An anti-CD38 antibody–drug conjugate (anti-CD38–Duostatin 5.2) that binds CD38 on clonal plasma cells, is internalized, and releases the Duostatin 5.2 cytotoxic payload to induce selective plasma-cell killing and reduce pathogenic light-chain production in systemic AL amyloidosis.
CD38-targeting antibody–drug conjugate that binds CD38 on plasma cells, is internalized, and releases an MMAF (Duostatin 5.2) cytotoxic payload to inhibit tubulin polymerization, causing G2/M arrest and apoptosis of CD38+ cells, thereby reducing pathogenic light-chain production in AL amyloidosis.
NO
INDIRECT
STI-6129 targets CD38 on the cell surface, is internalized, and releases an MMAF payload that binds the vinca site on β-tubulin to block polymerization, causing G2/M arrest and apoptosis. Tubulin expression alone does not lead to killing; only CD38+ cells are targeted.
Autologous, gene-modified cellular immunotherapy composed of peripheral blood monocytes engineered to express an anti-HER2 chimeric antigen receptor (CAR); administered as a single IV infusion (3 or 10 billion CAR+ cells). CAR recognition of HER2 on tumor cells activates monocytes, which traffic to tumors, differentiate into macrophages, and eliminate HER2+ cells via phagocytosis/cytotoxic effector functions while presenting tumor antigens and modulating the tumor microenvironment.
Autologous peripheral blood monocytes are engineered ex vivo to express an anti-HER2 chimeric antigen receptor. After infusion, CAR engagement of HER2 on tumor cells activates the monocytes, which traffic to tumors and differentiate into macrophages that eliminate HER2-positive cells via phagocytosis and other cytotoxic effector functions, while presenting tumor antigens and reshaping the tumor microenvironment to promote secondary adaptive immune responses.
YES
DIRECT
Anti-HER2 CAR–engineered monocytes/macrophages recognize HER2 and directly eliminate HER2+ cells via phagocytosis and macrophage cytotoxic effector functions.
An autologous, gene-modified CD19/CD20 dual-targeting CAR T-cell therapy given as a single IV infusion after conditioning; the CAR redirects T cells to CD19 and CD20 on malignant B cells to trigger cytotoxic killing and induce B-cell aplasia.
Autologous gene-modified T cells engineered to express a dual-specific chimeric antigen receptor that binds CD19 and CD20 on B cells; antigen engagement activates T-cell signaling, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B cells, leading to B-cell aplasia.
YES
DIRECT
CAR T cells engineered to target CD19 (and CD20) bind CD19 on B cells, become activated, and kill targets via perforin/granzyme-mediated cytolysis and apoptosis.
An autologous, gene-modified CD19/CD20 dual-targeting CAR T-cell therapy given as a single IV infusion after conditioning; the CAR redirects T cells to CD19 and CD20 on malignant B cells to trigger cytotoxic killing and induce B-cell aplasia.
Autologous gene-modified T cells engineered to express a dual-specific chimeric antigen receptor that binds CD19 and CD20 on B cells; antigen engagement activates T-cell signaling, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B cells, leading to B-cell aplasia.
YES
DIRECT
Dual-specific CAR T cells bind CD20 on B cells, triggering T-cell activation and perforin/granzyme-mediated cytolytic killing of the target cells.
Allogeneic, gene-modified T cells engineered to express a chimeric NK receptor that redirects them to tumor-associated ligands and activates T-cell cytotoxic signaling (via ITAM/CD3zeta), promoting perforin/granzyme-mediated killing and cytokine release against B7-H3-expressing neuroblastoma.
Allogeneic, gene-modified T cells engineered with a chimeric NK receptor that binds tumor-associated ligands on B7-H3–expressing neuroblastoma and signals through ITAM/CD3ζ to activate T-cell effector functions, driving perforin/granzyme-mediated cytolysis and cytokine release.
YES
INDIRECT
Engineered T cells bearing a chimeric NK receptor recognize tumor-associated ligands (not B7-H3) on B7-H3–positive tumor cells, signal via ITAM/CD3ζ, and kill via perforin/granzyme-mediated cytolysis.