Subcutaneous bispecific T-cell–engaging IgG1 antibody (CD3×CD20) that redirects cytotoxic T cells to kill CD20+ B cells.
Bispecific IgG1 antibody that binds CD3 on T cells and CD20 on B cells, crosslinking them to activate cytotoxic T lymphocytes and induce perforin/granzyme-mediated lysis of CD20-positive B-cell malignancies.
YES
DIRECT
Epcoritamab bridges CD3 on T cells to CD20 on target B cells, activating T cells to form an immunologic synapse and kill CD20+ cells via perforin/granzyme-mediated lysis.
Subcutaneous bispecific T-cell–engaging IgG1 antibody (CD3×CD20) that redirects cytotoxic T cells to kill CD20+ B cells.
Bispecific IgG1 antibody that binds CD3 on T cells and CD20 on B cells, crosslinking them to activate cytotoxic T lymphocytes and induce perforin/granzyme-mediated lysis of CD20-positive B-cell malignancies.
NO
INDIRECT
Epcoritamab binds CD3 on T cells to activate and redirect them to kill CD20+ B cells via perforin/granzyme-mediated cytolysis; CD3ε-expressing T cells are not themselves killed.
Autologous T cells engineered to express a chimeric antigen receptor targeting cadherin‑17 (CDH17). CAR engagement triggers CD3ζ/costimulatory signaling, leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of CDH17-positive tumor cells.
Autologous T cells engineered with a chimeric antigen receptor targeting CDH17. Upon CDH17 binding, the CAR delivers CD3-zeta and costimulatory signals that activate and expand T cells, leading to cytokine release and perforin/granzyme-mediated cytotoxic killing of CDH17-positive tumor cells.
YES
DIRECT
CAR-T cells bind CDH17 on target cells; CAR signaling activates T cells to kill via perforin/granzyme release and death-receptor pathways (e.g., Fas-FasL).
Investigational intratumoral immunotherapy biologic administered as subtherapeutic microdoses to trigger local immune-mediated effector functions within the tumor microenvironment; specific molecular targets are undisclosed and the study focuses on pharmacodynamic biomarker changes rather than efficacy.
Engineered NK cell engager that binds ROR1 on tumor cells and CD16 (FcγRIII) on NK cells to bring them into proximity, activate NK cells, and induce antibody-dependent cellular cytotoxicity and NK-mediated lysis of ROR1-positive tumor cells.
YES
DIRECT
The NK cell engager binds ROR1 on tumor cells and CD16 on NK cells, bridging and activating NK cells to induce ADCC and perforin–granzyme–mediated lysis of ROR1-positive cells.
Investigational intratumoral immunotherapy biologic administered as subtherapeutic microdoses to trigger local immune-mediated effector functions within the tumor microenvironment; specific molecular targets are undisclosed and the study focuses on pharmacodynamic biomarker changes rather than efficacy.
Engineered NK cell engager that binds ROR1 on tumor cells and CD16 (FcγRIII) on NK cells to bring them into proximity, activate NK cells, and induce antibody-dependent cellular cytotoxicity and NK-mediated lysis of ROR1-positive tumor cells.
NO
INDIRECT
The engager binds CD16 on NK cells and ROR1 on tumor cells, activating NK cells to perform ADCC and kill ROR1-positive tumor cells; CD16-expressing cells (NK cells) are not killed.