Targeting Natural Killer Cells to Acute Myeloid LeukemiaIn Vitrowith a CD16 × 33 Bispecific Killer Cell Engager and ADAM17 Inhibition

CD16 × 33 BiKE can overcome self-inhibitory signals and effectively elicit NK cell effector activity against AML. These in vitro studies highlight the potential of CD16 × 33 BiKE ± ADAM17 inhibition to enhance NK cell activation and specificity against CD33(+) AML, which optimally could be applied in patients with relapsed AML or for adjuvant antileukemic therapy posttransplantation.