A subcutaneous BCMA×CD3 bispecific IgG T-cell–engaging antibody that binds BCMA on malignant plasma cells and CD3 on T cells to form an immune synapse, activate T cells, and kill BCMA-positive myeloma cells.
Elranatamab is a BCMA×CD3 bispecific IgG antibody that binds BCMA on myeloma/plasma cells and CD3 on T cells, forming an immune synapse to activate and redirect T‑cell cytotoxicity and cytokine release, leading to lysis of BCMA‑positive myeloma cells.
BCMA×CD3 bispecific antibody links T cells to BCMA+ cells, triggering CD3-mediated activation and immune-synapse formation, leading to perforin/granzyme-dependent lysis and apoptosis of the target cells.
Humanized anti-HER2 IgG1 monoclonal antibody that inhibits HER2 signaling/dimerization and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 anti-HER2 monoclonal antibody that binds HER2 to block receptor dimerization and downstream signaling, may promote receptor downregulation, and recruits Fc gamma receptor–bearing immune cells to mediate antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
Binds HER2 on tumor cells and engages FcγR-expressing immune cells (e.g., NK cells) to mediate ADCC, killing HER2+ cells; HER2 signaling blockade can also promote apoptosis.
Autologous gene-modified T lymphocytes engineered to express a chimeric antigen receptor targeting B7-H3 (CD276), with an inducible caspase-9 (iC9) safety switch; designed to activate T-cell cytotoxicity against B7-H3–positive tumor cells.
Autologous T lymphocytes engineered to express a chimeric antigen receptor targeting B7-H3 (CD276). CAR engagement of B7-H3 on tumor cells triggers T-cell activation, cytokine release, and cytotoxic lysis of B7-H3–positive cells. The construct includes an inducible caspase-9 (iC9) safety switch that can be activated by a dimerizer (e.g., AP1903/rimiducid) to selectively ablate the infused CAR T cells if needed.
CAR T cells bind B7-H3 on target cells, become activated, and kill them via T-cell cytotoxic mechanisms (perforin/granzyme release and death receptor pathways).
Anti‑EGFR monoclonal antibody that inhibits EGFR signaling and may mitigate receptor tyrosine kinase feedback during KRAS inhibition.
Anti-EGFR monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream signaling (e.g., RAS/RAF/MEK/ERK), leading to anti-proliferative effects and potentially mitigating RTK feedback during KRAS inhibition.
Cetuximab binds EGFR and its Fc engages immune effectors to mediate ADCC (via Fcγ receptors on NK cells/macrophages) and can trigger CDC, killing EGFR+ cells; it also blocks EGFR signaling (anti-proliferative).
Fully human IgG1 anti-CD20 monoclonal antibody (brand name: Kesimpta) administered subcutaneously for relapsing-remitting multiple sclerosis; depletes CD20+ B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity/phagocytosis, and apoptosis, reducing B-cell antigen presentation and inflammatory activity while sparing stem cells and plasma cells.
Fully human IgG1 anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20+ B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity/phagocytosis, and apoptosis, reducing B-cell antigen presentation and inflammatory activity while sparing stem cells and plasma cells.
Binds CD20 on B cells and triggers complement-dependent cytotoxicity (MAC-mediated lysis) and Fc-mediated killing (ADCC by NK cells, ADCP by phagocytes); can also induce apoptosis.