Autologous, gene-engineered adoptive T-cell therapy in which patient T cells are transduced with an EBV-epitope-specific TCR and engineered to secrete a cytokine upon activation, enabling HLA-restricted recognition and killing of EBV-positive tumor cells and enhancing antitumor immunity.
Autologous T cells engineered to express an EBV epitope–specific TCR recognize EBV peptides presented by HLA on tumor cells, triggering TCR signaling and cytotoxic killing. Upon activation, the cells auto-secrete a cytokine that enhances their function, persistence, and recruitment/activation of endogenous immune cells, boosting antitumor immunity in EBV-positive tumors.
YES
DIRECT
Engineered TCR-T cells recognize the EBV peptide–HLA class I complex on tumor cells and kill them via CTL effector mechanisms (perforin/granzyme release and Fas–FasL–mediated apoptosis), with cytokine auto-secretion enhancing function and persistence.
Autologous, gene-engineered adoptive T-cell therapy in which patient T cells are transduced with an EBV-epitope-specific TCR and engineered to secrete a cytokine upon activation, enabling HLA-restricted recognition and killing of EBV-positive tumor cells and enhancing antitumor immunity.
Autologous T cells engineered to express an EBV epitope–specific TCR recognize EBV peptides presented by HLA on tumor cells, triggering TCR signaling and cytotoxic killing. Upon activation, the cells auto-secrete a cytokine that enhances their function, persistence, and recruitment/activation of endogenous immune cells, boosting antitumor immunity in EBV-positive tumors.
NO
INDIRECT
Cells expressing the cytokine’s receptors are not targeted for killing; the secreted cytokine activates/augments immune cells. Killing is directed at EBV peptide–HLA–positive tumor cells by the engineered TCR-T cells via perforin/granzyme (and Fas/FasL) cytolysis.
Antibody–drug conjugate targeting Nectin-4 that delivers a cytotoxic payload to kill Nectin-4–expressing tumor cells; associated with cutaneous adverse events.
Human monoclonal antibody targeting Nectin-4 linked via a cleavable linker to monomethyl auristatin E (MMAE). After binding to Nectin-4 on tumor cells, the complex is internalized and the linker is cleaved, releasing MMAE to bind tubulin and inhibit microtubule polymerization, leading to G2/M arrest and apoptosis in Nectin-4–expressing cells.
YES
DIRECT
The ADC binds Nectin-4, is internalized, the linker is cleaved to release MMAE, which inhibits microtubule polymerization (tubulin), causing G2/M arrest and apoptosis of Nectin-4–expressing cells.
Antibody–drug conjugate targeting Nectin-4 that delivers a cytotoxic payload to kill Nectin-4–expressing tumor cells; associated with cutaneous adverse events.
Human monoclonal antibody targeting Nectin-4 linked via a cleavable linker to monomethyl auristatin E (MMAE). After binding to Nectin-4 on tumor cells, the complex is internalized and the linker is cleaved, releasing MMAE to bind tubulin and inhibit microtubule polymerization, leading to G2/M arrest and apoptosis in Nectin-4–expressing cells.
NO
INDIRECT
The ADC binds Nectin-4 on tumor cells, is internalized, and releases MMAE, which binds the vinca site on beta‑tubulin to block microtubule polymerization, causing G2/M arrest and apoptosis. Beta‑tubulin expression alone does not determine killing; Nectin‑4 targeting does.
Human IgG1 monoclonal antibody targeting CD38 on malignant plasma cells; mediates NK cell ADCC, macrophage ADCP, complement-dependent cytotoxicity, and direct apoptosis; depletes CD38+ immunosuppressive cells (Tregs/Bregs/MDSCs) and expands T-cell populations.
Human IgG1 monoclonal antibody against CD38 that kills CD38+ myeloma cells via ADCC, ADCP, complement-dependent cytotoxicity, and direct apoptosis; also depletes CD38+ immunosuppressive cells (Tregs/Bregs/MDSCs) to enhance T‑cell responses.
YES
DIRECT
Daratumumab binds CD38 on target cells and triggers Fc-mediated ADCC (NK cells), ADCP (macrophages), complement-dependent cytotoxicity, and can induce apoptosis, leading to depletion of CD38+ cells.