An autologous, fully human anti-BCMA CAR T-cell therapy (CT103A) for relapsed/refractory multiple myeloma. Patient T cells are engineered to express a CAR targeting BCMA, leading to T-cell activation, expansion, cytokine release, and cytotoxic killing of BCMA-positive plasma cells.
Autologous T cells are engineered via lentiviral transduction to express a fully human anti-BCMA chimeric antigen receptor. Upon binding BCMA on malignant plasma cells, CAR signaling activates the T cells, inducing proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of BCMA-positive cells.
YES
DIRECT
Anti-BCMA CAR T cells bind BCMA on target cells, become activated, and kill via perforin/granzyme-mediated cytotoxicity (leading to lysis/apoptosis).
Patient-derived tumor-resident T cells isolated, expanded, and activated ex vivo, then reinfused to mediate antigen-specific cytotoxicity via TCR recognition of tumor antigens.
Autologous tumor-resident T cells are isolated from the patient’s tumor, expanded and activated ex vivo, then reinfused to recognize tumor antigens via their native TCRs presented on MHC, mediating antigen-specific cytotoxicity through perforin/granzyme release and cytokine secretion; supportive IL-2 can enhance survival and expansion.
YES
DIRECT
TILs recognize the neoantigen peptide–MHC I complex via their native TCR and directly lyse target cells through perforin/granzyme release (and Fas–FasL pathways).
Patient-derived tumor-resident T cells isolated, expanded, and activated ex vivo, then reinfused to mediate antigen-specific cytotoxicity via TCR recognition of tumor antigens.
Autologous tumor-resident T cells are isolated from the patient’s tumor, expanded and activated ex vivo, then reinfused to recognize tumor antigens via their native TCRs presented on MHC, mediating antigen-specific cytotoxicity through perforin/granzyme release and cytokine secretion; supportive IL-2 can enhance survival and expansion.
YES
DIRECT
Reinfused TILs recognize tumor-associated peptide–HLA class I complexes via their native TCRs and directly kill target cells through perforin/granzyme-mediated apoptosis (and Fas–FasL), with cytokines supporting cytotoxicity.
Patient-derived tumor-resident T cells isolated, expanded, and activated ex vivo, then reinfused to mediate antigen-specific cytotoxicity via TCR recognition of tumor antigens.
Autologous tumor-resident T cells are isolated from the patient’s tumor, expanded and activated ex vivo, then reinfused to recognize tumor antigens via their native TCRs presented on MHC, mediating antigen-specific cytotoxicity through perforin/granzyme release and cytokine secretion; supportive IL-2 can enhance survival and expansion.
YES
DIRECT
TILs recognize the neoantigen peptide–HLA class II complex via their native TCRs and directly kill target cells through perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis, with supportive cytokine effects.
Anti-HER2 antibody–drug conjugate delivering the topoisomerase I inhibitor DXd.
Humanized anti-HER2 monoclonal antibody linked to the topoisomerase I inhibitor DXd. Binds HER2 on tumor cells, is internalized, and releases DXd to inhibit Top1–DNA complexes, causing DNA damage, replication blockade, cell-cycle arrest, and apoptosis; also mediates ADCC and exerts a bystander killing effect due to a membrane-permeable payload.
YES
INDIRECT
After HER2-targeted uptake, the ADC releases the DXd payload, which inhibits Top1–DNA complexes, causing DNA damage and apoptosis; cells are killed only if they receive the payload (via HER2-mediated internalization or bystander uptake).