Targeting B7-H3 inhibits AML growth in vivo via NK cells. (A) Overlay plot showing B7-H3 expression in 4 AML PDX models. Cells were stained with primary anti-B7–H3 mAbs (blue) and secondary conjugated antibody as control (red), and B7-H3 expression was measured by flow cytometry. (B) Experimental schema. Two million AML-PDX cells were injected in NSG mice via the tail vein (TV), and upon >1% engraftment of hCD45+ cells in PB (wk 8), mice were treated with mouse IgG1 or anti-B7-H3 mAbs T-1A5, HEK5-1B3, or 58B1 at 1 mg/kg twice weekly via IP injection. (C) Percentage of human CD45⁺ cells in mouse PB. Mice blood samples were analyzed weekly by flow cytometry. When human CD45⁺ cells reached >95% or when mice became moribund (whichever happened first), mice were killed. (D) Kaplan-Meier survival plot representing the OS rates in the mice treated with different anti-B7–H3 mAbs (log-rank test). (E) Experimental design for xenograft model. Two million firefly luciferase GFP⁺ OCI-AML3 cells were injected in NSG mice via TV, and leukemia engraftment was measured weekly by bioluminescence imaging (BLI). The mice were treated with anti-B7–H3 mAb T-1A5 or mouse IgG1 at 1 mg/kg once a week via IP injections and NK cells (10 × 10⁶) twice weekly via TV. (F) Kaplan-Meier survival plot demonstrating the OS rates in mice treated with mAb T-1A5 or mouse IgG1 and NK cells.