Autologous, lentiviral-transduced PSMA-directed CAR T-cell therapy with a humanized J591-derived anti-PSMA scFv, CD2 costimulatory domain, and dual armoring via a dominant-negative TGFβ receptor and a PD1.CD28 switch receptor.
Autologous T cells are lentivirally engineered to express a PSMA-specific CAR (humanized J591 scFv) with a CD2 costimulatory domain. The cells are dually armored with a dominant-negative TGF-beta receptor to resist TGF-beta–mediated immunosuppression and a PD1.CD28 switch receptor that converts PD-1 inhibitory signals into CD28 costimulation, enhancing activation, persistence, and cytotoxic killing of PSMA-expressing tumor cells.
PSMA-targeted CAR T cells recognize PSMA on tumor cells and kill them via T-cell effector functions, including perforin/granzyme-mediated cytolysis and death-receptor signaling.
An investigational antibody–drug conjugate (ADC) in which a monoclonal antibody targeting an undisclosed tumor-associated antigen is linked to a cytotoxic payload; after antigen binding and internalization, the payload is released intracellularly to kill tumor cells.
Monoclonal antibody binds an undisclosed tumor-associated surface antigen, is internalized, and a cleavable linker releases a cytotoxic payload inside the cancer cell, resulting in intracellular cytotoxicity (e.g., DNA damage or microtubule disruption) and tumor cell death.
The ADC binds the tumor-associated surface antigen, is internalized, and a cleavable linker releases a cytotoxic payload inside the cell (e.g., DNA-damaging or microtubule-disrupting agent), leading to target cell death.
An allogeneic (off-the-shelf) anti-CD19 chimeric antigen receptor T-cell (CAR-T) therapy delivered as a single infusion after lymphodepleting chemotherapy. Gene-engineered T cells express a CAR recognizing CD19 to deplete CD19+ B cells (B-cell aplasia) and reset immunity to reduce pathogenic autoantibody production.
Allogeneic gene-engineered T cells expressing an anti-CD19 chimeric antigen receptor bind CD19 on B-lineage cells and kill them via T-cell cytotoxicity, causing deep B-cell depletion (B-cell aplasia) and an immune reset that reduces pathogenic autoantibody production.
Anti-CD19 CAR-T cells bind CD19 on target cells, form an immunologic synapse, and kill via T-cell cytotoxicity (perforin/granzyme-induced apoptosis, and Fas–FasL pathways).
Autologous chimeric antigen receptor T cells engineered to target glypican-3 (GPC3), enabling MHC-independent recognition and killing of GPC3-positive tumor cells; infused after lymphodepleting chemotherapy.
Autologous T cells engineered to express a chimeric antigen receptor targeting glypican‑3 (GPC3) bind GPC3 on tumor cells independent of MHC, triggering T‑cell activation, cytokine release, and cytotoxic killing of GPC3‑positive cancer cells; infused after lymphodepleting chemotherapy to enhance expansion and persistence.
GPC3-specific CAR-T cells bind GPC3 on target cells, become activated, and directly kill them via T-cell effector mechanisms (perforin/granzyme-mediated cytolysis and apoptosis).
Anti-CD33 antibody-drug conjugate that delivers calicheamicin; added to first induction in CD33-positive AML.
Humanized anti-CD33 monoclonal antibody linked to calicheamicin; binds CD33 on leukemic blasts, is internalized, and releases calicheamicin that binds the DNA minor groove causing double-strand breaks, inhibition of DNA synthesis, and apoptosis.
The ADC binds CD33, is internalized, and releases calicheamicin that causes DNA double-strand breaks, inhibiting DNA synthesis and inducing apoptosis in the target cell.