Polyclonal IgG biologic immunosuppressant targeting T lymphocytes, administered pre-transplant to prevent GVHD. Depletes and modulates T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; inhibits T-cell activation/proliferation and trafficking; may reduce antigen-presenting cell activity and inflammatory cytokine signaling.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; also suppresses T-cell activation/proliferation and trafficking and dampens APC activity and inflammatory cytokine signaling to prevent GVHD.
YES
DIRECT
Polyclonal IgG binds CD4 on T cells and triggers complement-dependent lysis and Fc-mediated ADCC; binding can also induce apoptosis, depleting CD4+ T cells.
Polyclonal IgG biologic immunosuppressant targeting T lymphocytes, administered pre-transplant to prevent GVHD. Depletes and modulates T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; inhibits T-cell activation/proliferation and trafficking; may reduce antigen-presenting cell activity and inflammatory cytokine signaling.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; also suppresses T-cell activation/proliferation and trafficking and dampens APC activity and inflammatory cytokine signaling to prevent GVHD.
YES
DIRECT
Polyclonal anti–T-cell IgG binds CD8 alpha on T cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC; crosslinking can also trigger apoptosis.
Polyclonal IgG biologic immunosuppressant targeting T lymphocytes, administered pre-transplant to prevent GVHD. Depletes and modulates T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; inhibits T-cell activation/proliferation and trafficking; may reduce antigen-presenting cell activity and inflammatory cytokine signaling.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, ADCC, and apoptosis; also suppresses T-cell activation/proliferation and trafficking and dampens APC activity and inflammatory cytokine signaling to prevent GVHD.
YES
DIRECT
ATLG binds CD5 on T cells; Fc engagement triggers complement-dependent cytotoxicity and ADCC, and can induce apoptosis, depleting CD5+ cells.
A Trop-2–targeted antibody–drug conjugate consisting of a humanized anti–Trop-2 monoclonal antibody linked via a hydrolyzable linker to SN-38 (the active metabolite of irinotecan). After binding Trop-2 on tumor cells and internalization, it releases SN-38 to inhibit topoisomerase I, causing DNA damage, S-phase arrest, and apoptosis, with potential bystander effect.
Humanized anti-Trop-2 monoclonal antibody linked via a hydrolyzable linker to SN-38. After binding Trop-2 on tumor cells and internalization, the linker is cleaved to release SN-38, which inhibits topoisomerase I by stabilizing topo I-DNA complexes, leading to DNA damage, S-phase arrest, and apoptosis, with potential bystander killing of neighboring cells.
YES
DIRECT
ADC binds Trop-2, is internalized, and releases SN-38, which inhibits topoisomerase I causing DNA damage and apoptosis (with potential bystander killing).
Disitamab vedotin is an anti-HER2 monoclonal antibody conjugated to the microtubule inhibitor MMAE. It binds HER2 on tumor cells, is internalized, and releases MMAE via a protease-cleavable linker in lysosomes, leading to microtubule disruption, G2/M cell-cycle arrest, and apoptotic cell death; the antibody component may also contribute to antitumor activity via Fc-mediated effector functions.
NO
INDIRECT
RC48 targets HER2, is internalized, and releases MMAE, which binds tubulin to disrupt microtubules causing G2/M arrest and apoptosis. Killing is driven by HER2-mediated delivery (with possible bystander effect), not by recognition of tubulin itself.