Type II, glycoengineered, humanized anti-CD20 monoclonal antibody that binds CD20 on B cells to induce direct cell death and enhance antibody-dependent cellular cytotoxicity and phagocytosis, depleting malignant CD20+ B cells.
Type II, glycoengineered humanized anti-CD20 IgG1 that binds CD20 on B cells and depletes malignant CD20+ cells by inducing direct cell death and enhancing FcγRIIIa-mediated ADCC and antibody-dependent phagocytosis; Fc glycoengineering (reduced fucosylation) increases effector function.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its Fc engages FcγRIIIa (CD16a) on NK cells/macrophages to trigger ADCC/ADCP against CD20+ B cells. CD16a-expressing cells act as effectors and are not killed by the drug.
Type II, glycoengineered, humanized anti-CD20 monoclonal antibody that binds CD20 on B cells to induce direct cell death and enhance antibody-dependent cellular cytotoxicity and phagocytosis, depleting malignant CD20+ B cells.
Type II, glycoengineered humanized anti-CD20 IgG1 that binds CD20 on B cells and depletes malignant CD20+ cells by inducing direct cell death and enhancing FcγRIIIa-mediated ADCC and antibody-dependent phagocytosis; Fc glycoengineering (reduced fucosylation) increases effector function.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its Fc engages Fcγ receptors (primarily CD16a on NK cells, and can engage CD16b on neutrophils) to mediate ADCC/phagocytosis against CD20+ cells. CD16b-expressing cells are effector cells, not targets, and are not directly killed.
Antibody–drug conjugate targeting integrin αvβ6; internalization releases the vedotin payload MMAE (monomethyl auristatin E), a microtubule-disrupting agent that causes G2/M arrest and apoptosis.
Monoclonal antibody targets integrin αvβ6 on tumor cells, is internalized, and releases the vedotin payload MMAE via a cleavable linker. MMAE disrupts microtubules by inhibiting tubulin polymerization, causing G2/M arrest and apoptosis, with potential bystander killing.
YES
DIRECT
ADC binds integrin αvβ6 on target cells, is internalized, and releases MMAE via a cleavable linker; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis (with potential bystander killing).
Antibody–drug conjugate targeting integrin αvβ6; internalization releases the vedotin payload MMAE (monomethyl auristatin E), a microtubule-disrupting agent that causes G2/M arrest and apoptosis.
Monoclonal antibody targets integrin αvβ6 on tumor cells, is internalized, and releases the vedotin payload MMAE via a cleavable linker. MMAE disrupts microtubules by inhibiting tubulin polymerization, causing G2/M arrest and apoptosis, with potential bystander killing.
YES
INDIRECT
The ADC binds integrin αvβ6, is internalized, and releases MMAE, which binds β-tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis (with potential bystander killing).
An autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy. Patient T cells are genetically engineered to express an anti-CD19 CAR; upon engagement of CD19 on B-lineage malignant cells, the CAR T cells activate and mediate cytotoxicity, leading to elimination of CD19+ tumor cells and on-target B-cell depletion. Administered as a single IV infusion (0.5–6×10^6 cells/kg).
Autologous patient T cells are engineered to express an anti-CD19 chimeric antigen receptor; upon binding CD19 on B-lineage malignant cells, the CAR T cells activate, proliferate, and mediate cytotoxic killing, eliminating CD19-positive tumor cells and causing on-target B-cell depletion.
YES
DIRECT
Anti-CD19 CAR T cells recognize CD19, become activated, and kill CD19+ cells via perforin/granzyme-mediated cytolysis and apoptosis (e.g., Fas/FasL), causing on-target B-cell depletion.