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.
YES
DIRECT
KD-496 CAR T cells recognize ULBP3 (an NKG2D ligand) together with CLDN18.2 on the same tumor cell, activating CAR signaling and killing via perforin/granzyme-mediated cytotoxicity.
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.
YES
DIRECT
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.
YES
DIRECT
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 dendritic cell (DC) vaccine made from the patient’s monocytes and loaded ex vivo with autologous glioblastoma (GBM) tumor antigens to activate tumor-specific T-cell responses.
Autologous dendritic cells are loaded ex vivo with patient-derived glioblastoma antigens and administered to present these antigens via MHC I/II, priming tumor-specific CD8+ cytotoxic and CD4+ helper T-cell responses that drive CTL-mediated lysis of GBM cells; GM-CSF is used to enhance dendritic cell maturation and activity.
YES
INDIRECT
The DC vaccine primes tumor-specific T cells. Vaccine-activated CD4+ T cells recognizing GBM neoantigen peptides on HLA class II can exert cytotoxicity, and they also help activate CD8+ CTLs that kill tumor cells via perforin/granzyme and Fas–FasL pathways.
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.
YES
DIRECT
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.