A glycoengineered type II anti-CD20 monoclonal antibody that enhances ADCC/ADCP and induces direct B-cell death; used pre-glofitamab to debulk and mitigate CRS.
Glycoengineered type II humanized anti-CD20 IgG1 that binds CD20 on B cells; afucosylated Fc increases affinity for Fc gamma RIIIa to enhance ADCC and ADCP, and it induces direct, caspase-independent B-cell death, depleting malignant CD20+ B cells.
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages FcγRIIIa on NK cells/macrophages to drive ADCC/ADCP and it also induces direct, caspase‑independent B‑cell death.
An antibody–drug conjugate (brand name Besponsa) comprising a humanized anti-CD22 IgG4 monoclonal antibody linked to the cytotoxic agent calicheamicin; it binds CD22 on B-lymphoblasts, is internalized, and releases calicheamicin intracellularly to induce DNA double-strand breaks and apoptosis.
Humanized anti-CD22 IgG4 antibody-drug conjugate; after binding CD22 on B cells and being internalized, it releases the cytotoxic payload calicheamicin, which binds the DNA minor groove and causes double-strand breaks, leading to apoptosis.
The anti-CD22 ADC binds CD22 on B cells, is internalized, and releases calicheamicin intracellularly, which induces DNA double-strand breaks leading to apoptosis of CD22+ cells.
Antigen-specific T cells expanded ex vivo and reinfused to recognize tumor peptides on MHC class I via the TCR, mediating cytotoxicity through perforin/granzyme release and IFN-gamma-mediated effects.
Autologous antigen-specific CTLs expanded ex vivo are reinfused to recognize tumor peptides presented on MHC class I via their endogenous TCR, inducing tumor-cell killing via perforin/granzyme release and death-receptor pathways (FasL/TRAIL), along with IFN-γ secretion to enhance antitumor immune responses.
Antigen-specific CTLs recognize tumor peptide–MHC I via the TCR and kill targets via perforin/granzyme release and by engaging TRAIL on CTLs with DR5 (TRAIL‑R2) on the tumor, triggering extrinsic apoptosis (caspase-8).
A subcutaneous CD20×CD3 bispecific T‑cell–engaging antibody that binds CD20 on B cells and CD3 on T cells to form an immune synapse, activate TCR/CD3 signaling, drive T‑cell proliferation and cytotoxic degranulation, and induce targeted B‑cell killing.
Subcutaneous bispecific antibody that binds CD20 on B cells and CD3 on T cells to form an immune synapse, activate TCR/CD3 signaling, expand and activate cytotoxic T cells, and induce perforin/granzyme‑mediated killing of CD20+ malignant B cells.
Epcoritamab bridges CD3 on T cells to CD20 on B cells, forming an immune synapse that activates T cells to release perforin and granzymes, causing cytolysis of CD20+ cells.
Anti-CD38 IgG1κ monoclonal antibody that binds CD38 on clonal plasma cells and other CD38+ cells, inducing complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity and phagocytosis, and apoptosis; also depletes CD38+ immunosuppressive cells and can inhibit CD38 ectoenzyme (NADase) activity.
Daratumumab binds CD38 on target cells and induces complement-dependent cytotoxicity (CDC), Fc-mediated ADCC by NK cells, ADCP by macrophages, and can trigger apoptosis upon crosslinking.