CD70-targeted CAR–NKT cell therapy: autologous natural killer T cells genetically engineered to express an anti-CD70 chimeric antigen receptor; designed to recognize CD70 on tumor cells and mediate cytotoxicity and cytokine release.
Autologous natural killer T cells engineered with an anti-CD70 chimeric antigen receptor bind CD70 on tumor cells, triggering CAR signaling that activates NKT-mediated cytotoxicity (perforin/granzyme) and proinflammatory cytokine release (e.g., IFN-γ, TNF-α), resulting in TCR-independent lysis of CD70-positive cancer cells and amplification of anti-tumor immunity.
Anti-CD70 CAR–NKT cells bind CD70 on target cells, triggering CAR signaling and NKT degranulation (perforin/granzyme) to induce apoptosis; TCR-independent.
Intravenous antibody–drug conjugate (IMMU-132; Trodelvy) targeting TROP-2 and delivering the topoisomerase I inhibitor SN-38.
Humanized anti–TROP-2 monoclonal antibody (hRS7) conjugated to SN-38 (topoisomerase I inhibitor). Binds TROP-2 on tumor cells, is internalized, and the linker is cleaved to release SN-38, which stabilizes topoisomerase I–DNA complexes, causing DNA strand breaks, inhibition of DNA replication, and apoptosis (with potential bystander effect).
ADC binds TROP-2 on tumor cells, is internalized, and releases SN-38, a topoisomerase I inhibitor, causing DNA damage and apoptosis (with possible bystander killing).
Rabbit polyclonal antilymphocyte globulin used for in vivo T-cell depletion to reduce graft-versus-host disease risk.
Rabbit polyclonal IgG against multiple human T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA) that depletes T lymphocytes via complement-dependent cytotoxicity, Fc-mediated ADCC/phagocytosis, and apoptosis, producing in vivo T‑cell immunosuppression to reduce GVHD risk.
rATG contains antibodies that bind LFA-1 (including CD18) on T cells, triggering complement-dependent lysis and Fc-mediated ADCC/phagocytosis, and can induce apoptosis, depleting the target-expressing cells.
HER3 (ERBB3)-targeting antibody–drug conjugate that delivers a topoisomerase I inhibitor payload; administered IV every 3 weeks; binds HER3, internalizes, and releases a DNA-damaging topo-I payload to kill HER3-expressing tumor cells; tested alone and with trastuzumab or osimertinib.
Humanized anti-HER3 IgG1 antibody-drug conjugate linked via a cleavable linker to a topoisomerase I inhibitor. After binding HER3 on tumor cells, the ADC is internalized and releases the topo I inhibitor, stabilizing the topo I–DNA complex to induce DNA breaks, block DNA replication, and trigger apoptosis in HER3-expressing tumor cells.
The anti-HER3 ADC binds HER3 on tumor cells, is internalized, and releases a topoisomerase I inhibitor that stabilizes the topo I–DNA complex, causing DNA breaks, replication arrest, and apoptosis of HER3-expressing cells.
Humanized anti-HER2 monoclonal antibody that blocks HER2/HER3 signaling; evaluated in combination with DB-1310.
Humanized monoclonal antibody that binds HER2 on tumor cells, blocks HER2/HER3 signaling and receptor dimerization, suppresses downstream PI3K/AKT and MAPK pathways, and mediates antibody‑dependent cellular cytotoxicity against HER2‑overexpressing cells.
Trastuzumab binds HER2 on tumor cells and engages FcγR-bearing effector cells (e.g., NK cells) to mediate ADCC; it also blocks HER2 signaling, promoting growth arrest and apoptosis of HER2+ cells.