Patient-derived tumor-resident T cells isolated, expanded, and activated ex vivo, then reinfused to mediate antigen-specific cytotoxicity via TCR recognition of tumor antigens.
Autologous tumor-resident T cells are isolated from the patient’s tumor, expanded and activated ex vivo, then reinfused to recognize tumor antigens via their native TCRs presented on MHC, mediating antigen-specific cytotoxicity through perforin/granzyme release and cytokine secretion; supportive IL-2 can enhance survival and expansion.
TILs recognize the tumor-associated peptide–MHC class II complex via their native TCRs and kill the presenting cell through perforin/granzyme-mediated cytolysis and Fas–FasL–induced apoptosis.
Allogeneic donor-derived T cells genetically modified to express a chimeric antigen receptor targeting CD19 on B-lineage leukemia cells; administered as a bridge to allo-HSCT to mediate antigen-specific cytotoxicity.
Allogeneic donor-derived T cells are genetically engineered to express a CD19-specific chimeric antigen receptor. Upon binding CD19 on B-lineage leukemia cells, CAR signaling (CD3ζ with costimulatory domains) activates the T cells, inducing proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of CD19+ malignant cells; used as a bridge to allo-HSCT.
CD19 CAR-T cells bind CD19 on target B cells, become activated, and kill them via perforin/granzyme-mediated cytolysis (and apoptosis).
Allogeneic donor-derived T cells engineered to express a chimeric antigen receptor targeting CD22; given sequentially post-transplant to address antigen-loss relapse and sustain leukemia control.
Allogeneic donor-derived T cells are genetically engineered to express a CD22-directed chimeric antigen receptor. CAR engagement of CD22 on B-lineage leukemia cells triggers CD3ζ/costimulatory signaling, activating T-cell cytotoxicity (perforin/granzyme) and cytokine release to eliminate target cells. Delivered sequentially post-allo-HSCT to mitigate antigen-loss relapse and sustain leukemia control.
CD22 CAR-T cells bind CD22 on target cells, triggering CD3ζ/costimulatory signaling and T‑cell effector functions (perforin/granzyme-mediated apoptosis; also Fas/FasL) to kill the CD22+ cells.
Autologous gene-modified T cells engineered to express a chimeric antigen receptor targeting EX02 on tumor cells; administered intratumorally or intraperitoneally (with possible IV infusion after lymphodepletion) to induce T-cell activation, cytotoxicity, and cytokine release against EX02-positive cancer cells.
Autologous T cells are engineered to express a chimeric antigen receptor that recognizes EX02 on tumor cells, enabling MHC-independent binding and activation of the T cell. CAR engagement triggers T‑cell activation, proliferation, cytokine release, and cytotoxic killing (e.g., perforin/granzyme) of EX02‑positive cancer cells. Administered intratumorally or intraperitoneally (with optional IV after lymphodepletion) to enhance expansion and persistence.
CAR T cells recognize EX02 on target cells and, upon engagement, kill them via contact-dependent cytotoxicity (perforin/granzyme release and death-receptor pathways).
Bispecific IgG1 monoclonal antibody targeting EGFR and LGR5; inhibits EGFR signaling, promotes receptor internalization, and mediates ADCC to eliminate EGFR+/LGR5+ HNSCC cells, including stem-like cells.
Bispecific IgG1 monoclonal antibody that binds EGFR and LGR5 on tumor cells to block EGFR signaling, promote receptor internalization/degradation, and leverage Fc-mediated ADCC to eliminate EGFR+/LGR5+ cancer cells, including stem-like populations.
IgG1 Fc engages FcγR+ effector cells (e.g., NK cells) to mediate ADCC against tumor cells co-expressing EGFR (and LGR5); EGFR blockade/internalization occurs but killing is primarily via ADCC.