Anti-HER2 IgG1 monoclonal antibody that blocks HER2 dimerization and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized anti-HER2 IgG1 that binds the HER2 extracellular dimerization domain, blocks HER2 dimerization and downstream signaling (e.g., PI3K/AKT/MAPK), and engages Fc-gamma receptor–bearing effector cells to mediate ADCC, leading to tumor cell growth inhibition and death.
Pertuzumab binds HER2, blocks HER2 dimerization/signaling (inducing apoptosis) and engages FcγR-bearing effector cells to mediate ADCC against HER2+ cells.
Anti-CD38 IgG1 monoclonal antibody that kills CD38-positive plasma cells via ADCC, CDC, ADCP, and direct apoptosis.
Humanized IgG1 monoclonal antibody targeting CD38 on plasma cells; induces cell death via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and direct apoptosis of CD38-expressing tumor cells.
Isatuximab binds CD38 on target cells and kills them via Fc-mediated ADCC (NK cells), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and can also induce direct apoptosis.
An intravenous antibody–drug conjugate (ABBV-400) consisting of a humanized anti–c-Met monoclonal antibody linked via a cleavable linker to a topoisomerase I–inhibitor payload; targets MET on tumor cells, is internalized, and releases the topo-I inhibitor to induce DNA damage and cell death with potential bystander effect.
Humanized anti–c-Met monoclonal antibody linked via a cleavable linker to a topoisomerase I inhibitor. After binding MET on tumor cells, the ADC is internalized and the linker is cleaved to release the topo‑I inhibitor, causing DNA damage and cell death, with potential bystander killing of adjacent tumor cells.
The anti-MET ADC binds MET on target cells, is internalized, and its cleavable linker releases a topoisomerase I inhibitor that causes DNA damage and cell death (with potential bystander killing).
Anti-CD20 monoclonal antibody that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Binds CD20 on B cells and induces killing via antibody-dependent cellular cytotoxicity (Fc-engaged NK/myeloid cells), complement-dependent cytotoxicity, and direct apoptosis signaling.
Adoptive cellular immunotherapy using virus-specific CTL lines engineered with glucocorticoid receptor (GR/NR3C1) knockout to resist steroid-mediated suppression/apoptosis; HLA-restricted recognition of adenovirus, BK virus, CMV, JC virus, or SARS-CoV-2 antigens on infected cells, leading to perforin/granzyme-mediated killing and antiviral cytokine release; administered intravenously with possible repeat dosing.
Adoptively transferred, virus-specific CTLs recognize viral peptides presented on HLA molecules via their native TCRs and eliminate infected cells through perforin/granzyme-mediated cytolysis and antiviral cytokine secretion. The cells are engineered with glucocorticoid receptor (NR3C1) knockout to resist steroid-induced suppression and apoptosis, improving persistence and antiviral activity in immunosuppressed patients.
Virus-specific CTLs recognize adenoviral peptide–HLA complexes via the TCR and kill infected cells by perforin/granzyme-mediated apoptosis (and potentially Fas–FasL signaling).