An antibody–drug conjugate (ADC) also known as iza-bren, izalontamab brengitecan (BMS-986507). The antibody targets a tumor-associated surface antigen, is internalized, and releases a 'gitecan' topoisomerase I inhibitor payload that induces DNA damage and tumor cell death.
Dual-targeting anti-EGFR/anti-HER3 antibody–drug conjugate. The antibody binds EGFR (HER1) and HER3 (ErbB3) on tumor cells, is internalized, and releases a 'gitecan' topoisomerase I inhibitor payload that induces DNA damage and tumor cell death.
NO
INDIRECT
BL-B01D1 does not target Topoisomerase I on the cell surface; it binds EGFR/HER3, is internalized, and releases a topoisomerase I–inhibiting payload that induces DNA damage and kills EGFR/HER3-positive cells.
Autologous genetically modified T cells expressing a chimeric antigen receptor targeting CD70, incorporating CD3ζ and costimulatory domains to activate, expand, secrete cytokines, and kill CD70-positive tumor cells after IV infusion.
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting CD70. Upon binding CD70 on tumor cells, the CAR’s CD3ζ and costimulatory domains activate the T cells, driving proliferation, cytokine release, and cytotoxic killing of CD70-positive cells via perforin/granzyme and death-receptor pathways.
YES
DIRECT
CAR-T cells recognize CD70 via the CAR, become activated (CD3ζ/costimulatory signaling), and kill CD70+ cells through perforin/granzyme release and death-receptor (Fas/TRAIL)–mediated apoptosis.
Antigen-specific T cells expanded ex vivo and reinfused to recognize tumor peptides on MHC class I via the TCR, mediating cytotoxicity through perforin/granzyme release and IFN-gamma-mediated effects.
Autologous antigen-specific CTLs expanded ex vivo are reinfused to recognize tumor peptides presented on MHC class I via their endogenous TCR, inducing tumor-cell killing via perforin/granzyme release and death-receptor pathways (FasL/TRAIL), along with IFN-γ secretion to enhance antitumor immune responses.
YES
DIRECT
Antigen-specific CTLs recognize the tumor peptide presented by HLA-A via their TCR and kill the presenting cells through perforin/granzyme-mediated cytolysis and death-receptor (FasL/TRAIL)–induced apoptosis.
An antibody–drug conjugate (GSK2857916) consisting of a humanized, afucosylated IgG1 monoclonal antibody targeting BCMA (TNFRSF17) conjugated to the cytotoxic payload monomethyl auristatin F (MMAF). It binds BCMA on plasma cells, is internalized, and releases MMAF to inhibit microtubules and induce apoptosis; the afucosylated antibody can also promote ADCC/ADCP.
Afucosylated anti-BCMA IgG1 ADC conjugated to MMAF. Binds BCMA on plasma cells, is internalized, and releases MMAF to inhibit tubulin polymerization causing G2/M arrest and apoptosis; afucosylation enhances ADCC/ADCP.
YES
DIRECT
Belantamab mafodotin binds BCMA on target cells, is internalized, and releases MMAF to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; its afucosylated Fc also mediates ADCC/ADCP against BCMA-expressing cells.
An antibody–drug conjugate (GSK2857916) consisting of a humanized, afucosylated IgG1 monoclonal antibody targeting BCMA (TNFRSF17) conjugated to the cytotoxic payload monomethyl auristatin F (MMAF). It binds BCMA on plasma cells, is internalized, and releases MMAF to inhibit microtubules and induce apoptosis; the afucosylated antibody can also promote ADCC/ADCP.
Afucosylated anti-BCMA IgG1 ADC conjugated to MMAF. Binds BCMA on plasma cells, is internalized, and releases MMAF to inhibit tubulin polymerization causing G2/M arrest and apoptosis; afucosylation enhances ADCC/ADCP.
NO
INDIRECT
Belantamab mafodotin targets BCMA on plasma cells, is internalized, and releases MMAF that binds beta‑tubulin to block microtubule polymerization, causing G2/M arrest and apoptosis; afucosylated Fc also promotes ADCC/ADCP. Tubulin expression alone is not sufficient for killing.