Anti-HER2 antibody–drug conjugate (T-DXd, DS-8201a) comprising trastuzumab linked to the topoisomerase I inhibitor deruxtecan (DXd); binds HER2, is internalized, and releases DXd to inhibit topo I and induce DNA damage, with a membrane-permeable payload enabling a bystander effect and potential ADCC via the Fc region.
Anti-HER2 monoclonal antibody (trastuzumab) conjugated to the topoisomerase I inhibitor deruxtecan (DXd). After binding HER2, the ADC is internalized and releases DXd, which inhibits topoisomerase I, causing DNA damage, replication arrest, and apoptosis; the membrane-permeable payload enables a bystander effect, and the Fc region can mediate ADCC.
The ADC binds HER2, is internalized, and releases the topoisomerase I inhibitor DXd, causing DNA damage, replication arrest, and apoptosis; Fc-mediated ADCC and a membrane-permeable payload enable additional bystander killing.
Adoptive cell therapy using Vα24+ invariant natural killer T cells that recognize glycolipid antigens via CD1d, rapidly secrete IFN-γ and other cytokines, directly lyse tumor cells, activate NK and dendritic cells, and remodel the immunosuppressive microenvironment to overcome PD‑1 resistance.
Autologous invariant natural killer T (iNKT; Va24-Ja18) cells expanded ex vivo and reinfused. They recognize glycolipid antigens presented by CD1d via their invariant TCR, rapidly secrete IFN-gamma and other cytokines, directly lyse tumor cells (perforin/granzyme, Fas/FasL), and activate NK and dendritic cells to remodel the immunosuppressive tumor microenvironment, enhancing antitumor immunity and helping overcome PD-1 resistance.
Adoptively transferred iNKT cells recognize glycolipid antigens presented by CD1d via their invariant TCR and directly kill CD1d+ cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.
Adoptive cell therapy using Vα24+ invariant natural killer T cells that recognize glycolipid antigens via CD1d, rapidly secrete IFN-γ and other cytokines, directly lyse tumor cells, activate NK and dendritic cells, and remodel the immunosuppressive microenvironment to overcome PD‑1 resistance.
Autologous invariant natural killer T (iNKT; Va24-Ja18) cells expanded ex vivo and reinfused. They recognize glycolipid antigens presented by CD1d via their invariant TCR, rapidly secrete IFN-gamma and other cytokines, directly lyse tumor cells (perforin/granzyme, Fas/FasL), and activate NK and dendritic cells to remodel the immunosuppressive tumor microenvironment, enhancing antitumor immunity and helping overcome PD-1 resistance.
iNKT cells recognize CD1d-presented glycolipid antigens via their invariant TCR and directly kill target cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.
Adoptive cell therapy using Vα24+ invariant natural killer T cells that recognize glycolipid antigens via CD1d, rapidly secrete IFN-γ and other cytokines, directly lyse tumor cells, activate NK and dendritic cells, and remodel the immunosuppressive microenvironment to overcome PD‑1 resistance.
Autologous invariant natural killer T (iNKT; Va24-Ja18) cells expanded ex vivo and reinfused. They recognize glycolipid antigens presented by CD1d via their invariant TCR, rapidly secrete IFN-gamma and other cytokines, directly lyse tumor cells (perforin/granzyme, Fas/FasL), and activate NK and dendritic cells to remodel the immunosuppressive tumor microenvironment, enhancing antitumor immunity and helping overcome PD-1 resistance.
iNKT cells express FasL and engage Fas (CD95) on target cells, triggering death receptor–mediated (caspase-8) apoptosis; they can also kill via perforin/granzyme.
A humanized IgG4 bispecific T‑cell–engager monoclonal antibody that binds CD3 on T cells and BCMA on malignant plasma cells to trigger T‑cell cytotoxicity (brand: TECVAYLI).
Humanized IgG4 bispecific antibody that binds CD3 on T cells and BCMA on malignant plasma cells, crosslinking T cells to tumor cells to activate cytotoxic T-cell responses (perforin/granzyme release and cytokine-mediated killing) against BCMA-expressing myeloma cells.
Teclistamab crosslinks CD3 on T cells to BCMA on target cells, activating T cells to kill BCMA+ cells via perforin/granzyme release and cytokine-mediated lysis.