An antibody–drug conjugate (brand name Besponsa) comprising a humanized anti-CD22 IgG4 monoclonal antibody linked to the cytotoxic agent calicheamicin; it binds CD22 on B-lymphoblasts, is internalized, and releases calicheamicin intracellularly to induce DNA double-strand breaks and apoptosis.
Humanized anti-CD22 IgG4 antibody-drug conjugate; after binding CD22 on B cells and being internalized, it releases the cytotoxic payload calicheamicin, which binds the DNA minor groove and causes double-strand breaks, leading to apoptosis.
YES
DIRECT
The anti-CD22 ADC binds CD22 on B cells, is internalized, and releases calicheamicin intracellularly, which induces DNA double-strand breaks leading to apoptosis of CD22+ cells.
An antibody–drug conjugate (brand name Besponsa) comprising a humanized anti-CD22 IgG4 monoclonal antibody linked to the cytotoxic agent calicheamicin; it binds CD22 on B-lymphoblasts, is internalized, and releases calicheamicin intracellularly to induce DNA double-strand breaks and apoptosis.
Humanized anti-CD22 IgG4 antibody-drug conjugate; after binding CD22 on B cells and being internalized, it releases the cytotoxic payload calicheamicin, which binds the DNA minor groove and causes double-strand breaks, leading to apoptosis.
NO
INDIRECT
The ADC binds CD22 on B cells, is internalized, and releases calicheamicin, which binds the DNA minor groove to cause double‑strand breaks and apoptosis. DNA is the payload’s intracellular target, not the surface determinant for cell killing.
Antigen-specific T cells expanded ex vivo and reinfused to recognize tumor peptides on MHC class I via the TCR, mediating cytotoxicity through perforin/granzyme release and IFN-gamma-mediated effects.
Autologous antigen-specific CTLs expanded ex vivo are reinfused to recognize tumor peptides presented on MHC class I via their endogenous TCR, inducing tumor-cell killing via perforin/granzyme release and death-receptor pathways (FasL/TRAIL), along with IFN-γ secretion to enhance antitumor immune responses.
YES
DIRECT
Antigen-specific CTLs recognize tumor peptide–MHC I via the TCR and kill targets via perforin/granzyme release and by engaging TRAIL on CTLs with DR5 (TRAIL‑R2) on the tumor, triggering extrinsic apoptosis (caspase-8).
Autologous gene-modified CAR T-cell therapy for relapsed/refractory multiple myeloma; patient T cells are engineered to express a CAR that recognizes myeloma-associated antigens and, upon binding, activates T-cell cytotoxicity.
Autologous patient T cells are genetically modified to express a chimeric antigen receptor that recognizes myeloma-associated surface antigens; upon antigen binding, CAR signaling activates and expands the T cells, inducing cytokine release and perforin/granzyme-mediated cytotoxic killing of malignant plasma cells.
NO
INDIRECT
LCAR-M61D CAR T cells are engineered to recognize myeloma-associated antigens (not CD19); therefore CD19+ cells are not targeted. When the CAR binds its cognate antigen, killing occurs via T-cell perforin/granzyme-mediated cytotoxicity.
A subcutaneous CD20×CD3 bispecific T‑cell–engaging antibody that binds CD20 on B cells and CD3 on T cells to form an immune synapse, activate TCR/CD3 signaling, drive T‑cell proliferation and cytotoxic degranulation, and induce targeted B‑cell killing.
Subcutaneous bispecific antibody that binds CD20 on B cells and CD3 on T cells to form an immune synapse, activate TCR/CD3 signaling, expand and activate cytotoxic T cells, and induce perforin/granzyme‑mediated killing of CD20+ malignant B cells.
YES
DIRECT
Epcoritamab bridges CD3 on T cells to CD20 on B cells, forming an immune synapse that activates T cells to release perforin and granzymes, causing cytolysis of CD20+ cells.