Autologous TCR-engineered T-cell therapy targeting HPV18-derived peptide presented by HLA-DRB1*09:01; administered as a single infusion to mediate antigen-specific cytotoxicity.
Autologous T cells are engineered to express a T-cell receptor that recognizes an HPV18-derived peptide presented by HLA-DRB1*09:01 on tumor cells. Antigen engagement triggers TCR signaling, activation, proliferation, cytokine release, and cytotoxic killing (perforin/granzyme and death receptor pathways) of HPV18-positive tumor cells.
YES
DIRECT
Engineered TCR-T cells recognize the HPV18-derived peptide presented by HLA-DRB1*09:01 and directly kill target cells via perforin/granzyme release and death receptor–mediated apoptosis.
Bispecific T-cell engager (BiTE) that links CD3 on T cells to CD19 on B cells, activating T-cell–mediated cytotoxicity.
A bispecific single-chain antibody (BiTE) that binds CD19 on B cells and CD3 on T cells, physically bringing T cells into contact with CD19+ cells to trigger TCR/CD3-mediated activation, cytolytic synapse formation, cytokine release, and perforin/granzyme-dependent killing of malignant B cells.
YES
DIRECT
Blinatumomab bridges CD3+ T cells to CD19+ cells, activating T cells to form a cytolytic synapse and kill targets via perforin/granzyme-dependent apoptosis.
Autologous TCR-engineered T-cell therapy targeting HPV18-derived peptide presented by HLA-DRB1*09:01; administered as a single infusion to mediate antigen-specific cytotoxicity.
Autologous T cells are engineered to express a T-cell receptor that recognizes an HPV18-derived peptide presented by HLA-DRB1*09:01 on tumor cells. Antigen engagement triggers TCR signaling, activation, proliferation, cytokine release, and cytotoxic killing (perforin/granzyme and death receptor pathways) of HPV18-positive tumor cells.
YES
DIRECT
TCR-engineered T cells recognize the HPV18-derived peptide presented by HLA-DRB1*09:01 on tumor cells and directly kill them via perforin/granzyme and death receptor pathways.
An allogeneic, off-the-shelf CD70-directed CAR T-cell therapy (UCAR-T). Gene-engineered T cells express a chimeric antigen receptor targeting CD70 to activate T-cell signaling (CD3ζ and costimulatory domains), leading to cytokine release and cytolytic elimination of CD70-positive tumor cells and modulation of the CD70–CD27 axis.
Allogeneic (off-the-shelf) T cells are gene-engineered to express a CD70-directed chimeric antigen receptor. Upon binding CD70 on tumor cells, CAR signaling (CD3zeta with costimulatory domains) activates T-cell effector functions, leading to cytokine release and targeted cytolytic killing of CD70-positive cells and modulation of the CD70–CD27 axis, independent of the native T-cell receptor.
YES
DIRECT
CD70-directed CAR T cells bind CD70 on target cells, triggering CAR signaling and T‑cell effector functions that kill CD70-positive cells via perforin/granzyme-mediated cytolysis (and death receptor pathways).
Chimeric IgG1 monoclonal antibody targeting EGFR to block ligand-mediated signaling and promote antibody-dependent cytotoxicity.
Chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream MAPK signaling and tumor cell proliferation; its Fc region also engages immune effector cells to promote antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
Cetuximab binds EGFR on target cells and its IgG1 Fc engages FcγR-bearing immune cells (e.g., NK cells) to induce ADCC (and potentially complement-mediated lysis), killing EGFR+ cells; signaling blockade is antiproliferative.