An anti-HER2 antibody-drug conjugate (ADC) carrying the microtubule inhibitor MMAE. It binds HER2 on tumor cells, is internalized, and releases MMAE to inhibit microtubule polymerization, causing mitotic arrest and apoptosis; the antibody component may also trigger Fc-mediated ADCC.
HER2-targeted IgG1 antibody-drug conjugate delivering the microtubule inhibitor MMAE. After binding HER2 and internalization, MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the antibody Fc may also mediate ADCC.
YES
DIRECT
The ADC binds HER2, is internalized, and releases MMAE that inhibits microtubule polymerization, causing G2/M arrest and apoptosis; Fc engagement may also mediate ADCC.
An anti-HER2 antibody-drug conjugate (ADC) carrying the microtubule inhibitor MMAE. It binds HER2 on tumor cells, is internalized, and releases MMAE to inhibit microtubule polymerization, causing mitotic arrest and apoptosis; the antibody component may also trigger Fc-mediated ADCC.
HER2-targeted IgG1 antibody-drug conjugate delivering the microtubule inhibitor MMAE. After binding HER2 and internalization, MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the antibody Fc may also mediate ADCC.
NO
INDIRECT
Disitamab vedotin binds HER2, is internalized, and releases MMAE that binds the vinca site on beta‑tubulin to disrupt microtubules, causing G2/M arrest and apoptosis in HER2+ cells (with possible Fc-mediated ADCC). Beta‑tubulin expression alone does not confer susceptibility.
Humanized anti-HER2 monoclonal antibody that blocks HER2 signaling/dimerization and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized monoclonal antibody to HER2 (ERBB2) that binds the extracellular domain, blocks receptor dimerization/signaling to inhibit PI3K/AKT and MAPK pathways, and mediates antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
YES
DIRECT
Trastuzumab binds HER2 and opsonizes target cells, engaging Fcγ receptor–bearing effector cells (e.g., NK cells) to mediate ADCC; may also activate complement (CDC).
Autologous, second-generation chimeric antigen receptor T cells engineered to recognize mesothelin on tumor cells and to secrete an IL-21–anti-PD-1 scFv fusion protein for localized cytokine support and checkpoint blockade, enhancing T-cell activation, proliferation, persistence, and cytotoxicity.
Autologous second-generation CAR T cells engineered to recognize mesothelin on tumor cells; CAR engagement (CD3ζ plus costimulatory signaling) activates T-cell cytotoxicity against mesothelin-positive cells, while secretion of an IL-21–anti-PD-1 scFv provides local IL-21 support and PD-1 checkpoint blockade to boost activation, proliferation, persistence, and resistance to exhaustion in the tumor microenvironment.
YES
DIRECT
Mesothelin-specific CAR T cells bind mesothelin on target cells and kill them via T-cell cytotoxic pathways (perforin/granzyme release and death-receptor signaling); IL-21–anti-PD-1 scFv enhances activation/persistence.
Autologous, second-generation chimeric antigen receptor T cells engineered to recognize mesothelin on tumor cells and to secrete an IL-21–anti-PD-1 scFv fusion protein for localized cytokine support and checkpoint blockade, enhancing T-cell activation, proliferation, persistence, and cytotoxicity.
Autologous second-generation CAR T cells engineered to recognize mesothelin on tumor cells; CAR engagement (CD3ζ plus costimulatory signaling) activates T-cell cytotoxicity against mesothelin-positive cells, while secretion of an IL-21–anti-PD-1 scFv provides local IL-21 support and PD-1 checkpoint blockade to boost activation, proliferation, persistence, and resistance to exhaustion in the tumor microenvironment.
NO
INDIRECT
The drug secretes an anti-PD-1 scFv that blocks PD-1 signaling to boost CAR-T activation; it does not target or kill PD-1-expressing cells. Cytotoxicity is directed against mesothelin-positive tumor cells via CAR-mediated T-cell killing.