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.
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.
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.
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.
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.
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.
An autologous CD19-directed CAR-T cell therapy generated by retroviral transduction; the CAR contains CD3ζ and costimulatory domains that enhance cytokine-driven JAK/STAT signaling to promote T-cell activation, proliferation, and cytotoxic killing of CD19-positive malignant B cells.
Autologous T cells are retrovirally transduced to express a CD19-specific chimeric antigen receptor containing CD3ζ and costimulatory domains. Engagement of CD19 on malignant B cells triggers CAR-mediated signaling (including cytokine-driven JAK/STAT pathways), leading to T-cell activation, proliferation, and targeted cytotoxic killing of CD19-positive cells.
CD19-directed CAR-T cells bind CD19 on target cells, become activated, and kill them via perforin/granzyme release and death-receptor (Fas/FasL)–mediated apoptosis.
Patient-derived T cells genetically engineered to express a chimeric antigen receptor that specifically recognizes Claudin18.2 (CLDN18.2), activating and expanding T cells to mediate targeted cytotoxicity against CLDN18.2-positive tumor cells; administered as up to three infusions.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting Claudin18.2 (CLDN18.2). Antigen engagement triggers CAR signaling, activating and expanding the T cells to mediate targeted cytotoxicity and cytokine release, leading to selective killing of CLDN18.2-positive tumor cells.
CAR T cells bind CLDN18.2 on target cells and kill them via T‑cell effector mechanisms (perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis).