Bispecific innate cell engager antibody that binds CD30 on tumor cells and CD16A on NK cells to bridge NK cells to CD30+ targets and trigger ADCC and cytokine release.
Tetravalent bispecific antibody that binds CD30 on tumor cells and CD16A (Fc gamma RIIIa) on NK cells, crosslinking NK cells to CD30-positive targets to activate NK-mediated cytotoxicity, induce ADCC and cytokine release, and drive tumor cell lysis.
YES
DIRECT
AFM13 bridges NK cells (via CD16A) to CD30+ cells, activating NK-mediated ADCC and perforin/granzyme-dependent lysis of the target cells.
Bispecific innate cell engager antibody that binds CD30 on tumor cells and CD16A on NK cells to bridge NK cells to CD30+ targets and trigger ADCC and cytokine release.
Tetravalent bispecific antibody that binds CD30 on tumor cells and CD16A (Fc gamma RIIIa) on NK cells, crosslinking NK cells to CD30-positive targets to activate NK-mediated cytotoxicity, induce ADCC and cytokine release, and drive tumor cell lysis.
NO
INDIRECT
AFM13 engages CD16A on NK cells to bridge them to CD30+ tumor cells, activating NK-mediated ADCC and cytotoxic granule release that kills the CD30+ targets; CD16A+ cells are effectors, not killed.
Humanized IgG1 bi-epitope anti-HER2 monoclonal antibody that binds HER2 extracellular domains 2 and 4 to block signaling, promote receptor internalization, and trigger ADCC.
Humanized IgG1 bi-epitope anti-HER2 monoclonal antibody that binds two non-overlapping HER2 extracellular domains (ECD2 and ECD4), blocking HER2 signaling, inducing receptor clustering and internalization/downregulation, and activating Fc-mediated effector functions (ADCC and ADCP) to eliminate HER2-overexpressing tumor cells.
YES
DIRECT
Zanidatamab binds HER2 ECD4 (and ECD2) on target cells and recruits immune effectors via its IgG1 Fc to trigger ADCC and ADCP, leading to killing of HER2-expressing cells; receptor clustering/internalization also occurs.
Autologous CMV-specific T cells genetically engineered to express an anti-CD19 chimeric antigen receptor, enabling targeted cytotoxicity against CD19-positive malignant B cells; endogenous CMV-specific TCRs allow antigen-driven recall responses to support in vivo expansion and persistence after transplant.
Autologous CMV-specific T cells engineered to express an anti-CD19 chimeric antigen receptor that redirects T-cell cytotoxicity to CD19-positive malignant B cells; native CMV-specific TCRs enable antigen-driven recall responses to enhance in vivo expansion and persistence, which can be boosted by CMV vaccination post-transplant.
YES
DIRECT
Anti-CD19 CAR-expressing T cells recognize CD19 on target cells and directly kill them via cytotoxic T-cell mechanisms (perforin/granzyme release and Fas/FasL-mediated apoptosis).