Autologous, dual-target CD19/BCMA chimeric antigen receptor (CAR) T-cell therapy; gene-modified T cells engineered to recognize CD19 and BCMA to deplete B cells and plasma cells; administered as a single intravenous infusion.
Autologous T cells engineered with dual CARs targeting CD19 and BCMA; upon infusion they recognize and eliminate CD19+ B cells and BCMA+ plasma cells via T‑cell activation and cytolytic activity, depleting B‑lineage cells (including autoreactive populations) and reducing autoantibody production.
YES
DIRECT
Dual CAR-T cells bind BCMA on target cells and directly kill them via T-cell cytotoxicity (perforin/granzyme release and Fas–FasL–mediated apoptosis).
Humanized IgG1 anti-HER3 monoclonal antibody that binds HER3 (ErbB3), blocks HER3 activation and heterodimerization (e.g., with EGFR/HER2), suppressing PI3K/AKT and MAPK signaling; its IgG1 Fc can engage ADCC.
HMBD-001 is a humanized IgG1 monoclonal antibody that binds HER3 (ERBB3), preventing ligand-induced activation and heterodimerization with EGFR/HER2. This blocks downstream PI3K/AKT and MAPK signaling to inhibit tumor cell growth and survival; its IgG1 Fc can also mediate ADCC.
YES
DIRECT
The anti‑HER3 IgG1 binds HER3 on target cells and its Fc engages Fcγ receptors on effector cells (e.g., NK cells) to trigger ADCC, leading to lysis of HER3-positive cells; signaling blockade is antiproliferative but not the primary killing mechanism.
Humanized IgG1 anti-HER3 monoclonal antibody that binds HER3 (ErbB3), blocks HER3 activation and heterodimerization (e.g., with EGFR/HER2), suppressing PI3K/AKT and MAPK signaling; its IgG1 Fc can engage ADCC.
HMBD-001 is a humanized IgG1 monoclonal antibody that binds HER3 (ERBB3), preventing ligand-induced activation and heterodimerization with EGFR/HER2. This blocks downstream PI3K/AKT and MAPK signaling to inhibit tumor cell growth and survival; its IgG1 Fc can also mediate ADCC.
NO
INDIRECT
HMBD-001 binds HER3 on target cells and its IgG1 Fc engages CD16A on NK cells to trigger ADCC, killing HER3-expressing cells. CD16A-expressing cells are effectors, not killed by the drug.
Chimeric IgG1 monoclonal antibody targeting EGFR; blocks ligand binding and receptor activation and can mediate ADCC.
Chimeric IgG1 monoclonal antibody against EGFR that binds the extracellular domain to block ligand binding and prevent receptor activation and dimerization, inhibiting downstream signaling (e.g., RAS/MAPK, PI3K/AKT) and tumor cell proliferation; its Fc region can engage immune effector cells to mediate ADCC.
YES
DIRECT
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptor–bearing immune cells (e.g., NK cells) to mediate antibody-dependent cellular cytotoxicity; it may also trigger complement-dependent cytotoxicity, while EGFR blockade mainly inhibits proliferation.
CD20×CD3 bispecific T‑cell–engaging antibody that binds CD20 on B cells and CD3 on T cells to activate cytotoxic T‑cell killing.
Bispecific anti-CD20×CD3 antibody that simultaneously binds CD20 on B cells and CD3 on T cells, cross-linking them to activate T-cell cytotoxicity and kill CD20-positive malignant B cells.
NO
INDIRECT
CD3 is on T cells; odronextamab binds CD3 to activate T cells, which then kill CD20+ B cells via T cell-mediated cytolysis (perforin/granzyme). CD3+ cells are not the cytotoxic target.