Polyclonal antibody preparation that depletes T cells and provides immunosuppression.
Polyclonal anti-thymocyte immunoglobulin that binds multiple T-cell surface antigens and depletes T lymphocytes via complement-dependent lysis and Fc-mediated effector functions (ADCC/phagocytosis), resulting in broad immunosuppression.
YES
DIRECT
ATG antibodies can bind HLA-DR on leukocytes and induce complement-dependent lysis and Fc-mediated ADCC/phagocytosis, depleting HLA-DR–expressing cells.
Chimeric monoclonal antibody that neutralizes TNF-α.
Chimeric monoclonal antibody that binds soluble and transmembrane TNF-alpha, blocking its interaction with TNFR1/TNFR2 and downstream NF-kappaB/MAPK signaling; suppresses pro-inflammatory cytokine activity and may induce complement/ADCC or apoptosis in TNF-alpha–expressing cells depending on context.
YES
DIRECT
Binds transmembrane TNF-alpha on cells; Fc region triggers ADCC/CDC via FcγR+ effectors and complement, and can induce apoptosis via reverse signaling in tmTNF-expressing cells.
CD30-directed antibody–drug conjugate (IgG1 mAb linked to MMAE) that binds CD30 on Hodgkin/Reed–Sternberg cells, is internalized, releases a microtubule-disrupting payload, and induces apoptosis.
CD30-directed IgG1 monoclonal antibody conjugated via a cleavable valine–citrulline linker to the microtubule inhibitor monomethyl auristatin E (MMAE). After binding CD30 on tumor cells and internalization, lysosomal cleavage releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis.
YES
DIRECT
The ADC binds CD30, is internalized, and lysosomal cleavage releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis of CD30-expressing cells.
A TROP-2–targeted antibody–drug conjugate (MK-2870/SKB264) that binds TROP-2 on tumor cells, is internalized, and releases a topoisomerase-I inhibitor payload to induce DNA damage and apoptosis.
TROP-2–targeted antibody–drug conjugate: the IgG1 antibody binds TROP-2 on tumor cells, is internalized, and a cleavable linker releases tirumotecan (a topoisomerase I–inhibiting belotecan derivative), leading to DNA replication inhibition, DNA damage, cell-cycle arrest, and apoptosis, with a bystander effect on neighboring tumor cells.
YES
DIRECT
The ADC binds TROP-2 on tumor cells, is internalized, and its cleavable linker releases the topoisomerase I inhibitor tirumotecan, causing DNA replication inhibition, DNA damage, cell-cycle arrest, and apoptosis (with some bystander effect).
CD30-directed antibody–drug conjugate (IgG1 mAb linked to MMAE) that binds CD30 on Hodgkin/Reed–Sternberg cells, is internalized, releases a microtubule-disrupting payload, and induces apoptosis.
CD30-directed IgG1 monoclonal antibody conjugated via a cleavable valine–citrulline linker to the microtubule inhibitor monomethyl auristatin E (MMAE). After binding CD30 on tumor cells and internalization, lysosomal cleavage releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis.
NO
INDIRECT
Brentuximab vedotin kills CD30-positive cells after binding CD30, internalization, and lysosomal release of MMAE, which binds the tubulin vinca domain to block polymerization and induce G2/M arrest and apoptosis. Tubulin expression alone does not confer susceptibility without CD30-mediated delivery.