HER2-directed antibody-drug conjugate linking trastuzumab to the maytansinoid microtubule inhibitor DM1, delivering the cytotoxic payload to HER2-expressing cancer cells to disrupt microtubules and inhibit proliferation.
HER2-directed antibody-drug conjugate linking trastuzumab to the maytansinoid DM1. Binds HER2 on tumor cells, is internalized, and releases DM1 intracellularly to inhibit microtubule function, causing mitotic arrest and apoptosis; also retains trastuzumab-mediated HER2 signaling blockade and ADCC.
YES
DIRECT
Binds HER2, is internalized, and releases the DM1 payload that disrupts microtubules, causing mitotic arrest and apoptosis (with additional Fc-mediated ADCC).
HER2-directed antibody-drug conjugate linking trastuzumab to the maytansinoid microtubule inhibitor DM1, delivering the cytotoxic payload to HER2-expressing cancer cells to disrupt microtubules and inhibit proliferation.
HER2-directed antibody-drug conjugate linking trastuzumab to the maytansinoid DM1. Binds HER2 on tumor cells, is internalized, and releases DM1 intracellularly to inhibit microtubule function, causing mitotic arrest and apoptosis; also retains trastuzumab-mediated HER2 signaling blockade and ADCC.
NO
INDIRECT
T-DM1 binds HER2, is internalized, then releases DM1 that binds β-tubulin to disrupt microtubules and trigger mitotic arrest/apoptosis. Killing depends on HER2 expression, not β-tubulin expression alone.
Anti-CD20 monoclonal antibody that depletes B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Binds CD20 on B cells and induces killing via Fc-mediated ADCC by effector cells, complement-dependent cytotoxicity, and direct apoptosis upon CD20 cross-linking.
Gene-modified autologous T cells expressing a chimeric antigen receptor targeting CD19 on malignant B cells; mediates cytotoxicity and cytokine release.
Autologous T cells genetically engineered to express a CD19-specific chimeric antigen receptor; upon binding CD19 on malignant B cells, the CAR provides activation and co-stimulatory signaling (e.g., CD3zeta with CD28/4-1BB), driving T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated lysis of CD19+ cells.
YES
DIRECT
CD19-specific CAR-T cells bind CD19 on target cells, become activated, and kill via perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis.
Chimeric IgG1 monoclonal antibody targeting GD2 on neuroblastoma cells; mediates ADCC and complement-dependent cytotoxicity.
Chimeric IgG1 monoclonal antibody that binds GD2 on tumor cells and induces immune-mediated killing via antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC), leading to lysis of GD2-expressing cells.
YES
DIRECT
Dinutuximab binds GD2 on target cells; its Fc engages FcγR-expressing effector cells to mediate ADCC and activates complement to induce CDC, causing lysis of GD2+ cells.