Anti-CD22 antibody–drug conjugate delivering calicheamicin to CD22-positive blasts.
Humanized anti-CD22 monoclonal antibody linked to calicheamicin; binds CD22 on B-cell blasts, is internalized, and releases calicheamicin, which binds the DNA minor groove to induce double-strand breaks and apoptosis.
YES
DIRECT
ADC binds CD22, is internalized, and releases calicheamicin that binds DNA minor groove, causing double-strand breaks and apoptosis in the target cell.
Anti-CD22 antibody–drug conjugate delivering calicheamicin to CD22-positive blasts.
Humanized anti-CD22 monoclonal antibody linked to calicheamicin; binds CD22 on B-cell blasts, is internalized, and releases calicheamicin, which binds the DNA minor groove to induce double-strand breaks and apoptosis.
NO
INDIRECT
DNA is not the targeted antigen. The ADC binds CD22, is internalized, then releases calicheamicin that binds DNA and causes double-strand breaks and apoptosis in CD22-positive cells.
Chimeric anti-CD20 monoclonal antibody used to deplete CD20+ B cells (including memory B cells) to reduce new anti-HLA antibody formation before transplant.
Chimeric anti-CD20 monoclonal IgG1 that binds CD20 on pre‑B and mature B lymphocytes, triggering complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity and inducing apoptosis, thereby depleting CD20+ B cells (including memory B cells) to reduce new anti-HLA antibody formation.
YES
DIRECT
Rituximab binds CD20 on B cells, triggering complement-dependent cytotoxicity and Fcγ receptor–mediated ADCC, and can induce apoptosis, leading to depletion of CD20+ cells.
Patient-derived tumor-infiltrating lymphocytes expanded ex vivo and infused after preparative chemotherapy; mediate tumor antigen-specific cytotoxicity via TCR recognition to repopulate with highly tumor-reactive T cells.
Autologous tumor-infiltrating lymphocytes expanded ex vivo are infused after lymphodepleting chemotherapy; they recognize tumor antigens via native TCRs and mediate antigen-specific cytotoxicity, persisting and expanding in vivo to repopulate with highly tumor-reactive T cells.
YES
DIRECT
Infused autologous TILs recognize tumor antigen peptide–HLA class I complexes via their native TCRs and directly kill target cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.
Patient-derived tumor-infiltrating lymphocytes expanded ex vivo and infused after preparative chemotherapy; mediate tumor antigen-specific cytotoxicity via TCR recognition to repopulate with highly tumor-reactive T cells.
Autologous tumor-infiltrating lymphocytes expanded ex vivo are infused after lymphodepleting chemotherapy; they recognize tumor antigens via native TCRs and mediate antigen-specific cytotoxicity, persisting and expanding in vivo to repopulate with highly tumor-reactive T cells.
YES
DIRECT
TILs recognize the tumor antigenic peptide–HLA-B complex via their native TCRs and directly kill target cells by perforin/granzyme release and Fas–FasL–mediated apoptosis.