Autologous T cells genetically engineered to express a chimeric antigen receptor targeting CD7 to eradicate CD7-positive malignant T lymphoblasts via CAR-mediated activation and cytotoxicity.
Autologous T cells are genetically engineered to express a CD7-specific chimeric antigen receptor. Binding to CD7 on malignant T lymphoblasts triggers CAR-mediated CD3ζ/co-stimulatory signaling, activating and expanding the T cells to kill targets via perforin/granzyme cytotoxicity, leading to depletion of CD7-positive cells.
CAR recognition of CD7 activates T cells via CD3ζ/co-stimulatory signaling, inducing perforin/granzyme-mediated cytolysis (and apoptosis) of CD7-positive cells.
Recombinant anti-EpCAM×CD3 T-cell–redirecting bispecific antibody administered by IV infusion; binds EpCAM on tumor cells and CD3 on T cells to form an immune synapse, activate CD3/TCR signaling, and induce T-cell–mediated cytotoxicity and cytokine release against EpCAM-positive epithelial cancers. Also referred to as 'Recombinant Anti-EpCAM-CD3 Antibody Injection.'
Recombinant bispecific antibody that simultaneously binds EpCAM (CD326) on epithelial tumor cells and CD3 on T cells, forming an immune synapse that activates CD3/TCR signaling and redirects cytotoxic T-cell activity to lyse EpCAM-positive tumor cells with associated cytokine release.
Bispecific T‑cell engager binds EpCAM on tumor cells and CD3 on T cells, forming an immune synapse that activates CTLs to kill EpCAM+ cells via perforin/granzyme (and Fas/FasL) with associated cytokine release.
Autologous tumor-infiltrating lymphocyte (TIL) cellular therapy manufactured from a patient’s tumor, expanded ex vivo, and reinfused to mediate antitumor activity through native TCR recognition, cytotoxic mechanisms, and cytokine secretion.
Autologous TILs expanded ex vivo and reinfused; they recognize patient-specific tumor antigens via native TCR–MHC interactions and mediate antitumor effects through cytotoxic killing (perforin/granzymes) and cytokine secretion within the tumor microenvironment.
Autologous TILs recognize the tumor neoantigen peptide–HLA class I complex via their native TCR, then kill the target cell by cytotoxic granule release (perforin/granzymes) and Fas–FasL–mediated apoptosis.
Humanized IgG1 monoclonal antibody targeting the HER2 extracellular dimerization domain (subdomain II); blocks HER2/HER3 dimerization, inhibiting downstream PI3K/AKT/MAPK signaling, and engages Fc-mediated ADCC to promote tumor cell killing.
Pertuzumab binds HER2 on tumor cells and engages Fcγ receptors on immune effectors to trigger ADCC; blockade of HER2/HER3 signaling also promotes apoptosis.