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. 2020 Aug 15;12(8):2303. doi: 10.3390/cancers12082303

Figure 2.

Figure 2

Ibrutinib elicits increased ADCP independent of BTK inhibition (A) Box plot showing ADCP of hMB “Double-Hit” lymphoma target cells and J774A.1 macrophages treated with alemtuzumab and conditioned media of ibrutinib pretreated hMB cells. (B) Box plot showing ADCP of hMB lymphoma cells co-cultured with ibrutinib-pretreated J774A.1 macrophages, both treated with alemtuzumab. (C) Box plot showing ADCP of ibrutinib-pretreated hMB lymphoma cells co-cultured with J774A.1 macrophages, both treated with alemtuzumab (n = 2). (D) Box plot showing ADCP of hMB lymphoma cells by combination of alemtuzumab with ibrutinib using primary peritoneal macrophages obtained from global BTK−/− mice as effector cells (E) Box plot showing ADCP by combination of alemtuzumab with ibrutinib and wild type (wt) hMB lymphoma cells and hMB with knock down in BTK. (F) Box plot showing ADCP of hMB lymphoma cells and J774A.1 macrophages treated with ibrutinib and second generation BTK inhibitor tirabrutinib. (G) Kaplan–Meier analysis comparing the survival of hMB transplanted male NSG mice receiving tirabrutinib and alemtuzumab as mono therapy or in combination. PBS was used as control. The treatment was given i.p. 10 days after i.v. hMB cell injection. All box plots show the median, the 25th and 75th quartiles, and the minimal and maximal value. Unless otherwise stated experiments were performed of at least three biological replicates. (* p < 0.05 and *** p ≤ 0.001).