A bispecific IgG1 monoclonal antibody targeting EGFR and MET that blocks ligand binding, promotes receptor internalization and degradation, and mediates Fc-dependent ADCC/ADCP against EGFR/MET-expressing tumor cells.
Amivantamab is a human bispecific IgG1 monoclonal antibody targeting EGFR and MET. It blocks ligand binding and receptor phosphorylation, induces receptor internalization and degradation, and engages Fc-dependent effector functions (ADCC/ADCP) to eliminate EGFR/MET-expressing tumor cells and inhibit downstream signaling.
Amivantamab binds MET on target cells and engages Fcγ receptor–bearing immune cells to mediate ADCC/ADCP, directly killing MET-expressing cells (with additional receptor internalization/degradation).
An anti-CD19 antibody–drug conjugate (ADC) that binds CD19 on B cells, is internalized, and releases a pyrrolobenzodiazepine (PBD) DNA-crosslinking cytotoxic payload to induce apoptosis.
An anti-CD19 antibody–drug conjugate that binds CD19 on B cells, is internalized, and releases a pyrrolobenzodiazepine (PBD) dimer payload which creates DNA interstrand crosslinks in the minor groove, inhibiting DNA replication and inducing apoptosis of CD19-expressing tumor cells.
ADC binds CD19, is internalized, and releases a PBD dimer that creates DNA interstrand crosslinks, blocking replication and inducing apoptosis of CD19+ cells.
An intravenous recombinant bispecific IgG monoclonal antibody that targets PD-L1 and CD47. It blocks PD-L1 to release the PD-1/PD-L1 immune checkpoint and blocks CD47 to disrupt the “don’t-eat-me” signal, enhancing macrophage-mediated phagocytosis and T-cell activation. Phase 1 dose escalation (0.1–6 mg/kg weekly) in advanced solid tumors.
Bispecific IgG that binds PD-L1 and CD47. Blocks PD-L1 to release the PD-1/PD-L1 immune checkpoint and restore T‑cell activation; blocks CD47 to disrupt CD47–SIRPα “don’t‑eat‑me” signaling, promoting macrophage-mediated phagocytosis. Fc effector function can add ADCP/ADCC, enhancing anti-tumor immunity.
IMM2520 binds PD-L1 with an IgG1 Fc, opsonizing PD-L1+ cells for Fc gamma receptor–mediated ADCC by NK cells and ADCP/phagocytosis by macrophages; simultaneous CD47 blockade removes the don’t-eat-me signal, further enhancing macrophage-mediated killing. (PD-1/PD-L1 blockade also restores CTL activity, an indirect effect.)
An intravenous recombinant bispecific IgG monoclonal antibody that targets PD-L1 and CD47. It blocks PD-L1 to release the PD-1/PD-L1 immune checkpoint and blocks CD47 to disrupt the “don’t-eat-me” signal, enhancing macrophage-mediated phagocytosis and T-cell activation. Phase 1 dose escalation (0.1–6 mg/kg weekly) in advanced solid tumors.
Bispecific IgG that binds PD-L1 and CD47. Blocks PD-L1 to release the PD-1/PD-L1 immune checkpoint and restore T‑cell activation; blocks CD47 to disrupt CD47–SIRPα “don’t‑eat‑me” signaling, promoting macrophage-mediated phagocytosis. Fc effector function can add ADCP/ADCC, enhancing anti-tumor immunity.
IMM2520 binds CD47 on target cells, blocking CD47–SIRPα “don’t‑eat‑me” signaling and engaging Fcγ receptors to drive macrophage-mediated phagocytosis (ADCP) and NK-cell ADCC, leading to death of CD47+ cells.
Third-generation, irreversible, mutant-selective EGFR tyrosine kinase inhibitor (also referred to as almonertinib in some sources).
Third-generation, irreversible, mutant-selective EGFR tyrosine kinase inhibitor that covalently binds the ATP site (e.g., Cys797) of mutant EGFR (including T790M), inhibits EGFR autophosphorylation and downstream MAPK and PI3K–AKT signaling, leading to growth arrest and apoptosis of EGFR-mutant tumor cells with relative sparing of wild-type EGFR.
Irreversible covalent inhibition of mutant EGFR (including T790M) at the ATP site blocks EGFR autophosphorylation and downstream MAPK/PI3K–AKT signaling, leading to growth arrest and apoptosis of EGFR-mutant tumor cells.