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.
ADC binds CD33 on target cells, is internalized, and releases calicheamicin, which induces DNA double‑strand breaks leading to apoptosis of the CD33+ cells.
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.
CAR T cells recognizing GPRC5D bind the antigen and kill target cells via perforin/granzyme-mediated cytotoxicity after CAR activation.
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.
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.
A broadly neutralizing monoclonal antibody targeting the V3‑glycan epitope on HIV‑1 Env (synonyms: 10‑1074‑LS, zinlirvimab); neutralizes virus and mediates Fc‑dependent effector functions (e.g., ADCC/ADCP).
Broadly neutralizing IgG1 monoclonal antibody (10-1074-LS/zinlirvimab) that binds the V3-glycan (N332) epitope on HIV-1 Env gp120, neutralizing virus by blocking Env-mediated entry; Fc domain engagement mediates effector functions (ADCC/ADCP). LS mutations extend serum half-life.
Antibody binds Env gp120 on infected cell surfaces; its IgG1 Fc engages Fcγ receptors on NK cells/macrophages to trigger ADCC/ADCP (and potentially complement), killing the Env-expressing cells.
Autologous T lymphocytes genetically modified to express a PSCA-targeted chimeric antigen receptor with 4-1BB co-stimulation and CD3ζ signaling, including a truncated CD19 tag for selection/tracking; administered intravenously after lymphodepletion.
Autologous T lymphocytes engineered to express a PSCA-specific chimeric antigen receptor (scFv-4-1BB-CD3zeta). CAR binding to PSCA on tumor cells delivers CD3zeta activation and 4-1BB co-stimulation, promoting T-cell proliferation, cytokine release, and perforin/granzyme-mediated killing of PSCA-positive cells. A truncated CD19 tag enables selection/tracking; given after lymphodepletion to support CAR-T expansion.
CAR-T cells bind PSCA on target cells and, via CD3ζ activation with 4-1BB co-stimulation, directly kill PSCA-positive cells through perforin/granzyme (and Fas–FasL) cytotoxicity.