Afucosylated humanized monoclonal antibody against IL-5 receptor alpha (IL-5Rα) that blocks IL-5 signaling and engages Fcγ receptors to drive enhanced antibody-dependent cellular cytotoxicity, inducing apoptosis and depletion of IL-5Rα-expressing eosinophils (and basophils) to reduce eosinophilic inflammation.
Benralizumab binds IL-5Rα on eosinophils/basophils and its afucosylated Fc engages FcγRIIIa on NK cells, triggering potent ADCC that induces apoptosis and depletion of IL-5Rα-expressing cells.
Celltrion’s proposed biosimilar of ocrelizumab, a humanized IgG1 monoclonal antibody that binds CD20 on pre‑B to mature B lymphocytes, depleting them via antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity and inducing apoptosis; plasma cells are spared. Administered intravenously.
Humanized IgG1 monoclonal antibody (biosimilar to ocrelizumab) that binds CD20 on pre-B to mature B lymphocytes and depletes them via antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity, with induction of apoptosis; plasma cells (CD20-negative) are spared. This B-cell depletion reduces antigen presentation, costimulation, and proinflammatory cytokines, modulating CNS autoimmunity in multiple sclerosis.
Anti-CD20 IgG1 binds CD20 on B cells and induces killing via antibody-dependent cellular cytotoxicity (FcγR-mediated) and complement-dependent cytotoxicity; can also trigger apoptosis.
US-licensed ocrelizumab, a humanized IgG1 anti-CD20 monoclonal antibody that depletes CD20+ B cells via antibody-dependent and complement-dependent cytotoxicity and induces apoptosis; plasma cells are spared. Administered intravenously.
Humanized IgG1 anti‑CD20 monoclonal antibody that binds CD20 on pre‑B to mature B lymphocytes and depletes them via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and apoptosis; plasma cells (CD20−) are spared, reducing B‑cell–mediated immune activity.
Anti-CD20 antibody binds CD20 on B cells and triggers killing via antibody-dependent cellular cytotoxicity (effector cells like NK cells), complement-dependent cytotoxicity, and induction of apoptosis.
EU-licensed ocrelizumab, a humanized IgG1 anti-CD20 monoclonal antibody that depletes CD20+ B cells via antibody-dependent and complement-dependent cytotoxicity and induces apoptosis; plasma cells are spared. Administered intravenously.
Humanized IgG1 anti‑CD20 monoclonal antibody that binds CD20 on pre‑B to mature B cells, depleting them via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and apoptosis; plasma cells (CD20−) are spared, reducing antigen presentation and pro‑inflammatory cytokine signaling.
Anti-CD20 mAb binds CD20 on B cells and triggers killing via Fc-mediated ADCC by NK/macrophages, complement-dependent cytotoxicity (CDC), and apoptosis of the bound cells.
Autologous, non–genetically engineered, ex vivo–expanded polyclonal multi–tumor-associated antigen (multiTAA)–specific T-cell therapy that recognizes multiple shared TAAs on pancreatic adenocarcinoma via native, MHC-restricted TCRs to mediate cytotoxic killing and cytokine-driven immune activation.
Autologous, ex vivo-expanded polyclonal CD4+/CD8+ T cells with native, MHC-restricted TCRs specific for multiple shared tumor-associated antigens on pancreatic adenocarcinoma. After infusion, these T cells recognize antigen-MHC complexes on tumor cells and mediate cytotoxic killing (perforin/granzyme) and cytokine-driven immune activation; multi-antigen targeting reduces antigen-loss escape and may improve durability.
Autologous multiTAA-specific T cells recognize WT1-derived peptides presented on MHC via native TCRs and directly kill target cells through perforin/granzyme-mediated cytotoxicity (with cytokine-driven activation).