Autologous T cells engineered to express a chimeric antigen receptor targeting BCMA (TNFRSF17) on plasma cells, activating T-cell cytotoxicity to eliminate malignant plasma cells in multiple myeloma.
Autologous T cells are engineered to express a chimeric antigen receptor that binds BCMA (TNFRSF17) on malignant plasma cells; CAR engagement activates T-cell signaling and cytotoxic effector functions (perforin/granzyme release, cytokines) to eliminate multiple myeloma cells.
NO
INDIRECT
BCMA-directed CAR-T cells recognize BCMA, not GPRC5D. They kill BCMA+ cells via CAR-activated T-cell cytotoxicity (perforin/granzyme); GPRC5D+ cells are not targeted unless they co-express BCMA.
Autologous T cells engineered to express a chimeric antigen receptor targeting GPRC5D, a GPCR highly expressed on plasma cells, to drive antigen-specific T-cell cytotoxicity against malignant plasma cells.
Autologous T cells engineered with a chimeric antigen receptor that recognizes GPRC5D on plasma cells; antigen binding triggers CAR signaling (CD3ζ with costimulatory domains) to activate T-cell cytotoxicity, cytokine release, and clonal expansion, leading to targeted lysis of GPRC5D-expressing malignant plasma cells.
YES
DIRECT
CAR-T cells bind GPRC5D, triggering CAR signaling (CD3ζ + costimulation) and T-cell effector functions that lyse target cells via perforin/granzyme release and Fas–FasL apoptosis.
Gene-edited autologous T-cell therapy in which CRISPR/Cas9 inserts a CD19-specific STAR receptor at the TRAC locus and ablates the endogenous TCR; the receptor signals via the native TCR–CD3 complex with OX40 costimulation to target CD19+ malignant B cells.
Autologous T cells are CRISPR/Cas9-edited to disrupt the endogenous TRAC and knock in a CD19-specific STAR receptor that grafts an anti-CD19 scFv onto TCR constant regions. This enables HLA-independent recognition of CD19 while signaling through the native TCR–CD3 complex with OX40 costimulation, driving activation, proliferation, and cytotoxic killing of CD19+ malignant B cells; TCR ablation reduces alloreactivity and GVHD risk.
YES
DIRECT
Engineered autologous T cells bearing a CD19-specific STAR receptor recognize CD19 on target cells and, via TCR–CD3 signaling with OX40 costimulation, induce T cell–mediated killing (perforin/granzyme and related cytotoxic pathways).
Anti-EGFR monoclonal antibody that blocks EGFR signaling, suppressing the RAS/RAF/MEK/ERK pathway in RAS/BRAF–wild type tumors.
HLX07 (pimurutamab) is a glycoengineered humanized anti-EGFR monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit EGFR-driven RAS/RAF/MEK/ERK signaling and tumor cell proliferation; glyco-optimization enhances ADCC.
YES
DIRECT
The anti‑EGFR antibody binds EGFR on target cells and its Fc engages FcγRIIIa (CD16) on NK cells to trigger ADCC, killing EGFR+ cells; complement activation and phagocytosis may also contribute, while signaling blockade is mainly cytostatic.
Humanized anti-HER2 monoclonal antibody that inhibits HER2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized monoclonal antibody targeting HER2; binds the extracellular domain to block HER2 signaling and receptor dimerization, and mediates antibody‑dependent cellular cytotoxicity (ADCC) against HER2‑overexpressing tumor cells.
YES
DIRECT
Trastuzumab binds HER2 on tumor cells and its Fc engages Fc gamma receptor–bearing immune cells (e.g., NK cells) to mediate ADCC (± complement), killing HER2-positive cells.