Bispecific T-cell engager (BiTE) biologic that binds CD19 on B-lineage cells and CD3 on T cells, redirecting cytotoxic T cells to eliminate CD19+ leukemia/minimal residual disease.
Blinatumomab is a bispecific CD19×CD3 antibody (BiTE) that bridges CD19+ B-lineage cells and CD3+ T cells, forming an immunologic synapse that activates and redirects cytotoxic T cells to lyse CD19-expressing leukemia cells and clear minimal residual disease, independently of MHC.
NO
INDIRECT
Blinatumomab binds CD3ε on T cells to activate and redirect them to kill CD19+ B cells; it does not kill CD3-expressing T cells.
Antibody–drug conjugate targeting CD79b on B cells; delivers MMAE to disrupt microtubules and induce apoptosis.
Monoclonal antibody targets CD79b on B cells; after internalization, a protease-cleavable linker releases MMAE, which inhibits microtubule polymerization, causing G2/M arrest and apoptosis in malignant B cells.
YES
DIRECT
An anti-CD79b antibody–drug conjugate binds CD79b on B cells, is internalized, and releases MMAE, which inhibits microtubule polymerization, causing G2/M arrest and apoptosis of CD79b-expressing cells.
Antibody–drug conjugate targeting CD79b on B cells; delivers MMAE to disrupt microtubules and induce apoptosis.
Monoclonal antibody targets CD79b on B cells; after internalization, a protease-cleavable linker releases MMAE, which inhibits microtubule polymerization, causing G2/M arrest and apoptosis in malignant B cells.
NO
INDIRECT
Polatuzumab vedotin targets CD79b, is internalized, and releases MMAE that binds the vinca site on beta-tubulin to inhibit microtubules, causing G2/M arrest and apoptosis. Beta-tubulin itself is not the targeted antigen.
Anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity and ADCC.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them primarily via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and antibody-dependent cellular phagocytosis (ADCP), leading to elimination of CD20-positive B cells.
YES
DIRECT
Rituximab binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated effector functions (ADCC and antibody-dependent phagocytosis), leading to lysis and clearance of CD20+ cells.
Humanized bispecific anti-CD20×CD3 monoclonal antibody that redirects T-cell cytotoxicity against CD20-positive B cells; given with step-up dosing to mitigate cytokine release syndrome.
Humanized bispecific antibody (2:1 CD20:CD3) that bridges CD20-positive B cells and CD3-positive T cells, activating T cells to form an immune synapse and kill target B cells via perforin/granzyme-mediated cytotoxicity; step-up dosing is used to mitigate cytokine release syndrome.
YES
DIRECT
Glofitamab bridges CD20 on target B cells to CD3 on T cells, forming an immune synapse that activates T cells to release perforin and granzymes, killing CD20+ cells.