Anti-HER2 monoclonal antibody that inhibits HER2 signaling, promotes receptor down-regulation, and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized anti-HER2 monoclonal antibody that binds the extracellular domain of HER2, inhibits HER2 signaling and receptor dimerization, promotes receptor internalization/downregulation, and mediates antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on target cells and its Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells) to mediate antibody‑dependent cellular cytotoxicity; complement activation may also contribute.
HER2-targeted antibody–drug conjugate delivering the microtubule inhibitor DM1, inducing mitotic arrest and apoptosis.
Ado‑trastuzumab emtansine (T‑DM1) is a HER2‑targeted antibody–drug conjugate in which trastuzumab delivers the microtubule inhibitor DM1 to HER2‑overexpressing tumor cells. After HER2 binding and internalization, lysosomal processing releases DM1 to inhibit microtubules, causing mitotic arrest and apoptosis; the trastuzumab moiety also inhibits HER2 signaling and can mediate ADCC.
The ADC binds HER2, is internalized, and releases the DM1 microtubule inhibitor intracellularly, causing microtubule disruption, mitotic arrest, and apoptosis (with additional Fc-mediated ADCC possible).
Autologous ex vivo–expanded tumor-infiltrating T cells administered as adoptive cell transfer to mediate antitumor immunity after lymphodepleting conditioning.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused after lymphodepleting conditioning. These polyclonal T cells use their native TCRs to recognize patient-specific tumor antigens in an HLA-restricted manner, engraft and expand (often supported by IL-2), and mediate antitumor effects via cytotoxic granule release and cytokine secretion.
TIL use native TCRs to recognize tumor antigenic peptide–HLA-A on target cells and directly kill them via perforin/granzyme release and Fas–FasL–mediated apoptosis.
Autologous ex vivo–expanded tumor-infiltrating T cells administered as adoptive cell transfer to mediate antitumor immunity after lymphodepleting conditioning.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused after lymphodepleting conditioning. These polyclonal T cells use their native TCRs to recognize patient-specific tumor antigens in an HLA-restricted manner, engraft and expand (often supported by IL-2), and mediate antitumor effects via cytotoxic granule release and cytokine secretion.
TILs use native TCRs to recognize the tumor peptide–HLA-B complex on target cells, triggering cytotoxic T-cell killing via perforin/granzyme release and death receptor pathways (e.g., Fas–FasL).
Autologous ex vivo–expanded tumor-infiltrating T cells administered as adoptive cell transfer to mediate antitumor immunity after lymphodepleting conditioning.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused after lymphodepleting conditioning. These polyclonal T cells use their native TCRs to recognize patient-specific tumor antigens in an HLA-restricted manner, engraft and expand (often supported by IL-2), and mediate antitumor effects via cytotoxic granule release and cytokine secretion.
TILs use their native TCRs to recognize tumor antigenic peptide–HLA-C complexes and directly lyse target cells via perforin/granzyme release (and Fas–FasL), with cytokine-mediated support.