Autologous, non-engineered, ex vivo–expanded polyclonal TIL therapy that recognizes tumor antigens via native TCRs and mediates cytotoxicity (perforin/granzyme, cytokines); administered IV at 9×10^10 cells.
Autologous, non-engineered, ex vivo–expanded polyclonal TILs that recognize tumor antigens via native TCR–MHC interactions and kill tumor cells through perforin/granzyme release and cytokine-mediated cytotoxicity after IV infusion.
YES
DIRECT
Infused TILs recognize the tumor-associated peptide–HLA class II complex via native TCRs and kill the presenting cell through perforin/granzyme release (and Fas–FasL/cytokine-mediated apoptosis).
Subcutaneous CD20×CD3 bispecific T‑cell–engaging monoclonal antibody that binds CD20 on B cells and CD3 on T cells to redirect T‑cell cytotoxicity against malignant B cells.
Humanized bispecific monoclonal antibody that binds CD20 on B cells and CD3 on T cells, cross-linking them to form an immune synapse and activate T-cell cytotoxicity (perforin/granzyme) to kill CD20+ malignant B cells.
NO
INDIRECT
Mosunetuzumab binds CD3 on T cells to recruit/activate them against CD20+ B cells, which are killed via perforin/granzyme; CD3+ T cells are not targeted for killing.
Recombinant fully human anti-CD38 monoclonal antibody immunotherapy that binds CD38 and eliminates CD38+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and antibody-dependent cellular phagocytosis; may also induce apoptosis and modulate CD38 enzymatic signaling.
Fully human IgG1 anti-CD38 monoclonal antibody that binds CD38 on malignant and immune cells and eliminates CD38+ cells via ADCC, CDC, and ADCP; can also induce apoptosis and modulate CD38 ectoenzyme signaling, leading to antitumor and immunomodulatory effects.
YES
DIRECT
Anti-CD38 IgG1 binds CD38 on target cells and triggers Fc-mediated ADCC (NK cells), CDC (complement), and ADCP (phagocytes); it may also induce direct apoptosis.
Anti-CD38 monoclonal antibody (reference product, DARZALEX) that depletes CD38+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and antibody-dependent cellular phagocytosis; may also induce apoptosis and modulate CD38 enzymatic signaling.
Human IgG1κ monoclonal antibody targeting CD38 that depletes CD38+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and antibody-dependent cellular phagocytosis; can also induce apoptosis and modulate CD38 enzymatic signaling, reducing CD38+ tumor and immunosuppressive cells.
YES
DIRECT
Anti-CD38 IgG1 mAb binds CD38 on target cells and uses its Fc to recruit immune effectors, causing ADCC (NK cells), CDC (complement), and ADCP (macrophages); can also induce apoptosis of CD38+ cells.
Anti–nectin-4 antibody-drug conjugate that delivers MMAE (vedotin), a microtubule-disrupting cytotoxin, to nectin-4–expressing urothelial cancer cells, inducing apoptosis.
Anti–nectin-4 monoclonal antibody linked via a cleavable linker to the microtubule toxin MMAE. After binding nectin-4 on tumor cells and internalization, MMAE is released to bind tubulin, inhibit polymerization, cause G2/M arrest, and induce apoptosis in nectin‑4–expressing cells.
YES
DIRECT
The ADC binds nectin-4 on target cells, is internalized, then releases MMAE via a cleavable linker; MMAE binds tubulin, inhibits microtubule polymerization, causes G2/M arrest, and induces apoptosis.