Anti-CD20 monoclonal antibody that depletes malignant B cells via antibody-dependent cellular cytotoxicity, complement activation, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive malignant B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and mediates killing via antibody-dependent cellular cytotoxicity (FcγR-engaged NK/macrophages), complement-dependent cytotoxicity (C1q/MAC), and can induce apoptosis upon CD20 cross-linking.
HER2-targeted antibody–drug conjugate that, after binding HER2, is internalized and releases MMAE to disrupt microtubules, causing mitotic arrest and apoptosis; can also mediate ADCC.
HER2-targeted monoclonal antibody linked to the cytotoxic payload MMAE. After binding HER2 on tumor cells, the ADC is internalized and the linker is cleaved to release MMAE, which disrupts microtubules to induce G2/M arrest and apoptosis; the antibody Fc can also mediate ADCC.
YES
DIRECT
The HER2-binding ADC is internalized after binding HER2; linker cleavage releases MMAE inside the cell, disrupting microtubules to cause G2/M arrest and apoptosis. The antibody Fc can also mediate ADCC against HER2+ cells.
HER2-targeted antibody–drug conjugate that, after binding HER2, is internalized and releases MMAE to disrupt microtubules, causing mitotic arrest and apoptosis; can also mediate ADCC.
HER2-targeted monoclonal antibody linked to the cytotoxic payload MMAE. After binding HER2 on tumor cells, the ADC is internalized and the linker is cleaved to release MMAE, which disrupts microtubules to induce G2/M arrest and apoptosis; the antibody Fc can also mediate ADCC.
NO
INDIRECT
RC48 binds HER2, is internalized, and releases MMAE, which binds beta‑tubulin to disrupt microtubules and trigger G2/M arrest and apoptosis in HER2+ cells; beta‑tubulin expression alone is not targeted or sufficient for killing.
CD79b-targeted antibody–drug conjugate that delivers monomethyl auristatin E (MMAE) to B cells, disrupting microtubules and inducing apoptosis.
Monoclonal antibody targets CD79b on B cells, is internalized, and releases the cytotoxin MMAE via a protease-cleavable linker; MMAE inhibits tubulin polymerization, disrupting microtubules, causing G2/M arrest and apoptosis of malignant B cells.
YES
DIRECT
Antibody-drug conjugate binds CD79b, is internalized, and releases MMAE after linker cleavage; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of CD79b+ cells.
CD79b-targeted antibody–drug conjugate that delivers monomethyl auristatin E (MMAE) to B cells, disrupting microtubules and inducing apoptosis.
Monoclonal antibody targets CD79b on B cells, is internalized, and releases the cytotoxin MMAE via a protease-cleavable linker; MMAE inhibits tubulin polymerization, disrupting microtubules, causing G2/M arrest and apoptosis of malignant B cells.
NO
INDIRECT
The ADC targets CD79b on B cells, is internalized, and releases MMAE; MMAE then binds beta-tubulin (vinca site) to disrupt microtubules, causing G2/M arrest and apoptosis. Tubulin is the payload’s intracellular target, not the cell-selection target.