A polyclonal immunoglobulin preparation that depletes T cells via complement-mediated lysis and apoptosis and exerts immune-modulatory effects; used peri-transplant to prevent graft-versus-host disease.
Polyclonal anti-thymocyte immunoglobulin that binds multiple T-cell surface antigens and depletes T cells via complement-mediated lysis, apoptosis, and Fc-dependent cytotoxicity, with additional immunomodulatory effects; used peri-transplant to suppress alloreactive T cells and prevent GVHD.
YES
DIRECT
ATG contains antibodies that bind HLA-DR on leukocytes, triggering complement-dependent lysis and Fc-mediated ADCC/phagocytosis, and can induce apoptosis via receptor crosslinking.
An antibody–drug conjugate composed of an anti–Nectin-4 IgG1 monoclonal antibody linked via a protease-cleavable linker to the microtubule-disrupting cytotoxin monomethyl auristatin E (MMAE). It binds Nectin-4 on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, leading to mitotic arrest and apoptosis; Fc-mediated effector functions may also contribute.
Anti–Nectin-4 IgG1 antibody linked via a protease-cleavable linker to MMAE. Upon binding Nectin-4 on tumor cells, the ADC is internalized and the linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptotic cell death; Fc-mediated effector functions may also contribute.
YES
DIRECT
The anti–Nectin-4 ADC binds Nectin-4 on target cells, is internalized, and releases MMAE after linker cleavage; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis. Fc-mediated effector functions may also contribute.
An antibody–drug conjugate composed of an anti–Nectin-4 IgG1 monoclonal antibody linked via a protease-cleavable linker to the microtubule-disrupting cytotoxin monomethyl auristatin E (MMAE). It binds Nectin-4 on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, leading to mitotic arrest and apoptosis; Fc-mediated effector functions may also contribute.
Anti–Nectin-4 IgG1 antibody linked via a protease-cleavable linker to MMAE. Upon binding Nectin-4 on tumor cells, the ADC is internalized and the linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptotic cell death; Fc-mediated effector functions may also contribute.
NO
INDIRECT
The ADC binds Nectin-4 on tumor cells, is internalized, and releases MMAE, which binds the vinca site on beta-tubulin to block microtubule polymerization, causing G2/M arrest and apoptosis in Nectin-4–positive cells; beta-tubulin is not the targeting antigen.
A CD19×CD3 bispecific antibody that binds CD3 on T cells and CD19 on B cells to redirect T‑cell cytotoxicity and deplete CD19+ B-lineage cells; administered IV or SC.
Bispecific antibody that binds CD3 on T cells and CD19 on B cells to crosslink and activate T cells, redirecting cytotoxicity to CD19+ B-lineage cells and depleting them.
YES
DIRECT
Bispecific antibody links CD3 on T cells to CD19 on target cells, forming an immune synapse and activating T-cell cytotoxicity (perforin/granzyme, Fas–FasL), leading to lysis/apoptosis of CD19+ cells.
Autologous dendritic cell (DC) vaccine made from the patient’s monocytes and loaded ex vivo with autologous glioblastoma (GBM) tumor antigens to activate tumor-specific T-cell responses.
Autologous dendritic cells are loaded ex vivo with patient-derived glioblastoma antigens and administered to present these antigens via MHC I/II, priming tumor-specific CD8+ cytotoxic and CD4+ helper T-cell responses that drive CTL-mediated lysis of GBM cells; GM-CSF is used to enhance dendritic cell maturation and activity.
NO
INDIRECT
GM-CSF acts on GM-CSF receptor on dendritic cells to enhance maturation and antigen presentation; cytotoxicity is mediated by vaccine-primed CD8+ T cells that kill GBM cells presenting the tumor antigens (perforin/granzyme), not GM-CSF receptor–expressing cells.