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.
NO
INDIRECT
PD-1 is blocked by the secreted anti-PD-1 nanobody to enhance T-cell activity; PD-1–expressing cells are not targeted for killing. Cytotoxicity is directed at MSLN+ tumor cells via CAR-mediated perforin/granzyme release.
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.
NO
INDIRECT
The therapy secretes an anti‑CTLA‑4 antibody to block CTLA‑4 signaling and enhance CAR T‑cell activation; killing is directed against mesothelin‑positive tumor cells via the CAR, not CTLA‑4–expressing cells.
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.
YES
DIRECT
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.
YES
DIRECT
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.
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.
NO
INDIRECT
Disitamab vedotin binds HER2, is internalized, and releases MMAE, which binds beta-tubulin to disrupt microtubules causing G2/M arrest and apoptosis. Beta-tubulin is not the cell-surface target; only HER2+ cells are directly targeted for payload delivery.