Autologous tumor-infiltrating lymphocyte (TIL) adoptive cell therapy administered intravenously after lymphodepleting chemotherapy to mediate TCR-dependent cytotoxicity against tumor cells.
Autologous TILs expanded ex vivo are reinfused after lymphodepleting chemotherapy. They recognize patient-specific tumor antigens via TCR-MHC and kill tumor cells through perforin/granzyme-mediated cytotoxicity and cytokine release, with IL-2 supporting T-cell activation, proliferation, and persistence.
YES
DIRECT
Infused autologous TILs recognize tumor neoantigen peptide–MHC I via their TCR and directly kill target cells through perforin/granzyme-mediated apoptosis (and Fas–FasL), supported by IL-2.
Cord blood–derived natural killer (NK) cells genetically engineered to express a CD19-directed chimeric antigen receptor for antigen-specific recognition and cytotoxic killing of CD19-positive B cells in B-cell malignancies.
Cord blood–derived NK cells are engineered to express a CD19-specific chimeric antigen receptor, enabling antigen-dependent recognition and cytotoxic killing of CD19-positive B cells in B-cell malignancies. In this construct, IL-15 supports NK activation, proliferation, and persistence, while IL-10 modulates inflammatory responses to enhance antitumor activity and potentially reduce toxicity.
NO
INDIRECT
Not targeted. The CAR-NK cells recognize CD19, not IL-10 receptor alpha; killing occurs only upon CD19 engagement via NK perforin/granzyme-mediated cytolysis of CD19+ cells.
Chimeric anti-CD20 monoclonal antibody immunotherapy that depletes B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity (CDC), recruits Fc receptor–bearing effector cells for antibody-dependent cellular cytotoxicity (ADCC), and can trigger apoptosis via CD20 cross-linking.
Anti-CD38 IgG1 monoclonal antibody targeting CD38 on clonal plasma cells, inducing ADCC, CDC, apoptosis, and immunomodulation.
Human IgG1κ monoclonal antibody targeting CD38 on clonal plasma cells; binding induces Fc-mediated cytotoxicity (ADCC, ADCP, CDC) and direct apoptosis, and depletes CD38+ immunosuppressive cells (Tregs, Bregs, MDSCs) to modulate the tumor microenvironment.
YES
DIRECT
Anti-CD38 IgG1 binds CD38 and triggers Fc-mediated ADCC by NK cells, ADCP by phagocytes, and complement-dependent cytotoxicity; can also induce apoptosis of CD38+ cells.
An antibody–drug conjugate consisting of a humanized anti–Trop-2 monoclonal antibody linked to SN-38 (active metabolite of irinotecan). It delivers a topoisomerase I inhibitor to Trop-2–expressing tumor cells, causing DNA damage and apoptosis with a bystander effect.
Humanized anti–Trop-2 monoclonal antibody linked to SN-38 (topoisomerase I inhibitor). Binds Trop-2 on tumor cells, is internalized, and releases SN-38 after cleavage, stabilizing topoisomerase I–DNA complexes to cause DNA breaks, inhibit replication, and trigger apoptosis; released payload can exert a bystander effect on neighboring cells.
YES
DIRECT
The ADC binds TROP2 on target cells, is internalized, and releases SN-38, a topoisomerase I inhibitor that causes DNA damage and apoptosis; released payload can also exert a bystander effect on neighboring cells.