TROP2-targeting antibody-drug conjugate that delivers a topoisomerase I inhibitor payload to TROP2-expressing tumor cells.
TROP2-targeting monoclonal antibody linked via a cleavable linker to a topoisomerase I inhibitor payload. Binding to TROP2 on tumor cells triggers internalization and intracellular release of the payload, which inhibits topoisomerase I to induce DNA damage and replication stress, leading to apoptosis, with potential bystander killing of adjacent tumor cells.
NO
INDIRECT
The ADC binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor that causes DNA damage and apoptosis; DNA topoisomerase I is the intracellular payload target, not the antigen used for cell targeting.
Humanized IgG1 monoclonal antibody targeting EGFR; blocks ligand binding and receptor activation, inhibiting RAS–RAF–MEK–ERK and PI3K–AKT signaling, and can induce antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody against EGFR that blocks ligand binding and receptor activation, inhibiting downstream RAS-RAF-MEK-ERK and PI3K-AKT signaling to suppress tumor cell proliferation and survival; can also mediate antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
The IgG1 antibody binds EGFR on target cells and its Fc engages Fc gamma receptors on immune effectors (e.g., NK cells, macrophages) to trigger ADCC, killing EGFR-positive cells; EGFR blockade can also promote apoptosis/growth arrest.
Chimeric IgG1 anti–TNF-α monoclonal antibody that neutralizes soluble and transmembrane TNF-α, suppressing TNF-driven signaling, cytokine release, leukocyte recruitment, and inducing apoptosis of activated immune cells.
Chimeric IgG1 monoclonal antibody that binds and neutralizes soluble and transmembrane TNF-α, blocking TNF receptor signaling (e.g., NF-κB activation), thereby reducing pro-inflammatory cytokine release and leukocyte recruitment, and can induce apoptosis of activated TNF-expressing immune cells.
NO
INDIRECT
Infliximab neutralizes soluble TNF-α, blocking TNF receptor signaling but not engaging target cells; it does not directly kill TNF-producing cells. Direct cytotoxicity (e.g., ADCC/apoptosis) occurs only when binding transmembrane TNF, not the soluble form.
Chimeric IgG1 anti–TNF-α monoclonal antibody that neutralizes soluble and transmembrane TNF-α, suppressing TNF-driven signaling, cytokine release, leukocyte recruitment, and inducing apoptosis of activated immune cells.
Chimeric IgG1 monoclonal antibody that binds and neutralizes soluble and transmembrane TNF-α, blocking TNF receptor signaling (e.g., NF-κB activation), thereby reducing pro-inflammatory cytokine release and leukocyte recruitment, and can induce apoptosis of activated TNF-expressing immune cells.
YES
DIRECT
Infliximab binds transmembrane TNF-α on activated immune cells; its IgG1 Fc recruits effector functions (ADCC by NK/myeloid cells and CDC) and crosslinking of tmTNF triggers reverse-signaling–mediated apoptosis of the TNF-expressing cells.
CD79b-directed antibody-drug conjugate that delivers monomethyl auristatin E (MMAE), a microtubule inhibitor.
CD79b-targeted monoclonal antibody linked via a protease-cleavable linker to monomethyl auristatin E (MMAE). After binding CD79b on B cells and internalization, MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis of CD79b-positive malignant B cells.
YES
DIRECT
The ADC binds CD79b on B cells, is internalized, and releases MMAE via a cleavable linker to inhibit tubulin polymerization, leading to G2/M arrest and apoptosis of CD79b-positive cells.