An anti-c-Met antibody–drug conjugate (ADC) that binds MET (c-Met) on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload causing DNA damage and cell death; disrupts MET-driven signaling.
Monoclonal antibody targets MET (c-Met) on tumor cells; after binding and internalization, releases a topoisomerase I inhibitor payload that induces DNA damage and cell death while disrupting MET-driven signaling.
NO
INDIRECT
The ADC targets MET (c-Met) on the cell surface, is internalized, and releases a topoisomerase I inhibitor that causes DNA damage. Topoisomerase I is the intracellular enzymatic payload target, not the antigen used for cell targeting.
An agonistic anti-CD40 monoclonal antibody immunotherapy delivered intratumorally to activate CD40 on antigen-presenting cells, enhancing dendritic cell activation, antigen presentation, and T-cell priming.
Mitazalimab is an agonistic IgG1 monoclonal antibody that binds CD40 and activates CD40 signaling on antigen-presenting cells, enhancing dendritic cell activation, antigen presentation, and T‑cell priming/expansion; it may also mediate ADCC against CD40-expressing tumor cells.
YES
DIRECT
Mitazalimab binds CD40 on target cells and its IgG1 Fc engages FcγR+ effector cells (e.g., NK cells, macrophages) to mediate antibody-dependent cellular cytotoxicity (ADCC), killing CD40+ cells.
Autologous, gene-modified T cells expressing an FMC63-derived anti-CD19 scFv with CD8 hinge, TNFRSF19 transmembrane, 4-1BB costimulatory, and CD3ζ signaling domains; designed to recognize CD19 on malignant B cells and mediate T-cell activation, proliferation, and cytotoxic killing.
Autologous T cells are gene-modified to express a CD19-directed CAR (FMC63 scFv, CD8 hinge, TNFRSF19 transmembrane, 4-1BB costimulatory, CD3ζ signaling). Upon binding CD19 on malignant B cells, the CAR triggers T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing, leading to targeted elimination of CD19+ cells and potential persistence for ongoing immune surveillance.
YES
DIRECT
Anti-CD19 CAR-T cells recognize CD19 and directly kill target cells via T-cell cytotoxic mechanisms, primarily perforin/granzyme-mediated apoptosis (and death-receptor pathways).
Humanized T-cell–engaging bispecific antibody targeting Claudin-6 on tumor cells and engaging T cells to promote immune synapse formation, T-cell activation, and cytotoxic killing of CLDN6-positive solid tumors; administered weekly with a priming dose.
Fc-silenced humanized IgG1 bispecific antibody that binds Claudin-6 on tumor cells and CD3 on T cells, redirecting cytotoxic T cells to CLDN6-positive tumors to form immune synapses, activate T cells, and drive targeted lysis of CLDN6-expressing solid tumor cells.
YES
DIRECT
CTIM-76 bridges CD3 on T cells to CLDN6 on tumor cells, forming an immune synapse and activating T cells to kill CLDN6+ cells via perforin/granzyme-mediated cytolysis.
Humanized T-cell–engaging bispecific antibody targeting Claudin-6 on tumor cells and engaging T cells to promote immune synapse formation, T-cell activation, and cytotoxic killing of CLDN6-positive solid tumors; administered weekly with a priming dose.
Fc-silenced humanized IgG1 bispecific antibody that binds Claudin-6 on tumor cells and CD3 on T cells, redirecting cytotoxic T cells to CLDN6-positive tumors to form immune synapses, activate T cells, and drive targeted lysis of CLDN6-expressing solid tumor cells.
NO
INDIRECT
CTIM-76 binds CD3E on T cells to recruit and activate them; the activated T cells kill CLDN6-positive tumor cells via perforin/granzyme–mediated cytolysis, not the CD3-expressing cells.