A T-cell–engaging bispecific monoclonal antibody (2:1 CD20:CD3) that binds CD20 on B cells and CD3 on T cells to activate cytotoxic T-cell killing of malignant B cells.
A 2:1 CD20:CD3 bispecific monoclonal antibody that co-binds CD20 on B cells and CD3 on T cells, cross-linking them to form an immunologic synapse and activate cytotoxic T-cell killing of CD20-positive malignant B cells.
NO
INDIRECT
Glofitamab binds CD3ε on T cells and CD20 on B cells to form an immunologic synapse, activating T-cell cytotoxicity that kills CD20+ B cells; CD3ε-expressing T cells are not killed.
An anti-CD79b antibody–drug conjugate that delivers the microtubule inhibitor MMAE to CD79b+ B cells, inducing mitotic arrest and apoptosis.
Anti-CD79b monoclonal antibody linked via a protease-cleavable linker to the microtubule inhibitor MMAE. After binding CD79b on B cells and internalization, MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in CD79b+ malignant B cells.
YES
DIRECT
ADC binds CD79b on B cells, is internalized, linker cleaved to release MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis of CD79b+ cells.
An anti-CD79b antibody–drug conjugate that delivers the microtubule inhibitor MMAE to CD79b+ B cells, inducing mitotic arrest and apoptosis.
Anti-CD79b monoclonal antibody linked via a protease-cleavable linker to the microtubule inhibitor MMAE. After binding CD79b on B cells and internalization, MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in CD79b+ malignant B cells.
NO
INDIRECT
Polatuzumab vedotin targets CD79b on B cells, is internalized, and releases MMAE, which binds beta-tubulin to disrupt microtubes, causing G2/M arrest and apoptosis. Beta-tubulin is the payload’s intracellular target, not the drug’s direct targeting antigen.
A glycoengineered type II anti-CD20 monoclonal antibody that enhances ADCC/ADCP and induces direct B-cell death; used pre-glofitamab to debulk and mitigate CRS.
Glycoengineered type II humanized anti-CD20 IgG1 that binds CD20 on B cells; afucosylated Fc increases affinity for Fc gamma RIIIa to enhance ADCC and ADCP, and it induces direct, caspase-independent B-cell death, depleting malignant CD20+ B cells.
YES
DIRECT
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages FcγRIIIa on NK cells/macrophages to drive ADCC/ADCP and it also induces direct, caspase‑independent B‑cell death.
A glycoengineered type II anti-CD20 monoclonal antibody that enhances ADCC/ADCP and induces direct B-cell death; used pre-glofitamab to debulk and mitigate CRS.
Glycoengineered type II humanized anti-CD20 IgG1 that binds CD20 on B cells; afucosylated Fc increases affinity for Fc gamma RIIIa to enhance ADCC and ADCP, and it induces direct, caspase-independent B-cell death, depleting malignant CD20+ B cells.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages FcγRIIIa (CD16a) on NK cells/monocytes to drive ADCC/ADCP, killing CD20+ B cells. CD16a+ cells serve as effectors and are not targeted for killing.