Fig. 4
From: Targeted inhibition of STAT/TET1 axis as a therapeutic strategy for acute myeloid leukemia
Effects of UC-514321 in treating AMLs. a Structures of NSC-370284 and UC-514321. b–e Effects of NSC-370284, UC-514321, and other JAK/STAT pathway inhibitors, i.e., Pacritinib, KW-2449, Stattic and sc-355979, on the viability of AML cell lines MONOMAC-6 (b), THP-1 (c), KASUMI1 (d), and NB4 (e). Cells were treated with drugs at indicated doses. Cell viability was detected by MTS 48 h post treatment. Error bar indicates SD of triplicate experiments. f–j Enhanced therapeutic effect of UC-514321, relative to NSC-370284, in treating TET1-high AMLs in vivo. Secondary BMT recipient mice were transplanted with primary leukemic BM cells with MLL-AF9 (f), AML-ETO9a (g), MLL-AF10(h), or FLT3-ITD/NPM1mut (i). Upon the onset of leukemia, the recipient mice were treated with DMSO (control) (n = 5 or 6), 2.5 mg/kg NSC-370284 (n = 5 or 6), or UC-514321 (n = 5 or 6), i.p., once per day, for 10 days. Kaplan–Meier curves are shown. The P values were determined by log-rank test. j Wright–Giemsa staining of mouse PB and BM, or H&E staining of mouse spleen and liver of MLL-AF9 AML secondary BMT recipients with or without drug treatment
