A TCR-based bispecific ImmTAC biologic that uses a high-affinity TCR to bind a PIWIL1-derived peptide presented by HLA-A*02:01 on tumor cells and an anti-CD3 domain to recruit/activate T cells; administered IV.
IMC-R117C is a soluble TCR–CD3 bispecific (ImmTAC) that uses an affinity-enhanced TCR to bind a PIWIL1-derived peptide presented by HLA-A*02:01 on tumor cells and an anti-CD3 domain to recruit and activate polyclonal T cells, driving synapse formation, cytokine release, and targeted T‑cell cytotoxicity against PIWIL1+ HLA-A*02:01 tumor cells.
NO
INDIRECT
IMC-R117C binds CD3ε on T cells to activate and redirect them against PIWIL1 peptide–HLA-A*02:01–positive tumor cells, which are killed by T-cell cytotoxic granules; CD3+ T cells are not killed.
CD79b-directed antibody–drug conjugate; binding to CD79b leads to internalization and release of the microtubule inhibitor MMAE, causing cell-cycle arrest and apoptosis.
CD79b-targeted antibody–drug conjugate; after binding CD79b on B cells, the complex is internalized and a protease-cleavable linker releases MMAE, which inhibits tubulin polymerization, causing G2/M cell-cycle arrest and apoptosis in CD79b-expressing malignant B cells.
YES
DIRECT
The ADC binds CD79b on B cells, is internalized, and releases MMAE, which inhibits tubulin polymerization leading to G2/M arrest and apoptosis of CD79b-expressing cells.
CD79b-directed antibody–drug conjugate; binding to CD79b leads to internalization and release of the microtubule inhibitor MMAE, causing cell-cycle arrest and apoptosis.
CD79b-targeted antibody–drug conjugate; after binding CD79b on B cells, the complex is internalized and a protease-cleavable linker releases MMAE, which inhibits tubulin polymerization, causing G2/M cell-cycle arrest and apoptosis in CD79b-expressing malignant B cells.
NO
INDIRECT
The ADC binds CD79b on B cells, is internalized, and releases MMAE, which then binds β‑tubulin (vinca site) to block microtubule polymerization, causing G2/M arrest and apoptosis. β‑tubulin expression alone is not sufficient—delivery requires CD79b targeting.
Chimeric anti-CD20 monoclonal antibody that depletes B cells via antibody-dependent cellular cytotoxicity, complement activation, and direct apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and direct induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and eliminates them via antibody-dependent cellular cytotoxicity (Fc-engaged NK cells/macrophages), complement-dependent cytotoxicity, and direct apoptosis upon CD20 cross-linking.
HER2-directed antibody–drug conjugate composed of an anti-ERBB2 monoclonal antibody linked to a cytotoxic payload; binds HER2, is internalized, and releases the payload to kill HER2-expressing tumor cells with potential bystander effect.
HER2-directed antibody–drug conjugate: a humanized anti-ERBB2 monoclonal antibody linked via a cleavable linker to a camptothecin-derived topoisomerase I inhibitor. After binding HER2 and internalization, the linker is cleaved to release the payload, which stabilizes TOP1–DNA complexes, induces DNA breaks, blocks replication, and triggers apoptosis in HER2-expressing tumor cells, with potential bystander killing.
YES
DIRECT
After binding HER2, the ADC is internalized and its cleavable linker releases a camptothecin-derived topoisomerase I inhibitor that stabilizes TOP1-DNA complexes, causing DNA breaks, replication arrest, and apoptosis in HER2-expressing cells (with potential bystander killing).