CD20×CD3 bispecific T‑cell–engaging antibody that redirects T cells to kill CD20+ B cells; administered IV with step‑up dosing.
Glofitamab is a CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells, bringing them into proximity to form an immune synapse and activate T cells, leading to perforin/granzyme‑mediated killing of CD20‑positive B‑cell malignancies.
YES
DIRECT
Bispecific binding to CD20 on B cells and CD3 on T cells forms an immune synapse and activates T cells to kill CD20+ cells via perforin/granzyme-mediated cytotoxicity.
Autologous gene-modified T cells engineered to express an anti-CD19 chimeric antigen receptor, enabling targeted depletion of CD19+ B cells to reduce autoantibody production and reset dysregulated humoral immunity.
Autologous T cells are engineered to express an anti-CD19 chimeric antigen receptor that recognizes CD19 on B cells and triggers T-cell activation and cytotoxic killing, depleting CD19+ B-cell subsets to reduce autoantibody production and B cell–mediated antigen presentation, thereby resetting dysregulated humoral immunity.
YES
DIRECT
CAR-T cells recognize CD19 via the CAR and directly kill CD19+ cells through T-cell cytotoxic mechanisms (perforin/granzyme-mediated lysis and Fas–FasL–induced apoptosis).
An anti-HER2 antibody–drug conjugate with a microtubule-inhibiting payload that binds HER2 (ERBB2) and kills HER2-expressing tumor cells.
HER2-directed antibody–drug conjugate that binds ERBB2 on tumor cells; after internalization, a cleavable linker releases the microtubule inhibitor MMAE, which blocks tubulin polymerization, leading to G2/M cell-cycle arrest and apoptosis in HER2-expressing cancer cells.
YES
DIRECT
The anti-HER2 ADC binds HER2 on tumor cells, is internalized, and releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis of HER2-expressing cells.
An anti-HER2 antibody–drug conjugate with a microtubule-inhibiting payload that binds HER2 (ERBB2) and kills HER2-expressing tumor cells.
HER2-directed antibody–drug conjugate that binds ERBB2 on tumor cells; after internalization, a cleavable linker releases the microtubule inhibitor MMAE, which blocks tubulin polymerization, leading to G2/M cell-cycle arrest and apoptosis in HER2-expressing cancer cells.
NO
INDIRECT
Disitamab vedotin targets HER2 on tumor cells, is internalized, and releases MMAE, which binds the beta‑tubulin vinca domain to block microtubule polymerization, causing G2/M arrest and apoptosis. Beta‑tubulin expression alone does not confer selective killing.
Intravenous anti–PD-L1 IgG1 monoclonal antibody immune checkpoint inhibitor; blocks PD-L1 from engaging PD-1/B7.1 to restore T-cell activity and can trigger NK cell–mediated ADCC via its Fc.
Human IgG1 anti–PD-L1 immune checkpoint inhibitor that blocks PD-L1 interaction with PD-1/B7.1 to release inhibitory signaling and restore T‑cell activity; its Fc can engage Fcγ receptors to trigger NK cell–mediated ADCC against PD-L1–expressing cells.
YES
DIRECT
Avelumab binds PD-L1 on target cells and its IgG1 Fc engages Fcγ receptors on NK cells to trigger antibody-dependent cellular cytotoxicity, leading to lysis of PD-L1–expressing cells.