An engineered bispecific IgM T-cell–engaging antibody administered intravenously that binds CD38 on myeloma cells and CD3 on T cells, redirecting T cells to mediate T-cell–dependent cellular cytotoxicity and triggering complement-dependent cytotoxicity.
Engineered bispecific IgM antibody that binds CD38 on tumor cells and CD3 on T cells, crosslinking to redirect T cells for T-cell-dependent cellular cytotoxicity; the IgM format also activates complement to mediate complement-dependent cytotoxicity against CD38-positive cells.
NO
INDIRECT
CD3ε on T cells is engaged to activate and redirect T cells; the drug also binds CD38 on tumor cells, leading to T‑cell–dependent killing and complement‑dependent cytotoxicity of CD38+ cells, not CD3+ cells.
IV investigational immunotherapy; the specific cellular target and mechanism are not disclosed in the trial record.
Anti-5T4 monoclonal antibody linked to the microtubule-disrupting payload monomethyl auristatin E (MMAE). After binding to 5T4-expressing tumor cells and internalization, MMAE inhibits tubulin polymerization, leading to G2/M cell-cycle arrest and apoptosis; 5T4 is overexpressed on many tumors with limited normal tissue expression.
YES
DIRECT
An anti-5T4 antibody-drug conjugate binds 5T4 on target cells, is internalized, and releases MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis of 5T4-expressing cells.
IV investigational immunotherapy; the specific cellular target and mechanism are not disclosed in the trial record.
Anti-5T4 monoclonal antibody linked to the microtubule-disrupting payload monomethyl auristatin E (MMAE). After binding to 5T4-expressing tumor cells and internalization, MMAE inhibits tubulin polymerization, leading to G2/M cell-cycle arrest and apoptosis; 5T4 is overexpressed on many tumors with limited normal tissue expression.
NO
INDIRECT
XB010 targets 5T4 on the cell surface; after 5T4-mediated internalization, its MMAE payload binds beta-tubulin to disrupt microtubules. Beta-tubulin expression alone does not trigger targeting or killing.
Fc-engineered humanized IgG1 anti-CD19 monoclonal antibody given IV; binds CD19 on B cells/leukemic blasts to enhance Fcγ receptor–mediated ADCC and ADCP via NK cells and macrophages and can induce direct apoptosis, leading to depletion of CD19+ cells in B-lineage ALL.
Fc‑engineered humanized IgG1 monoclonal antibody against CD19 that binds CD19 on B cells and leukemic blasts and enhances Fcγ receptor–mediated ADCC and ADCP by NK cells and macrophages; can also induce direct apoptosis, resulting in depletion of CD19‑positive cells.
YES
DIRECT
Binds CD19 on B cells and recruits Fcγ receptor–bearing effector cells (NK cells/macrophages) to mediate ADCC and ADCP; binding can also trigger direct apoptosis of CD19+ cells.
Fc-engineered humanized IgG1 anti-CD19 monoclonal antibody given IV; binds CD19 on B cells/leukemic blasts to enhance Fcγ receptor–mediated ADCC and ADCP via NK cells and macrophages and can induce direct apoptosis, leading to depletion of CD19+ cells in B-lineage ALL.
Fc‑engineered humanized IgG1 monoclonal antibody against CD19 that binds CD19 on B cells and leukemic blasts and enhances Fcγ receptor–mediated ADCC and ADCP by NK cells and macrophages; can also induce direct apoptosis, resulting in depletion of CD19‑positive cells.
NO
INDIRECT
Tafasitamab binds CD19 on B cells; its Fc engages CD16A on NK cells/macrophages to trigger ADCC/ADCP that kills CD19+ targets. CD16A-expressing effector cells are not killed by the drug.