Oral, small-molecule, highly selective HER2 tyrosine kinase inhibitor with CNS penetration; blocks HER2 phosphorylation and downstream PI3K/AKT/MAPK signaling.
Oral, selective HER2 (ErbB2) tyrosine kinase inhibitor that blocks HER2 autophosphorylation and downstream PI3K/AKT/MAPK signaling, leading to inhibition of proliferation and survival of HER2-overexpressing tumor cells; possesses CNS penetration supporting activity against brain metastases.
YES
DIRECT
Small-molecule HER2 TKI that blocks HER2 autophosphorylation and PI3K/AKT/MAPK survival signaling, causing cell-cycle arrest and apoptosis of HER2-expressing tumor cells (not immune-mediated).
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.
YES
DIRECT
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.
YES
DIRECT
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).
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.
NO
INDIRECT
T-DM1 binds HER2, is internalized, and releases DM1 that binds beta-tubulin to disrupt microtubules, causing mitotic arrest and apoptosis; beta-tubulin expression alone does not lead to targeting or killing.
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.
YES
DIRECT
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.