Humanized IgG1 monoclonal antibody targeting the HER2 (ERBB2) extracellular dimerization domain (subdomain II); prevents HER2/HER3 and HER2/EGFR heterodimerization and inhibits downstream PI3K/AKT and MAPK signaling in HER2-positive breast cancer.
Humanized IgG1 monoclonal antibody that binds the HER2 (ERBB2) extracellular dimerization domain (subdomain II), blocking HER2/HER3 and HER2/EGFR heterodimerization, thereby inhibiting PI3K/AKT and MAPK signaling and tumor cell proliferation; its Fc region can also mediate antibody-dependent cellular cytotoxicity (ADCC).
Pertuzumab binds HER2 on target cells and its Fc engages Fcγ receptor–bearing immune cells (e.g., NK cells) to trigger ADCC; blockade of HER2 dimerization/signaling can also induce apoptosis.
Humanized IgG1 monoclonal antibody that binds HER2 (ERBB2) domain IV, inhibits HER2 signaling, and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody that binds HER2 (ERBB2) domain IV on tumor cells, blocks HER2 receptor signaling and downstream PI3K/AKT and MAPK pathways, and mediates immune effector killing via antibody-dependent cellular cytotoxicity (ADCC).
Trastuzumab binds HER2 on tumor cells and its Fc engages FcγR-expressing effector cells (e.g., NK cells) to trigger antibody-dependent cellular cytotoxicity (ADCC), leading to target-cell killing; signaling blockade also contributes to growth inhibition.
Autologous genetically engineered T cells expressing a chimeric antigen receptor targeting BCMA (TNFRSF17) on plasma cells to induce T-cell activation, cytokine release, and cytotoxic killing in multiple myeloma.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes BCMA (TNFRSF17) on malignant plasma cells. Antigen engagement activates CD3ζ and costimulatory domains (e.g., 4-1BB or CD28), driving T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated killing of BCMA-positive multiple myeloma cells, with potential persistence for ongoing immunosurveillance.
CAR T cells recognizing BCMA form an immune synapse and kill BCMA+ cells via perforin/granzyme-mediated lysis and apoptosis (e.g., Fas/FasL).
Intravenous anti–PD-L1 monoclonal antibody immune checkpoint inhibitor that blocks PD-L1 to restore cytotoxic T-cell activity.
Human IgG1 anti–PD-L1 monoclonal antibody checkpoint inhibitor that binds PD-L1 and blocks its interaction with PD-1, preventing inhibitory signaling and restoring cytotoxic T-cell activity; can also mediate ADCC against PD-L1–expressing tumor cells.
Avelumab binds PD-L1 on target cells with its IgG1 Fc, engaging FcγR-expressing effector cells (e.g., NK cells) to mediate antibody-dependent cellular cytotoxicity (ADCC). It also blocks PD-1/PD-L1 to restore T-cell killing (indirect).
Low-fucose, fully human IgG1 bispecific monoclonal antibody targeting EGFR and MET; inhibits EGFR/MET signaling and active against EGFR activating/resistance mutations (e.g., T790M/C797S) and MET pathway activation.
Low-fucose, fully human IgG1 bispecific antibody that targets EGFR and MET (wild-type and mutant), blocks ligand binding and receptor phosphorylation, promotes receptor internalization/degradation, and mediates Fc-dependent ADCC; collectively shuts down EGFR/MET downstream signaling (e.g., MAPK, PI3K-AKT) and inhibits tumor cell proliferation, including in EGFR-activating/resistance and MET-driven settings.
Amivantamab binds EGFR on target cells and engages Fcγ receptors on immune effectors to trigger ADCC (and ADCP), killing EGFR-positive cells; it also induces receptor internalization/degradation and signaling blockade (mainly cytostatic).