Autologous, genetically modified CAR T-cell therapy engineered to dual-target NKG2D ligands (e.g., MICA/MICB/ULBP family) and CLDN18.2 on tumor cells, activating T-cell cytotoxicity to treat advanced NKG2DL+/CLDN18.2+ solid tumors.
Autologous T cells engineered with a tandem/bispecific CAR that recognizes NKG2D ligands (e.g., MICA, MICB, ULBP family) and CLDN18.2 on tumor cells. Target engagement activates CAR signaling, leading to T-cell cytotoxic killing via perforin/granzyme release and cytokine production, selectively lysing NKG2DL+/CLDN18.2+ cancer cells.
CAR T cells (KD-496) directly recognize ULBP4 as an NKG2D ligand together with CLDN18.2 on the same tumor cell, triggering CAR signaling and T-cell killing via perforin/granzyme-mediated cytolysis and cytokine release.
CD20×CD3 bispecific T‑cell–engaging antibody that binds CD20 on B cells and CD3 on T cells to activate cytotoxic T‑cell killing.
Bispecific anti-CD20×CD3 antibody that simultaneously binds CD20 on B cells and CD3 on T cells, cross-linking them to activate T-cell cytotoxicity and kill CD20-positive malignant B cells.
The CD20×CD3 bispecific antibody bridges CD3+ T cells to CD20+ cells, activating T cells to kill them via perforin/granzyme‑mediated cytotoxicity and apoptosis.
Autologous, genetically modified CAR T-cell therapy engineered to dual-target NKG2D ligands (e.g., MICA/MICB/ULBP family) and CLDN18.2 on tumor cells, activating T-cell cytotoxicity to treat advanced NKG2DL+/CLDN18.2+ solid tumors.
Autologous T cells engineered with a tandem/bispecific CAR that recognizes NKG2D ligands (e.g., MICA, MICB, ULBP family) and CLDN18.2 on tumor cells. Target engagement activates CAR signaling, leading to T-cell cytotoxic killing via perforin/granzyme release and cytokine production, selectively lysing NKG2DL+/CLDN18.2+ cancer cells.
KD-496 CAR T cells recognize ULBP5 (an NKG2D ligand) together with CLDN18.2 on the same cell, activating CAR signaling and T-cell degranulation (perforin/granzymes) to lyse the target cell.
Autologous, genetically modified CAR T-cell therapy engineered to dual-target NKG2D ligands (e.g., MICA/MICB/ULBP family) and CLDN18.2 on tumor cells, activating T-cell cytotoxicity to treat advanced NKG2DL+/CLDN18.2+ solid tumors.
Autologous T cells engineered with a tandem/bispecific CAR that recognizes NKG2D ligands (e.g., MICA, MICB, ULBP family) and CLDN18.2 on tumor cells. Target engagement activates CAR signaling, leading to T-cell cytotoxic killing via perforin/granzyme release and cytokine production, selectively lysing NKG2DL+/CLDN18.2+ cancer cells.
KD-496 CAR T cells recognize ULBP6 (an NKG2D ligand) together with CLDN18.2 on the same cell, triggering CAR activation and perforin/granzyme-mediated cytolysis.
Autologous T cells engineered to express a chimeric antigen receptor targeting GD2 with additional modules to resist tumor immunosuppression and enhance function/persistence for neuroblastoma.
Autologous T cells engineered to express a GD2‑specific chimeric antigen receptor. CAR engagement of GD2 on tumor cells activates T‑cell signaling to mediate targeted cytotoxicity; additional modules promote resistance to tumor immunosuppression and improve T‑cell function and persistence.
GD2-specific CAR T cells bind GD2 on target cells, triggering T-cell activation and immune synapse formation, leading to perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).