An anti-HER2 antibody–drug conjugate (RC48-ADC) that binds HER2, is internalized, and releases the microtubule inhibitor MMAE to induce cell cycle arrest and apoptosis; can also mediate ADCC and bystander killing.
Anti‑HER2 (ERBB2) antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE via a cleavable linker, leading to microtubule disruption, G2/M cell‑cycle arrest, and apoptosis; also can induce ADCC and bystander killing.
The ADC binds HER2, is internalized, and releases MMAE via a cleavable linker; MMAE disrupts microtubules, causing G2/M arrest and apoptosis. It can also induce ADCC and bystander killing.
Humanized IgG1 monoclonal antibody targeting the HER2 extracellular domain; inhibits HER2 signaling/dimerization and induces antibody-dependent cellular cytotoxicity; administered intravenously or subcutaneously in this trial.
Humanized IgG1 monoclonal antibody against HER2; binds the extracellular domain to block HER2 receptor activation and dimerization, inhibiting downstream PI3K/AKT and MAPK signaling, and recruits Fc gamma receptor-bearing immune cells (e.g., NK cells) to mediate antibody-dependent cellular cytotoxicity (ADCC).
Trastuzumab binds the HER2 extracellular domain and engages Fcγ receptors on NK cells to trigger antibody‑dependent cellular cytotoxicity (ADCC), killing HER2+ cells; it may also activate complement-dependent cytotoxicity.
A fully human IgG1-like bispecific monoclonal antibody targeting EGFR and MET; blocks ligand binding and receptor activation, disrupts EGFR–MET crosstalk, inhibits MAPK/ERK and PI3K/AKT signaling, and may mediate ADCC.
A fully human IgG1-like bispecific monoclonal antibody that binds EGFR and MET on tumor cells, blocking ligand binding and receptor activation, disrupting EGFR–MET crosstalk, and inhibiting downstream MAPK/ERK and PI3K/AKT signaling; its IgG1 Fc may also mediate ADCC.
IgG1 Fc engages FcγR+ effector cells (e.g., NK cells) to mediate ADCC against EGFR-expressing cells; EGFR/MET signaling blockade may also induce apoptosis.
A fully human IgG1-like bispecific monoclonal antibody targeting EGFR and MET; blocks ligand binding and receptor activation, disrupts EGFR–MET crosstalk, inhibits MAPK/ERK and PI3K/AKT signaling, and may mediate ADCC.
A fully human IgG1-like bispecific monoclonal antibody that binds EGFR and MET on tumor cells, blocking ligand binding and receptor activation, disrupting EGFR–MET crosstalk, and inhibiting downstream MAPK/ERK and PI3K/AKT signaling; its IgG1 Fc may also mediate ADCC.
As an IgG1-like bispecific antibody, it binds MET on target cells and its Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells) to induce ADCC (and potentially CDC), killing MET-expressing cells; signaling blockade itself is non-cytotoxic.
Gene-modified autologous T cells expressing a CD19-specific CAR; includes metabolic armoring intended to enhance T-cell fitness, expansion, and persistence; targets CD19+ malignant B cells.
Autologous T cells are gene-modified to express a CD19-specific chimeric antigen receptor. Binding to CD19 on malignant B cells triggers CAR signaling, activating cytotoxic functions (e.g., perforin/granzyme release and cytokine production) to kill target cells. Metabolic armoring is included to enhance T-cell metabolic fitness, expansion, and persistence in the tumor microenvironment.
CAR-T cells bind CD19 on target cells, triggering T-cell activation and immunologic synapse formation, leading to perforin/granzyme-mediated apoptosis (and related T-cell cytotoxic pathways).