ABBV-319 induces ADCC in vitro and in vivo. (A) Percentage specific lysis of RS4;11 cells in coculture with PBMC at an effector-to-target (E:T) ratio of 20:1 after 4-hour treatment with the indicated agents. Mean ± SEM are displayed. (B-C) Luciferase reporter activation in Jurkat cells expressing V158 (B) and F158 (C) FcγRIIIa after treatment with the indicated agents for 4 and 16 hours, respectively. Mean ± SEM are displayed. (D-F) Percentage specific lysis of RS4;11 (D), Raji (E), and KARPAS422 (F) in coculturing with PBMC at an E:T ratio of 20:1 after treatment with the indicated agent for 4 hours. Mean ± SEM are displayed. (G) Growth of OCI-LY19 tumors in CB17 SCID or CD34⁺ PBMC–engrafted NSG-Tg(Hu-IL15) mice after treatment with vehicle or a SD of ABBV-319 at 5 mg/kg. Mean ± SEM of tumor volumes were plotted for each treatment group vs days from randomization. ΔTGI_max and TGD₁₀₀₀ were calculated as described in the Methods. (H) Growth of OCI-LY19 tumors in CD34⁺ PBMC–engrafted NSG-Tg(Hu-IL15) mice after treatment with vehicle or a SD of ABBV-319 at 0.5, 1.5, and 5 mg/kg. Means ± SEM of tumor volumes were plotted for each treatment group vs days from randomization. (I) Flow cytometric immunophenotyping analysis of tail vein bleeds from OCI-LY19 tumor-bearing mice (H). B cells are presented as the percentage of CD45⁺ cells, whereas T and NK cells are presented as percentages of CD45⁺ cells without B cells. Details of the immunophenotyping methods are in supplemental Methods. (J) Growth of Raji tumors in CD34⁺ PMBC–engrafted NSG-Tg(Hu-IL15) mice after the indicated treatment regimen. Means ± SEM of tumor volumes were plotted for each treatment group vs days from randomization.