Anti-CD33 antibody–drug conjugate that delivers calicheamicin to CD33-positive AML blasts, causing DNA double-strand breaks and apoptosis.
Humanized anti-CD33 monoclonal antibody conjugated to calicheamicin; binds CD33 on AML blasts, is internalized, and releases calicheamicin that binds the DNA minor groove to induce double-strand breaks, inhibiting DNA synthesis and triggering apoptosis.
YES
DIRECT
ADC binds CD33 on target cells, is internalized, and releases calicheamicin, which induces DNA double‑strand breaks leading to apoptosis of the CD33+ cells.
Anti-CD33 antibody–drug conjugate that delivers calicheamicin to CD33-positive AML blasts, causing DNA double-strand breaks and apoptosis.
Humanized anti-CD33 monoclonal antibody conjugated to calicheamicin; binds CD33 on AML blasts, is internalized, and releases calicheamicin that binds the DNA minor groove to induce double-strand breaks, inhibiting DNA synthesis and triggering apoptosis.
NO
INDIRECT
Gemtuzumab ozogamicin binds CD33 on target cells, is internalized, and then releases calicheamicin that binds the DNA minor groove to cause double‑strand breaks and apoptosis; DNA is the payload site, not the selective determinant of which cells are killed.
Autologous anti-GPRC5D chimeric antigen receptor (CAR) T-cell therapy in which the patient’s T cells are genetically modified to express a CAR targeting GPRC5D on malignant plasma cells; upon antigen engagement, CAR-T cells activate, proliferate, release cytokines, and kill target cells. Given as a single infusion after lymphodepletion for relapsed/refractory multiple myeloma or primary plasma cell leukemia.
Autologous T cells genetically modified to express a chimeric antigen receptor targeting GPRC5D on malignant plasma cells; upon antigen binding, CAR T cells activate, proliferate, release cytokines, and kill target cells via perforin/granzyme-mediated cytotoxicity.
YES
DIRECT
CAR T cells recognizing GPRC5D bind the antigen and kill target cells via perforin/granzyme-mediated cytotoxicity after CAR activation.
Polyclonal antibody preparation that depletes T lymphocytes for induction immunosuppression.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional T-cell apoptosis and functional inhibition, producing potent immunosuppression.
NO
INDIRECT
ATG binds multiple T‑cell surface antigens (e.g., CD2, CD3, CD45, HLA‑DR) and depletes T cells via complement-dependent cytotoxicity and Fc-mediated ADCC; it is not directed against HLA‑C.
A broadly neutralizing monoclonal antibody targeting the CD4 binding site on HIV‑1 Env (synonyms: 3BNC117‑LS, teropavimab); neutralizes virus and mediates Fc‑dependent effector functions (e.g., ADCC/ADCP).
Broadly neutralizing monoclonal antibody (3BNC117-LS/teropavimab) that binds the CD4-binding site on HIV-1 Env gp120, preventing attachment to CD4 and viral entry; its Fc domain mediates effector functions (e.g., ADCC and ADCP, and potentially CDC) to promote clearance of virions and infected cells.
YES
DIRECT
The antibody binds gp120 on HIV‑infected cell surfaces; its Fc engages immune effectors to mediate ADCC and ADCP (and potentially CDC), leading to killing/clearance of Env-expressing cells.