Anti‑CD79b antibody–drug conjugate that delivers MMAE, a microtubule inhibitor, to B‑cell lymphomas.
Anti-CD79b monoclonal antibody–drug conjugate that binds CD79b on B cells, is internalized, and releases MMAE via a protease-cleavable linker; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of malignant B cells.
NO
INDIRECT
The ADC binds CD79b on B cells and is internalized; the released MMAE then binds beta-tubulin (vinca site) to inhibit microtubules, causing G2/M arrest and apoptosis. Tubulin expression alone does not target cells for killing.
Chimeric anti‑CD20 monoclonal antibody that mediates B‑cell depletion via ADCC and complement.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes them via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and antibody-dependent phagocytosis; may also trigger direct apoptosis of CD20-positive B cells.
YES
DIRECT
Binds CD20 on B cells and induces killing via Fc-mediated ADCC (NK cells/macrophages), complement-dependent cytotoxicity, antibody-dependent phagocytosis, and can trigger direct apoptosis of CD20+ cells.
An autologous NKG2D-based CAR T-cell therapy in which patient T cells are gene-engineered to express a chimeric antigen receptor using the NKG2D receptor ectodomain fused to intracellular activation/costimulatory domains (e.g., CD3ζ). The cells target stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumor cells to mediate cytotoxicity and cytokine release.
Autologous T cells are engineered to express an NKG2D-based CAR (NKG2D ectodomain fused to 4-1BB and CD3ζ signaling domains) that recognizes stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumors, activating T cells to release cytokines and mediate perforin/granzyme-dependent cytotoxicity against NKG2DL-positive cancer cells.
YES
DIRECT
NKG2D CAR T cells recognize and bind MICA on target cells, triggering 4-1BB/CD3ζ signaling and killing via perforin/granzyme-mediated cytotoxicity (with cytokine release).
Autologous, gene-modified T cells engineered with the Sleeping Beauty transposon/transposase system to stably express patient-specific, tumor-reactive T-cell receptors targeting mutation-derived neoantigen peptides presented on HLA; upon infusion, these cells activate TCR-CD3 signaling to mediate cytotoxic killing (perforin/granzyme) and may generate immunologic memory.
Autologous T cells are gene-modified with the Sleeping Beauty transposon/transposase system to stably express patient-specific, tumor-reactive TCRs that recognize mutation-derived neoantigen peptides presented on HLA (primarily MHC I). Upon infusion, engagement of the TCR-CD3 complex triggers activation, clonal expansion, cytokine release, and cytotoxic killing of tumor cells via perforin/granzyme, with potential development of immunologic memory.
YES
DIRECT
Engineered TCR-T cells bind the neoantigen peptide–HLA complex on tumor cells, triggering cytotoxic T-cell activity and killing via perforin/granzyme-mediated apoptosis (and Fas–FasL pathways).
Autologous, gene-modified T cells engineered with the Sleeping Beauty transposon/transposase system to stably express patient-specific, tumor-reactive T-cell receptors targeting mutation-derived neoantigen peptides presented on HLA; upon infusion, these cells activate TCR-CD3 signaling to mediate cytotoxic killing (perforin/granzyme) and may generate immunologic memory.
Autologous T cells are gene-modified with the Sleeping Beauty transposon/transposase system to stably express patient-specific, tumor-reactive TCRs that recognize mutation-derived neoantigen peptides presented on HLA (primarily MHC I). Upon infusion, engagement of the TCR-CD3 complex triggers activation, clonal expansion, cytokine release, and cytotoxic killing of tumor cells via perforin/granzyme, with potential development of immunologic memory.
YES
DIRECT
Engineered TCR-T cells recognize the neoantigen peptide–HLA-A complex via TCR/CD3, form an immune synapse, and induce apoptosis of target cells through perforin/granzyme release (and Fas–FasL).