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 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.
YES
DIRECT
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).
Anti-HER2 antibody–drug conjugate (RC48) that binds HER2 (ERBB2), is internalized, and releases the cytotoxic payload MMAE to disrupt microtubules, causing mitotic arrest and cell death; may also enhance ADCC.
HER2 (ERBB2)-targeted antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the payload monomethyl auristatin E (MMAE), which inhibits tubulin polymerization to disrupt microtubules, causing G2/M arrest and apoptosis; may also enhance antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
HER2-binding ADC is internalized and releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis; Fc-mediated ADCC may also contribute.
Anti-HER2 antibody–drug conjugate (RC48) that binds HER2 (ERBB2), is internalized, and releases the cytotoxic payload MMAE to disrupt microtubules, causing mitotic arrest and cell death; may also enhance ADCC.
HER2 (ERBB2)-targeted antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the payload monomethyl auristatin E (MMAE), which inhibits tubulin polymerization to disrupt microtubules, causing G2/M arrest and apoptosis; may also enhance antibody-dependent cellular cytotoxicity (ADCC).
YES
INDIRECT
HER2-targeted ADC binds HER2, is internalized, then releases MMAE, which binds beta-tubulin and inhibits microtubule polymerization, causing G2/M arrest and apoptosis.
Autologous, dual-target CD19/BCMA chimeric antigen receptor (CAR) T-cell therapy; gene-modified T cells engineered to recognize CD19 and BCMA to deplete B cells and plasma cells; administered as a single intravenous infusion.
Autologous T cells engineered with dual CARs targeting CD19 and BCMA; upon infusion they recognize and eliminate CD19+ B cells and BCMA+ plasma cells via T‑cell activation and cytolytic activity, depleting B‑lineage cells (including autoreactive populations) and reducing autoantibody production.
YES
DIRECT
CD19 on target cells is recognized by the CD19-directed CAR on infused T cells, triggering T‑cell activation and cytolytic killing via perforin/granzyme release and apoptosis pathways (e.g., Fas/FasL).