Yago Nieto, MD, PhD, discusses AFM13, how it works, and its effect as a bispecific antibody that targets CD30 and CD16.
Yago Nieto, MD, PhD, professor of stem cell transplantation & cellular therapy, The University of Texas MD Anderson Cancer Center, Houston, discusses AFM13, how it works, and its effect as a bispecific antibody that targets CD30 and CD16.
“AFM13 is a bispecific antibody conjugate that targets both CD30, which is expressed on many types of lymphomas. It's universally expressed on Hodgkin's lymphoma cells, also on other T-cell lymphomas and some B-cell lymphomas. And on the other hand, AFM13 also binds CD16, which is a marker of natural killer [NK] cells,” explains Nieto.
AFM13 activates NK cells to kill CD30+ cells.1 First, the NK cells are activated with cytokines, expanded in the presence of artificial antigen-presenting cells and complexed with AFM13 prior to being infused into a patient. Additionally, precomplexed AFM13-NK cells are more readily able to find and eliminate CD30-positive lymphoma cells.
In this video, Nieto also explains how NK cells function in the immune response against cancer, and what advantages they offer in cell therapy compared with T cells.
“A big advantage of allogeneic NK cells over allogeneic T cells is that NK cells do not cause graft-vs-host disease, even in settings of deep HLA mismatch, as it was in our trial. So, that makes the product much easier to manage and much safer,” adds Nieto.
Currently, a phase 1 trial (NCT04074746) is assessing the combination of AFM13 and expanded NK cells precomplexed with AFM13 (AFM13-NK) in 42 patients with relapsed refractory lymphoma.
According to findings published in Nature Medicine, the combination led to an overall response rate (ORR) of 92.9% and a complete response (CR) rate of 66.7%. At a median follow-up of 20 months, the 2-year event-free survival (EFS) and overall survival (OS) rates of 26.2% and 76.2%, respectively.
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