Anti-CD79b antibody-drug conjugate that delivers MMAE to CD79b-positive B cells, disrupting microtubules and inducing 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-positive malignant B cells.
YES
DIRECT
ADC binds CD79b on B cells, is internalized, linker is cleaved, and MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis of CD79b-positive cells.
Anti-CD79b antibody-drug conjugate that delivers MMAE to CD79b-positive B cells, disrupting microtubules and inducing 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-positive malignant B cells.
NO
INDIRECT
The ADC binds CD79b on B cells, is internalized, and releases MMAE, which binds the vinca site on beta-tubulin to disrupt microtubules and induce apoptosis; tubulin expression alone does not lead to targeting or killing.
Anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and direct apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and eliminates them via complement-dependent cytotoxicity and Fc-mediated ADCC by NK cells/macrophages; CD20 crosslinking can also trigger apoptosis.
Human IgG1 monoclonal antibody targeting PD-L1, blocking PD-L1/PD-1 interactions to enhance T-cell responses; can mediate ADCC.
Human IgG1 monoclonal antibody that binds PD-L1 and blocks its interaction with PD-1, releasing inhibitory checkpoint signaling to restore and enhance T‑cell antitumor activity; its Fc can also mediate ADCC against PD‑L1–expressing tumor cells.
YES
DIRECT
Avelumab binds PD-L1 on target cells and, via its IgG1 Fc, engages Fcγ receptor–bearing effector cells (e.g., NK cells) to trigger ADCC that kills PD-L1–expressing cells; checkpoint blockade also indirectly enhances T-cell killing.
A bispecific T-cell–engaging antibody (PF-06863135) targeting BCMA on myeloma cells and CD3 on T cells to redirect T-cell cytotoxicity against BCMA-positive cells.
Elranatamab is a bispecific antibody that binds BCMA on malignant plasma cells and CD3 on T cells, cross-linking them to form an immune synapse and activate cytotoxic T-cell killing of BCMA-positive myeloma cells.
YES
DIRECT
Elranatamab bridges CD3 on T cells and BCMA on target cells, forming an immune synapse that activates T-cell cytotoxicity (perforin/granzyme-mediated killing) of BCMA-positive cells.