhibitors via a GRP78-ATF6-CHOP axis

a Viability of primary FLT3-ITD+ AML blasts treated with increasing concentrations of HPA-12 (0, 60, 80, and 100 μM) for 48 h. Cell viability was measured by the CCK-8 assay. Viability of FLT3-ITD+ CD34+ primary AML cells (b) and CD34+ hematopoietic stem and progenitor cells (c). CD34+ cells were enriched with anti-hCD34 microbeads. Annexin V/PI staining of primary FLT3-ITD+ AML cells from Patient #5 (d) and FLT3-TKD+ AML cells from Patient #6 (e) treated with increasing concentrations of HPA-12 for 48 h. Annexin V/PI staining of primary FLT3-ITD + AML cells from Patient #5 (f) and FLT3-TKD + AML cells from Patient #6 (g) treated with with HPA-12 (80 µM) and Creno (6 µM) alone or in combination for 48 h. h Expression of GRP78, ATF6, and CHOP determined by western blotting of primary FLT3-ITD+ AML cells from Patient #5 in (h). Expression of GRP78 and ATF6 determined by western blotting in primary FLT3-TKD+ AML cells from Patient #6 (i) and primary FLT3-ITD+ AML cells from Patient #7 (j). The data are presented as the means ± SDs. The characteristics of the AML patients and healthy donors in this figure are shown in Table S9–10. Source data are provided as a source data file.