Monoclonal IgG1 antibody targeting B7-H3 (CD276) on tumor cells; engages NK cells via Fc to drive antibody-dependent cellular cytotoxicity (ADCC).
Humanized, Fc‑engineered IgG1 monoclonal antibody targeting B7‑H3 (CD276) on tumor cells; binding flags tumor cells for immune elimination by engaging FcγRIIIa (CD16) on NK cells to drive potent antibody‑dependent cellular cytotoxicity (ADCC), with additional Fc‑mediated effector functions (e.g., macrophage engagement) possible. No payload; primary effect is target‑specific immune‑mediated cytotoxicity.
YES
DIRECT
Enoblituzumab binds B7-H3 on target cells and engages NK cells via Fc-gamma receptor (CD16) to trigger antibody-dependent cellular cytotoxicity (perforin/granzyme); additional Fc-mediated effector functions (e.g., macrophage phagocytosis) may contribute.
Monoclonal IgG1 antibody targeting B7-H3 (CD276) on tumor cells; engages NK cells via Fc to drive antibody-dependent cellular cytotoxicity (ADCC).
Humanized, Fc‑engineered IgG1 monoclonal antibody targeting B7‑H3 (CD276) on tumor cells; binding flags tumor cells for immune elimination by engaging FcγRIIIa (CD16) on NK cells to drive potent antibody‑dependent cellular cytotoxicity (ADCC), with additional Fc‑mediated effector functions (e.g., macrophage engagement) possible. No payload; primary effect is target‑specific immune‑mediated cytotoxicity.
NO
INDIRECT
The antibody binds B7-H3 on tumor cells; its Fc engages CD16a on NK cells to trigger ADCC that kills B7-H3–positive tumor cells. CD16a-expressing cells (NK cells) are not killed.
Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy; patient T cells are gene-modified to express a CD19-targeted CAR that, upon antigen engagement, activates T-cell cytotoxicity to eliminate CD19-positive B-cell malignancies and induce B-cell aplasia.
Autologous T cells are gene‑modified to express an anti‑CD19 chimeric antigen receptor; binding to CD19 on B cells activates CAR signaling and T‑cell cytotoxicity, leading to elimination of CD19‑positive malignant B cells and on‑target B‑cell aplasia.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target B cells and kill them via T-cell cytotoxicity (perforin/granzyme-mediated apoptosis and Fas–FasL signaling).
Therapeutic cancer vaccine using a recombinant gorilla adenoviral vector encoding HPV16/18 E6/E7 antigens; delivered subcutaneously to prime and expand HPV-specific CD8+ and CD4+ T cells by antigen presentation in dendritic cells.
Replication-deficient gorilla adenoviral vector delivers genes encoding HPV16/18 E6/E7 antigens to antigen-presenting cells, leading to intracellular expression and presentation on MHC I/II, priming and expanding HPV-specific CD8+ cytotoxic and CD4+ helper T cells and inducing antibody responses, which target and lyse HPV16/18 E6/E7–expressing tumor cells.
YES
INDIRECT
Therapeutic vaccination primes HPV16 E6–specific CD8+ T cells that recognize E6-derived peptides on MHC I of tumor cells and kill them via perforin/granzyme-mediated cytolysis (with CD4+ help).
Therapeutic cancer vaccine using a recombinant gorilla adenoviral vector encoding HPV16/18 E6/E7 antigens; delivered subcutaneously to prime and expand HPV-specific CD8+ and CD4+ T cells by antigen presentation in dendritic cells.
Replication-deficient gorilla adenoviral vector delivers genes encoding HPV16/18 E6/E7 antigens to antigen-presenting cells, leading to intracellular expression and presentation on MHC I/II, priming and expanding HPV-specific CD8+ cytotoxic and CD4+ helper T cells and inducing antibody responses, which target and lyse HPV16/18 E6/E7–expressing tumor cells.
YES
INDIRECT
Therapeutic vaccine primes HPV16 E7-specific CD8+ T cells; CTLs recognize E7 peptides on MHC I of tumor cells and kill them via perforin/granzyme (and Fas–FasL) pathways.