Anti-CD79b antibody–drug conjugate that delivers MMAE to CD79b+ 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 of malignant B cells.
YES
DIRECT
Anti‑CD79b ADC binds CD79b on B cells, is internalized, and releases MMAE after linker cleavage; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of the target cells.
Anti-CD79b antibody–drug conjugate that delivers MMAE to CD79b+ 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 of malignant B cells.
NO
INDIRECT
The ADC binds CD79b on B cells, is internalized, and releases MMAE, which binds beta-tubulin to block microtubule polymerization, causing mitotic arrest and apoptosis. Beta-tubulin expression alone is not sufficient; only CD79b+ cells are killed.
Anti-CD20 monoclonal antibody that mediates B-cell depletion via CDC, ADCC, and apoptosis.
Anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature 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 kills via complement-dependent cytotoxicity (MAC lysis), antibody-dependent cellular cytotoxicity by FcγR-bearing effector cells, and direct apoptosis upon crosslinking.
Autologous cellular immunotherapy comprising dendritic cells and activated effector T cells; dendritic cells present tumor antigens via MHC I/II to prime tumor-specific T cells, and infused T cells mediate cytotoxicity via perforin/granzyme and IFN-γ.
Autologous dendritic cells loaded with tumor antigens present peptides via MHC I/II to prime and expand tumor-specific T cells, while co-infused activated effector T cells mediate tumor cell killing through perforin/granzyme release and IFN-γ–driven Th1 cytotoxic responses.
YES
DIRECT
Vaccine-primed/infused CD8+ T cells recognize the tumor peptide–HLA class I complex via the TCR and kill target cells via perforin/granzyme-mediated cytotoxicity (±Fas–FasL), supported by IFN-γ–driven Th1 responses.
Autologous cellular immunotherapy comprising dendritic cells and activated effector T cells; dendritic cells present tumor antigens via MHC I/II to prime tumor-specific T cells, and infused T cells mediate cytotoxicity via perforin/granzyme and IFN-γ.
Autologous dendritic cells loaded with tumor antigens present peptides via MHC I/II to prime and expand tumor-specific T cells, while co-infused activated effector T cells mediate tumor cell killing through perforin/granzyme release and IFN-γ–driven Th1 cytotoxic responses.
YES
INDIRECT
DC vaccination primes tumor-specific T cells; these T cells recognize the tumor peptide–HLA class II complex via the TCR and kill target cells mainly via perforin/granzyme (with IFN-γ–driven Th1 responses and Fas/FasL contributing).