Autologous cellular immunotherapy using ex vivo–generated dendritic cells pulsed with patient-specific tumor neoantigen peptides to prime/expand neoantigen-specific CD8+ and CD4+ T cells.
Autologous dendritic cells are generated ex vivo and pulsed with patient-specific tumor neoantigen peptides. After infusion, the DCs migrate to lymphoid tissues and present these neoantigens on HLA class I and II, providing costimulation (e.g., CD80/CD86) and cytokines to prime and expand neoantigen-specific CD8+ cytotoxic T cells and CD4+ helper T cells, thereby promoting tumor-specific immune responses and immunologic memory.
NO
INDIRECT
Neoantigen-pulsed dendritic cells use CD80/CD86 to costimulate and prime neoantigen-specific T cells, which then kill tumor cells presenting the neoantigen–HLA via perforin/granzyme or Fas–FasL. The CD80/CD86+ dendritic cells themselves are not targeted for killing.
Chimeric anti-CD20 monoclonal antibody that depletes B cells via ADCC, complement activation, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive malignant and normal B cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and eliminates them via Fc-mediated ADCC by NK/macrophages, complement-dependent cytotoxicity (CDC), and can directly induce apoptosis upon CD20 crosslinking.
IgG-based bispecific antibody–drug conjugate targeting HER3 (ERBB3) and TROP2; binds tumor cells, induces receptor-mediated internalization, and releases an intracellular cytotoxic payload to kill cancer cells, potentially dampening HER3 signaling and addressing antigen heterogeneity.
IgG-based bispecific antibody–drug conjugate that binds HER3 (ERBB3) and TROP2 on tumor cells, induces receptor-mediated internalization, and releases an intracellular cytotoxic payload to kill cancer cells; dual targeting may also dampen HER3 signaling and address antigen heterogeneity.
YES
DIRECT
The bispecific ADC binds HER3 on tumor cells, undergoes receptor-mediated internalization, and releases an intracellular cytotoxic payload that kills the cell (e.g., via DNA damage or microtubule disruption).
IgG-based bispecific antibody–drug conjugate targeting HER3 (ERBB3) and TROP2; binds tumor cells, induces receptor-mediated internalization, and releases an intracellular cytotoxic payload to kill cancer cells, potentially dampening HER3 signaling and addressing antigen heterogeneity.
IgG-based bispecific antibody–drug conjugate that binds HER3 (ERBB3) and TROP2 on tumor cells, induces receptor-mediated internalization, and releases an intracellular cytotoxic payload to kill cancer cells; dual targeting may also dampen HER3 signaling and address antigen heterogeneity.
YES
DIRECT
ADC binds TROP2 on tumor cells, is internalized, and releases an intracellular cytotoxic payload that kills the cell.
Autologous, gene-modified CAR T-cell therapy expressing two CARs targeting the EGFR 806 epitope and IL13Rα2; delivered intrathecally to induce T-cell activation, cytokine release, and cytotoxic killing of glioblastoma cells while aiming to reduce antigen escape through dual targeting.
Autologous T cells genetically engineered (lentiviral) to co-express two chimeric antigen receptors targeting the EGFR 806 epitope and IL13Ra2. Engagement of either antigen on glioblastoma cells triggers CAR signaling to activate T cells, leading to cytokine release, clonal expansion, and perforin/granzyme-mediated cytotoxic killing. Dual targeting is intended to reduce antigen escape; administered intrathecally for CNS tumor access.
YES
DIRECT
CAR T cells recognize the EGFR 806 epitope, form an immune synapse, and kill target cells via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).