Recombinant cytokine–toxin fusion (IL-3 linked to truncated diphtheria toxin) that binds CD123 (IL-3Rα) on AML cells, is internalized, and inhibits protein synthesis via EF-2 ADP-ribosylation to kill CD123+ blasts/progenitors.
Recombinant IL-3–diphtheria toxin fusion that binds CD123 (IL-3R alpha) on target cells, is internalized, and the diphtheria toxin catalytic domain ADP-ribosylates EF-2 to halt protein synthesis, leading to death of CD123-positive blasts/progenitors.
NO
INDIRECT
Tagraxofusp binds CD123 (not EF-2); after CD123-mediated internalization, its diphtheria toxin moiety ADP-ribosylates EF-2 to halt protein synthesis and kill CD123-positive cells.
Anti-CD33 antibody–drug conjugate that delivers calicheamicin; after binding CD33 and internalization, releases calicheamicin to induce DNA double-strand breaks and apoptosis in AML blasts.
Humanized anti-CD33 monoclonal antibody linked to calicheamicin; after CD33 binding and internalization, calicheamicin is released to bind the DNA minor groove, inducing double-strand breaks and apoptosis in CD33-positive AML cells.
YES
DIRECT
The anti-CD33 ADC binds CD33, is internalized, and releases calicheamicin, which binds the DNA minor groove to cause double-strand breaks and apoptosis in CD33+ cells.
Anti-CD33 antibody–drug conjugate that delivers calicheamicin; after binding CD33 and internalization, releases calicheamicin to induce DNA double-strand breaks and apoptosis in AML blasts.
Humanized anti-CD33 monoclonal antibody linked to calicheamicin; after CD33 binding and internalization, calicheamicin is released to bind the DNA minor groove, inducing double-strand breaks and apoptosis in CD33-positive AML cells.
NO
INDIRECT
The ADC targets CD33 on AML cells; after internalization it releases calicheamicin, which binds the DNA minor groove and causes double-strand breaks leading to apoptosis. DNA minor groove is not the selecting (antibody) target.
Bispecific T-cell–engager antibody immunotherapy that bridges CD19+ B cells and T cells, binding CD19 on B cells and engaging T cells to activate a cytotoxic response against CD19-expressing cells; administered IV once weekly; evaluated as monotherapy in relapsed/refractory CD19+ B-ALL.
Bispecific antibody that links CD19+ B-lineage leukemia cells to T cells—binding CD19 on tumor cells and engaging T cells (via CD3) to trigger T-cell activation and cytotoxic killing of CD19-expressing cells.
YES
DIRECT
The bispecific antibody binds CD19 on target cells and CD3 on T cells, forming an immune synapse that activates T cells to kill CD19+ cells via perforin/granzyme-mediated cytotoxicity.
Autologous, gene-edited TCR-T cell therapy engineered to express an HLA-A*11:01–restricted TCR specific for the KRAS G12D neoantigen; administered as an infusion with dose escalation to mediate antigen-specific cytotoxicity against KRAS G12D–mutant tumors.
Autologous T cells are gene-edited to express an HLA-A*11:01–restricted TCR specific for the KRAS G12D neoantigen. After infusion, these engineered TCR-T cells recognize KRAS G12D peptide–MHC I complexes on tumor cells, activate via TCR signaling, and kill target cells through antigen-specific cytotoxic mechanisms (e.g., perforin/granzyme).
YES
DIRECT
Engineered TCR-T cells recognize KRAS G12D peptide–HLA-A*11:01 on target cells via their TCR and kill them through cytotoxic granule release (perforin/granzymes) and death-receptor signaling.