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. Author manuscript; available in PMC: 2020 May 4.
Published in final edited form as: Invest New Drugs. 2019 May 17;38(2):340–349. doi: 10.1007/s10637-019-00786-4

Fig 1. In vitro activity of pacritinib in various FLT3-ITD+ models.

Fig 1

(A) Activity of pacritinib against different FLT3 mutants in a binding assay. (B) Activity of pacritinib against FLT3-ITD and FLT3 D835Y in a kinase assay. (C) Activity of pacritinib in Ba/F3 cells transfected with different FLT3 mutants in a cell viability assay (mean ± SEM, n=12, two experiments). (D) Signaling inhibition with pacritinib in Ba/F3 cells expressing different FLT3 double mutants via Western blot (representative images from two experiments). (E) Activity of pacritinib in AML cell lines in a viability assay (mean ± SD, n=12). Activity of pacritinib in (F) murine primary FLT3-ITD+/−/IDH2-R140Q+/− leukemia cells and (G) pre-treatment patient primary blast samples in a viability assay (mean ± SD, n=3). Baseline mutations in each patient are denoted in parentheses.