An anti-HER2 antibody-drug conjugate comprising the humanized IgG1 monoclonal antibody trastuzumab linked via a cleavable linker to the membrane-permeable topoisomerase I inhibitor deruxtecan (DXd). It binds HER2 on tumor cells, is internalized, and releases DXd intracellularly to inhibit Topo-I, causing DNA damage and apoptosis; the payload’s bystander effect can kill adjacent low-HER2 cells, and the IgG1 Fc may engage ADCC.
Humanized anti-HER2 IgG1 (trastuzumab) linked via a cleavable linker to the membrane-permeable topoisomerase I inhibitor deruxtecan (DXd). After binding HER2 and internalization, the linker is cleaved to release DXd, which inhibits Topo-I, causing DNA damage, cell-cycle arrest, and apoptosis; the payload exerts a bystander killing effect on adjacent low-HER2 cells and the IgG1 Fc can engage ADCC.
NO
INDIRECT
The ADC targets HER2 (not topoisomerase I) on tumor cells, is internalized, and releases deruxtecan, which inhibits Topo I to cause DNA damage and apoptosis (with bystander killing). Cell kill is determined by HER2-mediated delivery, not by expression of Topo I itself.
Off-the-shelf allogeneic, gene-modified T cells engineered with a lentiviral CD7-directed chimeric antigen receptor to recognize and kill CD7-positive malignant T/NK lineage cells; designed for persistence to control CD7+ disease.
Allogeneic gene‑modified T cells engineered with a lentiviral CD7‑specific chimeric antigen receptor that binds CD7 on malignant T/NK lineage cells, triggering CAR‑mediated activation, proliferation, cytokine release, and perforin/granzyme‑dependent cytotoxic killing independent of the native TCR; designed for persistence to control CD7‑positive disease.
YES
DIRECT
CD7-directed CAR T cells bind CD7 on target cells, become activated, and kill them via perforin/granzyme-mediated cytolysis (and death-receptor apoptosis).
Recombinant humanized anti-HER2 monoclonal antibody that binds HER2, augments HER2 pathway blockade, and promotes ADCC.
Humanized IgG1 monoclonal antibody targeting HER2/ERBB2 on tumor cells; binds the extracellular domain to block HER2 signaling/heterodimerization and enhances pathway blockade, while engaging Fcγ receptors to mediate antibody‑dependent cellular cytotoxicity (ADCC) against HER2‑overexpressing cells.
YES
DIRECT
IgG1 anti-HER2 antibody binds HER2 on tumor cells and engages Fcγ receptors on effector cells to trigger antibody-dependent cellular cytotoxicity (ADCC), killing HER2+ cells (potentially with some complement involvement).
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.
YES
DIRECT
Anti-thymocyte globulin binds CD2 on T cells and triggers complement-dependent lysis and Fc-mediated ADCC/phagocytosis; crosslinking can also induce apoptosis.
Humanized IgG1 monoclonal antibody against HER2/ERBB2 that binds the receptor on tumor cells, blocks HER2 activation/dimerization and downstream PI3K/AKT/MAPK signaling, promotes receptor internalization, and mediates Fcγ-dependent ADCC against HER2-overexpressing cells.
YES
DIRECT
Trastuzumab coats HER2-expressing cells and engages Fcγ receptors on NK cells/macrophages to trigger antibody-dependent cellular cytotoxicity (ADCC), killing the target cells; it also blocks HER2 signaling (growth inhibition).