Biosimilar of infliximab (Remsima/CT-P13), a chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-α to block TNFR1/2 signaling and downstream NF-κB activation, reducing proinflammatory cytokines, adhesion molecules, leukocyte recruitment, and keratinocyte hyperproliferation; may mediate Fc-dependent lysis/apoptosis of TNF-α–expressing cells.
IgG1 monoclonal antibody biosimilar to infliximab that binds soluble and transmembrane TNF-alpha, neutralizing TNF and blocking TNFR1/2 signaling and downstream NF-kB activation; decreases proinflammatory cytokines and adhesion molecules, limits leukocyte recruitment and keratinocyte hyperproliferation; may induce Fc-mediated lysis/apoptosis of TNF-alpha-expressing cells.
IgG1 binds transmembrane TNF-α on cells and, via its Fc, triggers ADCC by FcγR+ effector cells and complement-dependent cytotoxicity; ligation of tmTNF can also induce reverse-signaling apoptosis in the target cell.
Autologous, gene-modified TCR-T cell product. Patient T cells are engineered ex vivo to express a personalized T-cell receptor matched to the patient’s HLA class I type that recognizes tumor-specific peptides; cells are expanded and reinfused to mediate cytotoxic killing via TCR/CD3 activation, perforin/granzyme release, and cytokine secretion.
Autologous T cells are genetically engineered ex vivo to express a personalized T-cell receptor matched to the patient’s HLA class I that recognizes tumor-specific peptides. Upon peptide–HLA engagement, TCR/CD3 signaling activates the transferred T cells to kill tumor cells via perforin/granzyme release and cytokine secretion.
Engineered TCR-T cells recognize the tumor peptide–HLA class I complex via the introduced TCR, activate through TCR/CD3, form an immunologic synapse, and induce target-cell death by perforin/granzyme–mediated apoptosis (with cytokine-mediated support).
Anti-CD20 chimeric monoclonal antibody that depletes B cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity (C1q activation/MAC lysis), and can trigger apoptosis signaling.
CD20×CD3 bispecific monoclonal antibody (T‑cell engager) that binds CD20 on B cells and CD3 on T cells, activating T‑cell cytotoxicity to eliminate CD20+ cells.
Mosunetuzumab is a humanized CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells, cross-linking them to activate TCR signaling and immune synapse formation, redirecting T-cell cytotoxicity (perforin/granzyme) to kill and deplete CD20+ malignant B cells.
Bispecific T-cell engager crosslinks CD20 on target cells with CD3 on T cells, forming an immune synapse and inducing perforin/granzyme-mediated cytotoxicity against CD20+ cells.
Chimeric anti‑CD20 IgG1 monoclonal antibody that depletes B cells via ADCC, CDC, ADCP, and apoptosis.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and induction of apoptosis.
Rituximab binds CD20 on B cells and depletes them via Fc-mediated ADCC (NK cells), CDC (complement activation), ADCP (macrophages), and can also induce apoptosis.