Figure S10 from Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma

NBI-961 does not alter FLT3 expression or its downstream substrate with greater cytotoxicity than sorafenib. (A) Western blot analysis of FLT3 in NBI-961 treated SUDHL5 in lysates from the same three independent experiments showing NEK2 degradation in Figure 4A. (B) Western blot analysis of phosphorylated mTOR (a known downstream substrate of FLT3) in newly NBI-961 treated SUDHL5 lysates from three independent experiments. NEK2 degradation was confirmed. Quantification of p-mTOR band intensity normalized to ACTIN is shown below. (C) Cell viability curves after 96 h NBI-961 treatment of RIVA (red dashed line) and SUDHL5 (blue dashed line) DLBCL cells compared to sorafenib treatment (solid lines) at a higher serial dilution (40 – 0.039 M; left panel) and at the same serial dilution as NBI-961 (2 – 0.00195 M; right panel). Sorafenib GI50 (95% C.I.): RIVA, 4.15 M (3.24 – 5.31); SUDHL5, 3.32 M (2.43 – 4.54).