Monoclonal antibody targeting the GD2 ganglioside on neuroblastoma cells; facilitates NK cell–mediated ADCC via CD16.
Monoclonal antibody that binds the GD2 ganglioside on neuroblastoma cells; the Fc region engages FcγRIIIa (CD16) on NK cells to drive antibody-dependent cellular cytotoxicity (ADCC), and can also trigger complement-dependent cytotoxicity and macrophage antibody-dependent cellular phagocytosis, leading to tumor cell killing.
NO
INDIRECT
Anti-GD2 binds GD2 on tumor cells; its Fc engages CD16a on NK cells to trigger ADCC (and complement/macrophage effector functions) that kill GD2-positive tumor cells. CD16a-expressing cells serve as effectors and are not killed.
Ex vivo expanded TILs infused to restore antitumor immunity and kill tumor cells via TCR recognition and cytotoxic effector functions.
Autologous TILs are isolated from the tumor, expanded ex vivo, and reinfused as a polyclonal T‑cell product that recognizes tumor antigens via native, HLA‑restricted TCRs and eliminates tumor cells through cytotoxic effector functions (perforin/granzyme) and cytokine release, restoring antitumor immunity without genetic engineering.
YES
DIRECT
Infused TILs recognize the EBV peptide–HLA class I complex via their native TCRs and directly kill target cells by releasing perforin and granzymes (with possible Fas/FasL-mediated apoptosis).
IgG1 monoclonal antibody targeting CD38; depletes CD38+ cells via ADCC, CDC, and ADCP; can induce direct apoptosis; inhibits CD38 ectoenzyme (NADase/cyclase) activity, reducing adenosine and modulating immune signaling.
Humanized IgG1 anti-CD38 monoclonal antibody that depletes CD38+ cells via ADCC, CDC, and ADCP and can directly induce apoptosis; also inhibits CD38 ectoenzyme (NADase/cyclase) activity, reducing adenosine and modulating immune signaling.
YES
DIRECT
Isatuximab binds CD38 on target cells and triggers Fc-mediated ADCC (NK cells), CDC (complement), and ADCP (phagocytes), and can also directly induce apoptosis of CD38+ cells.
Teclistamab (Tecvayli) is an anti-BCMA×CD3 bispecific IgG4 monoclonal antibody T-cell engager that binds BCMA on multiple myeloma cells and CD3 on T cells to activate TCR/CD3 signaling and drive T-cell–mediated cytotoxicity against BCMA-positive myeloma cells.
Teclistamab is a bispecific IgG4 antibody that binds BCMA on malignant plasma cells and CD3 on T cells, cross-linking them to form an immune synapse. This activates TCR/CD3 signaling, leading to T‑cell proliferation, cytokine release, and cytotoxic effector activity (perforin/granzymes) that selectively lyses BCMA‑positive myeloma cells.
YES
DIRECT
Teclistamab bridges CD3 on T cells to BCMA on target cells, forming an immune synapse and activating TCR/CD3 signaling, leading to perforin/granzyme-mediated cytotoxic lysis of BCMA-positive cells.
Teclistamab (Tecvayli) is an anti-BCMA×CD3 bispecific IgG4 monoclonal antibody T-cell engager that binds BCMA on multiple myeloma cells and CD3 on T cells to activate TCR/CD3 signaling and drive T-cell–mediated cytotoxicity against BCMA-positive myeloma cells.
Teclistamab is a bispecific IgG4 antibody that binds BCMA on malignant plasma cells and CD3 on T cells, cross-linking them to form an immune synapse. This activates TCR/CD3 signaling, leading to T‑cell proliferation, cytokine release, and cytotoxic effector activity (perforin/granzymes) that selectively lyses BCMA‑positive myeloma cells.
NO
INDIRECT
Teclistamab binds CD3 on T cells to recruit/activate them; the activated T cells kill BCMA-positive myeloma cells via perforin/granzyme cytotoxicity. CD3+ cells are not the targets of killing.