Anti-HER2 antibody–drug conjugate (RC48) that binds HER2 (ERBB2), is internalized, and releases the cytotoxic payload MMAE to disrupt microtubules, causing mitotic arrest and cell death; may also enhance ADCC.
HER2 (ERBB2)-targeted antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the payload monomethyl auristatin E (MMAE), which inhibits tubulin polymerization to disrupt microtubules, causing G2/M arrest and apoptosis; may also enhance antibody-dependent cellular cytotoxicity (ADCC).
HER2-binding ADC is internalized and releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis; Fc-mediated ADCC may also contribute.
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.
CD19 on target cells is recognized by the CD19-directed CAR on infused T cells, triggering T‑cell activation and cytolytic killing via perforin/granzyme release and apoptosis pathways (e.g., Fas/FasL).
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.
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.
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.
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.
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.