Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy; patient T cells are engineered to express an anti-CD19 scFv with CD28/CD3ζ signaling domains, triggering activation, expansion, and cytotoxic killing of CD19-positive B-cell lymphoma.
Autologous T cells are transduced to express a CD19-specific CAR with an anti-CD19 scFv, CD28 costimulatory, and CD3ζ signaling domains. After infusion, the CAR T cells recognize CD19 on B cells independent of MHC, become activated, proliferate, release cytotoxic mediators and cytokines, and selectively kill CD19-positive malignant B cells.
Anti-CD19 CAR T cells bind CD19 on target cells and kill them via T-cell cytolysis (immune synapse formation, perforin/granzyme release, apoptosis).
Autologous, gene-modified CD19-directed chimeric antigen receptor (CAR) T-cell therapy derived from the patient's T cells and given as a single infusion to deplete CD19+ B cells and reduce autoantibody production in SLE.
Autologous T cells engineered to express a CD19-specific chimeric antigen receptor; upon binding CD19 on B-lineage cells, the CAR T cells activate, proliferate, and kill CD19+ cells via cytotoxic mechanisms, depleting B cells and reducing autoantibody production to reset humoral autoimmunity.
CD19 CAR T cells bind CD19 on target cells, become activated, and kill CD19+ cells via perforin/granzyme-mediated cytolysis and apoptosis (e.g., Fas–FasL), depleting B cells.
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.
The ADC binds HER2, is internalized, and releases the topoisomerase I inhibitor deruxtecan, causing DNA damage, cell-cycle arrest, and apoptosis in HER2+ cells; the IgG1 Fc can also engage ADCC, with a bystander effect from the membrane-permeable payload.
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.
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.
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).