Fig. 1

VEN and MEN1i synergistically inhibited KMT2Ar-AML proliferation. A IC50 of VEN in different AML cell lines (72 h); B IC50 of MI-503 in different AML cell lines (7 days); C Growth inhibition and synergistic index (combination index [CI] was calculated via CalcuSyn software) in THP-1 (expressing KMT2A-MLLT3), MV4-11 (expressing KMT2A-AFF1), and MOLM13 (expressing KMT2A-MLLT3) cells after treatments with different concentrations of VEN, MI-503, and their combination (72 h); D Apoptotic induction (Annexin V-positive cells) was determined after treatments with VEN, MI-503, and their combination (72 h) [two-tailed Student's t-tests; **P < 0.01, ***P < 0.001]; E Growth inhibition and synergistic index of VEN plus MI-503 in primary bone marrow MNCs from KMT2Ar-AML patients (72 h); F Detecting the progression of tumor burden via fluorescence imaging after treating the CDX mouse model constructed by MOLM13-Luciferase with DMSO, VEN, MI-503 and their combination. G The relative luminescence unit (RLU) value was calculated for indicating leukemic burdens of treated mice (28 days) [two-tailed Student's t-tests; *P < 0.05, **P < 0.01, ***P < 0.001]. H Kaplan–Meier survival curves in the MOLM13 xenotransplantation model [two-tailed Student's t-tests; *P < 0.05, **P < 0.01, ***P < 0.001]