Bispecific T-cell engager (CD19xCD3) that redirects T cells to kill CD19-positive B-ALL blasts.
Blinatumomab is a CD19xCD3 bispecific single-chain antibody (BiTE) that binds CD19 on B cells and CD3 on T cells, bringing them into proximity to activate T cells and form an immunologic synapse, resulting in perforin/granzyme-mediated killing of CD19-positive B-lymphoblasts.
YES
DIRECT
Blinatumomab links CD3 on T cells to CD19 on target cells, activating T cells to kill CD19-positive cells via perforin/granzyme-mediated cytotoxicity.
Bispecific T-cell engager (CD19xCD3) that redirects T cells to kill CD19-positive B-ALL blasts.
Blinatumomab is a CD19xCD3 bispecific single-chain antibody (BiTE) that binds CD19 on B cells and CD3 on T cells, bringing them into proximity to activate T cells and form an immunologic synapse, resulting in perforin/granzyme-mediated killing of CD19-positive B-lymphoblasts.
NO
INDIRECT
Blinatumomab binds CD3 on T cells to activate them and link to CD19+ cells; the T cells then kill CD19+ targets via perforin/granzyme. CD3+ cells are not directly killed.
An antibody–drug conjugate where a trastuzumab-based anti-HER2 antibody targets HER2-expressing tumor cells and delivers a deruxtecan (DXd) topoisomerase I inhibitor payload, causing DNA damage and apoptosis; the membrane-permeable payload enables a bystander effect and the Fc region may mediate ADCC.
A trastuzumab-based anti-HER2 antibody binds HER2 on tumor cells, is internalized, and releases the deruxtecan (DXd) payload, a membrane-permeable topoisomerase I inhibitor that induces DNA damage and apoptosis; the payload can exert a bystander effect on neighboring cells, and the antibody Fc region may mediate ADCC.
YES
DIRECT
The anti-HER2 ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage and apoptosis; Fc-mediated ADCC and a membrane-permeable bystander effect can add killing.
An antibody–drug conjugate where a trastuzumab-based anti-HER2 antibody targets HER2-expressing tumor cells and delivers a deruxtecan (DXd) topoisomerase I inhibitor payload, causing DNA damage and apoptosis; the membrane-permeable payload enables a bystander effect and the Fc region may mediate ADCC.
A trastuzumab-based anti-HER2 antibody binds HER2 on tumor cells, is internalized, and releases the deruxtecan (DXd) payload, a membrane-permeable topoisomerase I inhibitor that induces DNA damage and apoptosis; the payload can exert a bystander effect on neighboring cells, and the antibody Fc region may mediate ADCC.
NO
INDIRECT
The ADC binds HER2, is internalized, and releases DXd, which inhibits topoisomerase I to cause DNA damage and apoptosis. Topoisomerase I is the payload’s intracellular enzyme target, not the binding antigen; cells are not selectively killed for expressing topoisomerase I unless they receive the payload via HER2-mediated delivery or bystander diffusion.
Chimeric IgG1 monoclonal antibody against EGFR; blocks ligand-induced EGFR signaling (RAS/RAF/MEK/ERK; PI3K/AKT) and opsonizes tumor cells to enhance NK cell ADCC.
Cetuximab is a chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding, receptor activation and dimerization, thereby inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling to suppress tumor proliferation. Its Fc region also opsonizes EGFR-expressing tumor cells to promote NK cell–mediated ADCC.
YES
DIRECT
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on NK cells to mediate ADCC (and can trigger complement-dependent cytotoxicity), leading to lysis of EGFR-positive cells; EGFR blockade mainly inhibits proliferation.