Autologous, genetically engineered TCR-T cell therapy expressing an HLA-A*11:01–restricted T cell receptor specific for the KRAS G12V neoantigen; administered after lymphodepletion with a single IV infusion to recognize KRAS G12V peptides on tumor HLA-A*11:01, expand (with low-dose IL-2 support), and mediate cytotoxic killing of tumor cells in advanced solid tumors.
Autologous T cells genetically engineered to express an HLA-A*11:01–restricted TCR specific for the KRAS G12V neoantigen; after lymphodepletion and low-dose IL-2 support, the infused cells recognize KRAS G12V peptides presented on tumor HLA-A*11:01, expand, and mediate cytotoxic killing of mutant KRAS–expressing tumor cells.
YES
DIRECT
Engineered TCR-T cells recognize the KRAS G12V peptide presented by HLA-A*11:01 on tumor cells and directly induce apoptosis via perforin/granzyme release and Fas–FasL signaling.
Anti-CD79b antibody-drug conjugate that delivers the microtubule inhibitor MMAE (monomethyl auristatin E) to B cells.
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 CD79b-expressing malignant B cells.
YES
DIRECT
ADC binds CD79B on B cells, is internalized, linker is cleaved to release MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis of CD79B-expressing cells.
Anti-CD79b antibody-drug conjugate that delivers the microtubule inhibitor MMAE (monomethyl auristatin E) to B cells.
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 CD79b-expressing malignant B cells.
NO
INDIRECT
The ADC targets CD79b on B cells; only CD79b-positive cells internalize the drug and release MMAE, which then binds the beta-tubulin (vinca) site to block microtubules and induce apoptosis. Tubulin expression alone does not confer susceptibility without CD79b-mediated uptake.
Anti-CD20 chimeric monoclonal antibody that depletes CD20-positive B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20-positive cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and eliminates them via Fc-mediated ADCC (NK cells/macrophages), complement-dependent cytotoxicity, and direct induction of apoptosis.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks EGFR/MET signaling, promotes receptor internalization/degradation, and mediates Fc-dependent cytotoxicity (ADCC/ADCP); administered IV.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks EGFR/MET signaling, induces receptor internalization and degradation, and engages Fc receptors to mediate ADCC/ADCP against tumor cells.
YES
DIRECT
Amivantamab binds EGFR on target cells and engages Fcγ receptors on NK cells/macrophages to trigger ADCC/ADCP, leading to killing of EGFR-expressing cells.