A bispecific T-cell–redirecting antibody that binds GPRC5D on myeloma/plasma cells and CD3 on T cells, inducing T-cell–mediated cytotoxicity.
Bispecific humanized antibody that binds CD3 on T cells and GPRC5D on myeloma cells, cross-linking and activating T cells to mediate cytotoxic killing of GPRC5D-expressing tumor cells.
Talquetamab links CD3 on T cells to GPRC5D on target cells, activating cytotoxic T cells to kill GPRC5D+ cells via perforin/granzyme–mediated apoptosis.
Autologous genetically engineered T cells expressing a chimeric antigen receptor targeting CD19, using CD3ζ signaling with 4-1BB or CD28 costimulation to mediate cytokine release and cytotoxic killing of CD19+ B-cell malignancies.
Autologous T cells are engineered to express a CD19-specific chimeric antigen receptor; binding to CD19 triggers CD3ζ signaling with 4-1BB or CD28 costimulation, leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated killing of CD19+ B-cell malignancies.
CAR T cells bind CD19 on target cells, become activated, and kill via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
An antibody–drug conjugate targeting Nectin-4 that delivers the microtubule inhibitor monomethyl auristatin E (MMAE), leading to microtubule disruption, G2/M arrest, and apoptosis.
Enfortumab vedotin is an anti–Nectin-4 monoclonal antibody linked via a cleavable linker to the microtubule inhibitor MMAE. After binding Nectin-4 on tumor cells and internalization, the linker is proteolytically cleaved to release MMAE, which binds tubulin, inhibits microtubule polymerization, induces G2/M arrest, and triggers apoptosis.
The ADC binds Nectin-4, is internalized, and releases MMAE intracellularly; MMAE inhibits tubulin polymerization, causing microtubule disruption, G2/M arrest, and apoptosis of Nectin-4–expressing cells.
Antibody–drug conjugate targeting CD30; upon internalization releases MMAE to disrupt microtubules, causing G2/M arrest and apoptosis.
Anti-CD30 monoclonal antibody conjugated to MMAE via a cleavable linker; after CD30 binding and internalization, MMAE is released to inhibit tubulin polymerization, causing G2/M cell-cycle arrest and apoptosis in CD30-positive tumor cells.
An anti-CD30 antibody–drug conjugate binds CD30, is internalized, and releases MMAE intracellularly; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of CD30-positive cells.
Bispecific antibody targeting DLL3 on neuroendocrine tumor cells and CD47 to block the CD47–SIRPα 'don't‑eat‑me' signal, enhancing macrophage phagocytosis and Fc effector functions.
Bispecific antibody that binds DLL3 on neuroendocrine tumor cells while blocking CD47 to inhibit the CD47–SIRPα 'don't-eat-me' signal, thereby enhancing macrophage-mediated phagocytosis and Fc effector functions (e.g., ADCP/ADCC) against DLL3-positive tumor cells.
The bispecific antibody binds DLL3 on tumor cells and blocks CD47, removing the “don’t‑eat‑me” signal and engaging Fcγ receptors to trigger macrophage-mediated phagocytosis (ADCP) and NK cell ADCC, killing DLL3+ cells.