Autologous dual-target BCMA/CD19 chimeric antigen receptor T-cell (CAR-T) therapy produced via lentiviral transduction; single IV infusion to deplete CD19+ B cells and BCMA+ plasma cells in autoimmune kidney disease.
Autologous T cells are lentivirally engineered to express dual chimeric antigen receptors targeting CD19 and BCMA. On engagement with these antigens on B cells and plasma cells, the CAR-T cells become activated and kill targets via perforin/granzyme and death receptor pathways, depleting CD19+ B cells and BCMA+ plasmablasts/plasma cells to reduce pathogenic autoantibody production in autoimmune kidney disease.
YES
DIRECT
BCMA-directed CAR-T cells bind BCMA on target cells and kill them via T-cell cytotoxicity (perforin/granzyme release and death receptor pathways).
Anti-CD38 IgG1 monoclonal antibody that targets CD38 on T-ALL blasts and mediates complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity/phagocytosis, apoptosis, and immunomodulation.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on malignant cells, triggering complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), and direct apoptosis; also depletes CD38+ immunosuppressive cells, leading to immunomodulation.
YES
DIRECT
Daratumumab binds CD38 on target cells and induces complement-dependent cytotoxicity (CDC), Fc-mediated ADCC by NK cells, ADCP by macrophages, and can trigger apoptosis upon crosslinking.
Patient-derived dendritic cells pulsed ex vivo with DKK1 peptide to present the antigen and induce DKK1-specific antitumor T-cell responses in myeloma.
Autologous dendritic cells are generated ex vivo and pulsed with DKK1 peptide; after reinfusion they present DKK1 via MHC to prime DKK1-specific CD8+ and CD4+ T cells, inducing cytotoxic T-cell killing of DKK1-expressing myeloma/plasma cells and potentially anti-DKK1 antibodies, thereby generating tumor-specific immunity.
YES
INDIRECT
The DC vaccine primes DKK1-specific cytotoxic T cells that recognize DKK1 peptides on MHC and kill DKK1-expressing cells via CTL mechanisms (perforin/granzyme, Fas–FasL).
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting CD30 (TNFRSF8) for TCR-independent recognition and killing of CD30-positive Hodgkin/Reed–Sternberg cells.
Autologous T lymphocytes engineered to express a chimeric antigen receptor that binds CD30 (TNFRSF8) on Hodgkin/Reed–Sternberg cells, enabling TCR-independent recognition and activation through CD3ζ and co-stimulatory domains, resulting in T-cell expansion, cytokine release, and perforin/granzyme-mediated lysis of CD30-positive tumor cells.
YES
DIRECT
CAR T cells bind CD30 on target cells and, upon activation via CD3ζ/co-stimulatory domains, kill CD30+ cells by perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis.
An antibody–drug conjugate comprising a humanized anti–Trop-2 IgG linked to SN-38 (active metabolite of irinotecan), delivering a topoisomerase I inhibitor to Trop-2–expressing tumor cells to induce DNA damage and apoptosis.
Humanized anti–Trop-2 IgG linked to SN-38 (active irinotecan metabolite). The antibody binds Trop-2 on tumor cells, is internalized, and releases SN-38 after cleavage. SN-38 inhibits topoisomerase I by stabilizing Topo I–DNA complexes, causing DNA strand breaks, blocking replication, and inducing apoptosis, with potential bystander cytotoxicity.
YES
DIRECT
ADC binds TROP2 on tumor cells, is internalized, and releases SN-38 intracellularly; SN-38 inhibits topoisomerase I, causing DNA breaks and apoptosis (with possible bystander killing).