Engineered Toxin Body biologic protein that binds CTLA-4 and delivers a toxin-based kill signal to selectively deplete CTLA-4–expressing cells (e.g., regulatory T cells) within tumors to dismantle the immunosuppressive tumor microenvironment.
Engineered toxin body with biparatopic VHHs that bind CTLA-4 on tumor-infiltrating cells (primarily Tregs), internalize, and release the Shiga-like toxin A subunit, which depurinates 28S rRNA to block protein synthesis and induce apoptosis, selectively depleting CTLA-4+ immunosuppressive cells and enhancing anti-tumor T-cell responses.
Biparatopic VHHs bind CTLA-4 on target cells, internalize, and release Shiga-like toxin A that depurinates 28S rRNA, blocks protein synthesis, and induces apoptosis of CTLA-4+ cells.
Monoclonal antibody targeting Claudin 18.2 that promotes immune effector–mediated cytotoxicity (ADCC/CDC) and may disrupt CLDN18.2 signaling on tumor cells.
Monoclonal antibody against Claudin 18.2 (CLDN18.2) that binds the antigen on tumor cells, induces Fc-mediated ADCC and CDC to kill CLDN18.2-positive cells, and may disrupt CLDN18.2 signaling to inhibit tumor cell proliferation.
Antibody binds CLDN18.2 on tumor cells and engages Fc effector functions to trigger ADCC (via NK cells/macrophages) and complement-dependent cytotoxicity (CDC), leading to lysis of CLDN18.2+ cells.
An anti-HER2 IgG1 antibody–drug conjugate linked to the microtubule inhibitor MMAE. It binds HER2 (ERBB2) on tumor cells, is internalized, and releases MMAE to disrupt tubulin polymerization, causing mitotic arrest and apoptosis; may also induce ADCC and bystander killing.
Anti-HER2 (ERBB2) IgG1 antibody–drug conjugate carrying the microtubule inhibitor MMAE. Upon binding HER2 on tumor cells, it is internalized and releases MMAE to inhibit tubulin polymerization, leading to G2/M arrest and apoptosis; may also engage Fc-mediated ADCC and enable bystander killing.
The ADC binds HER2, is internalized, and releases MMAE that inhibits tubulin polymerization, causing G2/M arrest and apoptosis; Fc-mediated ADCC and limited bystander killing may also contribute.
Fully human anti-CD20 IgG1κ monoclonal antibody (brand name Kesimpta) administered subcutaneously; binds a membrane-proximal epitope on CD20 on B lymphocytes to induce rapid, sustained depletion of circulating CD20+ B cells via CDC, ADCC, and phagocytosis while sparing stem cells and plasma cells; reduces BCR-driven activity, antigen presentation, proinflammatory cytokine release, and autoantibody contribution to dampen CNS inflammation in RMS.
Fully human anti-CD20 IgG1κ monoclonal antibody that binds a membrane-proximal epitope on CD20 on B lymphocytes, inducing rapid, sustained depletion of CD20+ B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and phagocytosis; spares stem cells and plasma cells, thereby reducing B-cell receptor signaling, antigen presentation, proinflammatory cytokine release, and autoantibody production.
Ofatumumab binds CD20 on B cells and induces complement-dependent cytotoxicity (MAC-mediated lysis) and Fc-mediated ADCC/antibody-dependent phagocytosis, depleting CD20+ cells.
An autologous CD19-directed CAR T-cell therapy in which a patient’s T cells are engineered ex vivo to express a chimeric antigen receptor targeting CD19, leading to T-cell activation, proliferation, cytokine release, and cytotoxic killing of CD19+ B cells; evaluated in relapsed/refractory CD19+ B-cell non-Hodgkin lymphoma.
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor targeting CD19. CAR engagement with CD19 triggers CD3ζ/co-stimulatory signaling, leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated killing of CD19+ malignant (and normal) B cells in an MHC-independent manner.
CD19-directed CAR T cells bind CD19 on target cells; CAR signaling activates T cells to kill via perforin/granzyme-mediated cytolysis (MHC-independent).