TROP2-targeted antibody-drug conjugate delivering a topoisomerase I inhibitor payload; binds TROP2 on tumor cells, internalizes, and releases cytotoxin to induce DNA damage and apoptosis (with potential bystander effect).
TROP2-targeted antibody–drug conjugate; binds TROP2 on tumor cells, is internalized, and releases a cleavable topoisomerase I inhibitor payload (tirumotecan) that inhibits Topo I, inducing DNA damage, replication arrest, and apoptosis, with potential bystander killing.
YES
DIRECT
ADC binds TROP2 on target cells, is internalized, and releases a topoisomerase I inhibitor payload that induces DNA damage/replication arrest, leading to apoptosis (with possible bystander killing).
TROP2-targeted antibody-drug conjugate delivering a topoisomerase I inhibitor payload; binds TROP2 on tumor cells, internalizes, and releases cytotoxin to induce DNA damage and apoptosis (with potential bystander effect).
TROP2-targeted antibody–drug conjugate; binds TROP2 on tumor cells, is internalized, and releases a cleavable topoisomerase I inhibitor payload (tirumotecan) that inhibits Topo I, inducing DNA damage, replication arrest, and apoptosis, with potential bystander killing.
NO
INDIRECT
SKB264 binds TROP2, is internalized, and releases a Topo I–inhibitor payload that induces DNA damage and apoptosis. Topoisomerase I is the intracellular enzymatic payload target, not the antigen bound by the ADC, so Topo I expression alone is not directly targeted for killing.
Autologous, non–genetically modified tumor-infiltrating lymphocyte (TIL) therapy providing ex vivo expanded tumor‑reactive T cells to mediate cytotoxicity against tumor cells.
Autologous, non-genetically modified tumor-infiltrating lymphocytes expanded ex vivo; upon reinfusion, native TCRs recognize patient-specific tumor antigens and mediate cytotoxic killing of tumor cells via perforin/granzyme release and cytokine-driven immune activation.
YES
DIRECT
Infused TILs use native TCRs to recognize tumor-derived peptide–HLA class I complexes on tumor cells and kill them via perforin/granzyme release and death-receptor pathways (e.g., Fas/FasL).
Autologous, non–genetically modified tumor-infiltrating lymphocyte (TIL) therapy providing ex vivo expanded tumor‑reactive T cells to mediate cytotoxicity against tumor cells.
Autologous, non-genetically modified tumor-infiltrating lymphocytes expanded ex vivo; upon reinfusion, native TCRs recognize patient-specific tumor antigens and mediate cytotoxic killing of tumor cells via perforin/granzyme release and cytokine-driven immune activation.
YES
DIRECT
Reinfused TILs use native TCRs to recognize the tumor-derived peptide–HLA class II complex and directly kill the presenting cell via perforin/granzyme-mediated cytolysis, supported by cytokines (e.g., IFN-γ, TNF-α).
Anti-CD38 IgG1 monoclonal antibody that induces myeloma cell death via ADCC, CDC, and ADCP; can trigger direct apoptosis, inhibit CD38 ectoenzyme/adenosine signaling, and deplete CD38+ immunosuppressive cells.
Isatuximab is an anti‑CD38 IgG1 monoclonal antibody that binds CD38 on malignant plasma cells, inducing cell death via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), antibody‑dependent cellular phagocytosis (ADCP), and direct apoptosis. It also inhibits CD38 ectoenzyme/adenosine signaling and depletes CD38‑positive immunosuppressive cells, enhancing anti‑tumor immunity.
YES
DIRECT
Isatuximab binds CD38 on target cells and induces Fc-mediated ADCC and ADCP, activates complement (CDC), and can trigger direct apoptosis.