An allogeneic, CD19-directed CAR T-cell therapy engineered ex vivo using CRISPR-Cas9; administered as a single IV infusion after lymphodepleting chemotherapy. Donor T cells are modified to express a CD19-specific chimeric antigen receptor that activates cytotoxic pathways (perforin/granzyme release and cytokine-mediated killing) to lyse malignant B cells in relapsed/refractory B-cell malignancies.
Allogeneic donor T cells are CRISPR-Cas9–engineered to express a CD19-specific chimeric antigen receptor and to knock out endogenous TCR, TGFBR2, and Regnase-1. After infusion, CAR binding to CD19 on B cells activates cytotoxic pathways (perforin/granzyme release and cytokine-mediated killing) to eliminate CD19-positive malignant B cells, while edits reduce GVHD risk and enhance potency and persistence.
CD19-directed CAR T cells bind CD19 on target B cells and induce killing via perforin/granzyme-mediated cytolysis and apoptosis (death receptor/cytokine pathways).
Adoptive natural killer (NK) cell therapy intended to eliminate HER2-expressing tumor cells via NK-mediated cytotoxicity; used as a cellular immunotherapy.
Adoptive transfer of ex vivo expanded natural killer (NK) cells designed to recognize and eliminate HER2-expressing tumor cells via NK-mediated cytotoxicity (perforin/granzyme and death-receptor pathways), with lymphodepletion used to enhance NK-cell engraftment and persistence.
HER2-targeted adoptive NK cells recognize HER2+ tumor cells and kill them via NK cytotoxicity, including perforin/granzyme release and death-receptor (e.g., Fas/TRAIL) pathways.
Autologous CAR T-cell gene therapy made by non-viral electroporation of CD3+ T cells to express a mesothelin-specific CAR (alpaca VHH, CD28, CD3ζ) and to secrete anti-PD-1 nanobody and anti-CTLA-4 antibody for local checkpoint blockade in MSLN+ solid tumors.
Autologous T cells are engineered via non-viral electroporation to express a mesothelin-targeted CAR (alpaca VHH binder with CD28 costimulation and CD3ζ signaling) that mediates antigen-specific cytotoxicity against MSLN+ tumor cells. The cells also secrete an anti-PD-1 nanobody and an anti-CTLA-4 antibody to provide local checkpoint blockade within the tumor microenvironment, enhancing T-cell activation, proliferation, and persistence while reducing exhaustion and Treg-mediated suppression.
CAR T cells bind mesothelin on target cells, become activated, and kill them via perforin/granzyme-mediated cytolysis (and death-receptor pathways).
A fully human BCMA-targeted chimeric antigen receptor (CAR) autologous T-cell therapy. Patient T cells are engineered to express an anti-BCMA scFv linked to CD3ζ signaling and a 4-1BB (CD137) co-stimulatory domain to enhance activation, proliferation, persistence, and cytotoxic activity against BCMA-expressing multiple myeloma cells.
Autologous T cells engineered via lentiviral transduction to express a fully human anti-BCMA CAR with CD3ζ signaling and 4-1BB co-stimulation. Upon binding BCMA on myeloma cells, CAR signaling activates the T cells, enhancing proliferation and persistence and mediating cytotoxic killing (perforin/granzymes, cytokine release), also depleting normal BCMA+ plasma cells.
BCMA-expressing cells are recognized by anti-BCMA CAR-T cells, which upon engagement are activated to kill targets via perforin/granzyme-mediated cytolysis (and Fas/FasL, cytokines), depleting BCMA+ tumor and normal plasma cells.
Anti-HER2 antibody-drug conjugate (RC-48) that delivers the microtubule-disrupting payload MMAE after HER2-mediated internalization; the IgG1 backbone can mediate ADCC.
HER2-targeted IgG1 antibody-drug conjugate that binds HER2 (ErbB2) on tumor cells, undergoes receptor-mediated internalization, and releases the cytotoxic payload MMAE to inhibit microtubule polymerization, causing G2/M cell-cycle arrest and apoptosis; the IgG1 Fc can also mediate ADCC.
The ADC binds HER2 and is internalized; lysosomal release of MMAE inhibits microtubules, causing G2/M arrest and apoptosis. The IgG1 Fc can also recruit immune effector cells for ADCC.