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.
NO
INDIRECT
Talquetamab bridges CD3 on T cells to GPRC5D on myeloma cells, activating T cells to kill GPRC5D+ tumor cells via perforin/granzyme; CD3+ T cells are not targeted for killing.
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.
YES
DIRECT
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.
YES
DIRECT
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.
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.
NO
INDIRECT
The ADC targets Nectin-4, is internalized, and releases MMAE; MMAE binds beta-tubulin to block microtubule polymerization, causing G2/M arrest and apoptosis. Beta-tubulin expression alone is not sufficient for targeting or killing.
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.
YES
DIRECT
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.