An intravenously administered bispecific T-cell–engaging antibody that binds CD19 on B cells and CD3 on T cells, forming an immune synapse and activating TCR/CD3 signaling to drive T-cell–mediated cytotoxicity against malignant CD19+ B cells.
Intravenous bispecific antibody that binds CD19 on B cells and CD3 on T cells, creating an immune synapse that activates TCR/CD3 signaling and redirects T-cell cytotoxicity to eliminate malignant CD19+ B cells.
The bispecific antibody bridges CD19 on target cells to CD3 on T cells, forming an immune synapse that activates TCR/CD3 signaling and redirects T-cell killing (perforin/granzyme-mediated apoptosis) of CD19+ cells.
Investigational intravenously infused antibody-based therapy targeting CD19 on B cells, intended to eliminate malignant B cells via immune effector mechanisms; evaluated in a first-in-human Phase 1 trial in relapsed/refractory CD19+ B-cell malignancies.
CD19-targeted, afucosylated IgG1 antibody-drug conjugate that binds CD19 on B cells to trigger ADCC and, after internalization, delivers a glucocorticoid receptor modulator payload that suppresses GR-dependent pro-survival/proliferative gene programs, leading to apoptosis and inhibition of proliferation in CD19+ malignant B cells.
ABBV-319 binds CD19, triggers enhanced ADCC via its afucosylated IgG1 Fc, and after internalization delivers a GR-modulator payload that suppresses pro-survival signaling and induces apoptosis in CD19+ cells.
Lutetium-177–DOTA–girentuximab, a CAIX-targeted radioimmunotherapy delivering beta radiation to CAIX-positive tumors.
177Lu-TLX250 (Lutetium-177–DOTA–girentuximab) is a CAIX-targeted monoclonal antibody radioconjugate. Girentuximab binds CAIX on tumor cells and delivers the beta-emitting radionuclide 177Lu, producing localized radiation (including cross-fire) that induces DNA double-strand breaks and tumor cell death while sparing CAIX-negative tissues.
Girentuximab binds CAIX and delivers 177Lu beta radiation to the bound cell, causing DNA double-strand breaks and radiation-induced cell death (with some cross-fire to nearby cells).
An anti-EGFR IgG1 monoclonal antibody that blocks EGFR signaling on tumor cells.
Cetuximab is a chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization, thereby inhibiting downstream signaling (e.g., RAS-RAF-MEK-ERK, PI3K-AKT) to reduce tumor cell proliferation and survival; it may also mediate ADCC.
Cetuximab binds EGFR on target cells and its IgG1 Fc engages FcγR-expressing effector cells (e.g., NK cells) to mediate ADCC; it can also trigger complement-dependent cytotoxicity, while EGFR blockade inhibits survival signaling and may promote apoptosis.
Fully human afucosylated IgG1 monoclonal antibody targeting the BAFF receptor (BAFF-R/BR3/TNFRSF13C); blocks BAFF binding to BAFF-R and depletes BAFF-R–expressing B cells via enhanced ADCC/ADCP, reducing autoreactive B-cell activity.
Ianalumab is a fully human afucosylated IgG1 monoclonal antibody that binds the BAFF receptor (BAFF-R/TNFRSF13C), blocks BAFF-BAFF-R signaling, and depletes BAFF-R–expressing B cells via enhanced antibody-dependent cellular cytotoxicity and phagocytosis, reducing survival and activity of autoreactive B cells.
Ianalumab binds BAFF-R on B cells and, via its afucosylated IgG1 Fc, engages Fcγ receptors on effector cells to trigger ADCC and ADCP (NK cell–mediated lysis and macrophage phagocytosis), depleting BAFF-R–expressing cells; BAFF signaling blockade may also promote apoptosis.