Anti-CD38 IgG1 monoclonal antibody that depletes CD38+ plasmablasts and plasma cells to reduce anti-FVIII alloantibody production.
Human IgG1 anti‑CD38 monoclonal antibody that binds CD38 on plasmablasts, plasma cells, and other CD38+ immune cells and depletes them via Fc‑mediated effector functions (ADCC, ADCP) and complement‑dependent cytotoxicity (CDC), thereby reducing anti‑FVIII alloantibody production and modulating immune responses.
YES
DIRECT
Daratumumab binds CD38 on target cells and triggers Fc-mediated ADCC (NK cells), ADCP (macrophages), and complement-dependent cytotoxicity (CDC), with possible direct apoptotic signaling upon cross-linking.
An autologous, gene-modified TCR-T cell therapy composed of engineered CD8+ and CD4+ T cells that express an HLA-A*11:01–restricted TCR specific for the KRAS G12V neoantigen, co-express a wild-type CD8α/β coreceptor to strengthen TCR signaling, and include a Fas–4-1BB switch receptor to convert Fas signals into 4-1BB costimulation, enhancing resistance to apoptosis and improving activation/persistence.
Autologous gene-modified CD8+ and CD4+ T cells engineered to express an HLA-A*11:01-restricted TCR specific for the KRAS G12V neoantigen. After infusion, the cells recognize KRAS G12V peptide presented on MHC-I and mediate tumor cell killing via TCR-driven cytotoxicity and cytokine release. A co-expressed wild-type CD8alpha/beta coreceptor strengthens TCR signaling and enables CD4+ T-cell recognition, while a Fas-4-1BB switch receptor converts FasL death signals into 4-1BB costimulation, enhancing activation, resistance to apoptosis, and persistence.
YES
DIRECT
Engineered TCR-T cells recognize KRAS G12V peptide presented by HLA-A*11:01 on tumor cells and directly kill them via TCR-triggered cytotoxicity (perforin/granzyme-mediated lysis and related effector mechanisms).
An autologous, gene-modified TCR-T cell therapy composed of engineered CD8+ and CD4+ T cells that express an HLA-A*11:01–restricted TCR specific for the KRAS G12V neoantigen, co-express a wild-type CD8α/β coreceptor to strengthen TCR signaling, and include a Fas–4-1BB switch receptor to convert Fas signals into 4-1BB costimulation, enhancing resistance to apoptosis and improving activation/persistence.
Autologous gene-modified CD8+ and CD4+ T cells engineered to express an HLA-A*11:01-restricted TCR specific for the KRAS G12V neoantigen. After infusion, the cells recognize KRAS G12V peptide presented on MHC-I and mediate tumor cell killing via TCR-driven cytotoxicity and cytokine release. A co-expressed wild-type CD8alpha/beta coreceptor strengthens TCR signaling and enables CD4+ T-cell recognition, while a Fas-4-1BB switch receptor converts FasL death signals into 4-1BB costimulation, enhancing activation, resistance to apoptosis, and persistence.
NO
INDIRECT
AFNT-211 TCR-T cells recognize the KRAS G12V peptide presented by HLA-A*11:01 and kill the presenting cell via TCR-mediated cytotoxicity (perforin/granzyme). HLA-A*11:01 heavy chain alone is not a cytotoxic target; killing requires the KRAS G12V peptide–HLA complex.
An autologous, gene-modified TCR-T cell therapy composed of engineered CD8+ and CD4+ T cells that express an HLA-A*11:01–restricted TCR specific for the KRAS G12V neoantigen, co-express a wild-type CD8α/β coreceptor to strengthen TCR signaling, and include a Fas–4-1BB switch receptor to convert Fas signals into 4-1BB costimulation, enhancing resistance to apoptosis and improving activation/persistence.
Autologous gene-modified CD8+ and CD4+ T cells engineered to express an HLA-A*11:01-restricted TCR specific for the KRAS G12V neoantigen. After infusion, the cells recognize KRAS G12V peptide presented on MHC-I and mediate tumor cell killing via TCR-driven cytotoxicity and cytokine release. A co-expressed wild-type CD8alpha/beta coreceptor strengthens TCR signaling and enables CD4+ T-cell recognition, while a Fas-4-1BB switch receptor converts FasL death signals into 4-1BB costimulation, enhancing activation, resistance to apoptosis, and persistence.
NO
INDIRECT
FasL is not a killing target; the Fas-4-1BB switch receptor converts FasL engagement into 4-1BB costimulation, enhancing T-cell activation and persistence. Killing occurs only when the TCR recognizes KRAS G12V peptide-HLA-A*11:01, leading to perforin/granzyme-mediated lysis.
Chimeric monoclonal antibody against EGFR that inhibits downstream signaling (RAS/MAPK, PI3K/AKT) and mediates antibody‑dependent cellular cytotoxicity (ADCC).
Chimeric monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization/activation, thereby inhibiting downstream RAS/MAPK and PI3K/AKT signaling and tumor cell proliferation; also mediates NK cell–dependent ADCC.
YES
DIRECT
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on NK cells to trigger ADCC, leading to lysis of EGFR+ cells (with possible CDC/phagocytosis); EGFR signaling blockade may also promote apoptosis.