Autologous tumor-infiltrating lymphocyte (TIL) adoptive cell therapy consisting of ex vivo–expanded, polyclonal CD8+/CD4+ T cells that recognize patient-specific tumor antigens via native TCRs and kill tumor cells through cytotoxic granules and cytokines.
Autologous ex vivo–expanded polyclonal CD8+/CD4+ tumor-infiltrating lymphocytes that recognize patient-specific tumor antigens via native TCRs and eliminate tumor cells through perforin/granzyme-mediated cytotoxicity and cytokine secretion (e.g., IFN-γ, TNF).
Autologous TILs recognize the neoantigen–HLA class II complex via native TCRs (primarily CD4+ T cells) and directly kill target cells through perforin/granzyme release and death-receptor pathways, with IFN-γ/TNF further promoting apoptosis.
Autologous T cells engineered to express a chimeric antigen receptor targeting carcinoembryonic antigen (CEA/CEACAM5); administered intraperitoneally to mediate CAR signaling and cytotoxic killing of CEA-positive tumor cells.
Autologous T cells engineered to express a chimeric antigen receptor specific for CEA (CEACAM5). CAR engagement with CEA on tumor cells triggers CD3ζ/co-stimulatory signaling, activating T-cell cytotoxicity and cytokine release to kill CEA-positive cancer cells. Administered intraperitoneally to target peritoneal tumor deposits.
CEA-targeted CAR-T cells bind CEACAM5 on tumor cells, trigger CD3ζ/co-stimulatory activation, and kill via perforin/granzyme-mediated cytolysis and death-receptor pathways.
Autologous tumor-infiltrating lymphocyte (TIL) adoptive cell therapy consisting of ex vivo–expanded, polyclonal CD8+/CD4+ T cells that recognize patient-specific tumor antigens via native TCRs and kill tumor cells through cytotoxic granules and cytokines.
Autologous ex vivo–expanded polyclonal CD8+/CD4+ tumor-infiltrating lymphocytes that recognize patient-specific tumor antigens via native TCRs and eliminate tumor cells through perforin/granzyme-mediated cytotoxicity and cytokine secretion (e.g., IFN-γ, TNF).
Native TCRs on infused TILs recognize the tumor-associated peptide–HLA class II complex and directly lyse the presenting cells via perforin/granzyme release (with supportive cytokines such as IFN-γ/TNF).
Humanized anti-HER2 monoclonal antibody (trastuzumab-like) that binds the HER2 extracellular domain, inhibits HER2 signaling, and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized anti-HER2 monoclonal antibody that binds the HER2 extracellular domain, blocks HER2 receptor activation and dimerization to inhibit downstream signaling and tumor cell proliferation, and recruits immune effector cells to mediate antibody-dependent cellular cytotoxicity (ADCC).
Binds HER2 on tumor cells and engages Fcγ receptor–bearing immune cells (e.g., NK cells) to trigger ADCC, leading to lysis of HER2+ cells; also blocks HER2 signaling (primarily cytostatic).
Humanized monoclonal antibody targeting the HER2 extracellular dimerization domain (subdomain II); blocks HER2 heterodimerization, especially HER2/HER3, thereby inhibiting downstream PI3K/AKT and MAPK signaling and leading to tumor cell growth inhibition and apoptosis (with potential ADCC contribution).
Pertuzumab binds HER2, blocks HER2 dimerization and survival signaling to induce apoptosis, and its Fc engages Fcγ receptor–bearing immune cells to mediate ADCC against HER2-expressing cells.