Donor-derived memory T cells genetically engineered to express an NKG2D-based chimeric antigen receptor targeting stress-induced NKG2D ligands (MICA/MICB/ULBPs) on tumor cells, intended to trigger T-cell cytotoxicity and overcome immune evasion; administered intravenously with optional intratumoral injection after lymphodepleting conditioning.
Donor-derived memory T cells are genetically engineered to express an NKG2D-based chimeric antigen receptor that recognizes stress-induced NKG2D ligands (MICA/MICB/ULBPs) on tumor cells, leading to CAR-mediated T-cell activation, cytokine release, and targeted cytotoxic killing, with the memory phenotype supporting persistence and the approach aiming to overcome tumor immune evasion.
NKG2D-CAR T cells bind ULBP5 (an NKG2D ligand) on target cells, triggering CAR signaling and T‑cell cytotoxicity via perforin/granzyme release and apoptosis-inducing pathways.
Donor-derived memory T cells genetically engineered to express an NKG2D-based chimeric antigen receptor targeting stress-induced NKG2D ligands (MICA/MICB/ULBPs) on tumor cells, intended to trigger T-cell cytotoxicity and overcome immune evasion; administered intravenously with optional intratumoral injection after lymphodepleting conditioning.
Donor-derived memory T cells are genetically engineered to express an NKG2D-based chimeric antigen receptor that recognizes stress-induced NKG2D ligands (MICA/MICB/ULBPs) on tumor cells, leading to CAR-mediated T-cell activation, cytokine release, and targeted cytotoxic killing, with the memory phenotype supporting persistence and the approach aiming to overcome tumor immune evasion.
NKG2D-CAR T cells recognize ULBP6 on target cells via the NKG2D-based CAR, activating T-cell killing through perforin/granzyme release (and death receptor/cytokine pathways), leading to direct lysis of ULBP6-expressing cells.
Chimeric anti‑CD20 monoclonal antibody that depletes CD20+ B cells via antibody‑dependent cellular cytotoxicity (ADCC) and complement‑dependent cytotoxicity (CDC).
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via antibody‑dependent cellular cytotoxicity (ADCC) and complement‑dependent cytotoxicity (CDC), leading to elimination of malignant B lymphocytes.
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC by NK cells/macrophages and complement-dependent cytotoxicity (MAC-mediated lysis).
Monoclonal antibody targeting the GD2 ganglioside on neuroblastoma cells; facilitates NK cell–mediated ADCC via CD16.
Monoclonal antibody that binds the GD2 ganglioside on neuroblastoma cells; the Fc region engages FcγRIIIa (CD16) on NK cells to drive antibody-dependent cellular cytotoxicity (ADCC), and can also trigger complement-dependent cytotoxicity and macrophage antibody-dependent cellular phagocytosis, leading to tumor cell killing.
Anti-GD2 mAb binds GD2 on tumor cells; its Fc engages CD16 on NK cells to drive ADCC, activates complement for CDC, and opsonizes cells for macrophage ADCP, resulting in killing of GD2+ cells.
Autologous, gene-edited TCR-engineered T-cell (TCR-T) therapy targeting the KRAS G12V neoantigen presented by HLA-A*11:01; infused T cells recognize KRAS G12V peptide–HLA on tumor cells and mediate cytotoxicity.
Autologous T cells are gene-edited to express a T-cell receptor specific for the KRAS G12V neoantigen presented by HLA-A*11:01. After infusion, these TCR-T cells recognize the KRAS G12V peptide–HLA complex on tumor cells, become activated, and mediate MHC-restricted cytotoxicity (e.g., perforin/granzyme release and cytokine-driven killing).
Engineered TCR-T cells recognize the KRAS G12V peptide presented by HLA-A*11:01 and directly kill target cells via TCR-triggered cytolysis (perforin/granzyme and Fas/FasL-mediated apoptosis).