Bispecific antibody-drug conjugate (izalontamab brengitecan; BMS-986507) targeting EGFR and HER3; after binding and internalization, releases a topoisomerase I inhibitor payload (brengitecan) that induces DNA damage and tumor cell death.
Bispecific ADC targeting EGFR and HER3; after receptor binding and internalization, the linker is cleaved to release the topoisomerase I inhibitor brengitecan, inducing DNA damage and apoptosis in EGFR/HER3-expressing tumor cells.
YES
DIRECT
The ADC binds EGFR on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and apoptosis.
Autologous, gene-edited tumor-infiltrating lymphocyte (TIL) therapy engineered to inactivate SOCS1 and Regnase-1 (ZC3H12A) to enhance T-cell activation, cytokine production, proliferation, persistence, and tumor killing.
Autologous tumor-infiltrating lymphocytes edited with CRISPR-Cas9 to inactivate SOCS1 and Regnase-1 (ZC3H12A), removing intrinsic brakes on cytokine/JAK-STAT signaling and mRNA stability. This enhances T-cell activation, cytokine production, proliferation, persistence, and cytotoxic killing of tumor cells after infusion.
NO
INDIRECT
Regnase-1 is knocked out within the infused TILs to enhance their function; it is not a killing target. The edited TILs then kill tumor cells they recognize via TCR, primarily through perforin/granzyme release and Fas–FasL interactions.
Bispecific antibody-drug conjugate (izalontamab brengitecan; BMS-986507) targeting EGFR and HER3; after binding and internalization, releases a topoisomerase I inhibitor payload (brengitecan) that induces DNA damage and tumor cell death.
Bispecific ADC targeting EGFR and HER3; after receptor binding and internalization, the linker is cleaved to release the topoisomerase I inhibitor brengitecan, inducing DNA damage and apoptosis in EGFR/HER3-expressing tumor cells.
YES
DIRECT
The bispecific ADC binds HER3 on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and apoptosis of the HER3-expressing cells.
Bispecific antibody-drug conjugate (izalontamab brengitecan; BMS-986507) targeting EGFR and HER3; after binding and internalization, releases a topoisomerase I inhibitor payload (brengitecan) that induces DNA damage and tumor cell death.
Bispecific ADC targeting EGFR and HER3; after receptor binding and internalization, the linker is cleaved to release the topoisomerase I inhibitor brengitecan, inducing DNA damage and apoptosis in EGFR/HER3-expressing tumor cells.
NO
INDIRECT
BL-B01D1 binds EGFR/HER3 on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan that causes DNA damage and apoptosis. Topoisomerase I is the intracellular enzymatic target of the payload, not the antigen recognized by the ADC.
Human afucosylated IgG1 monoclonal antibody (AMG 451; KHK4083) administered subcutaneously that targets OX40 (TNFRSF4) on activated T cells, blocking OX40–OX40L co-stimulatory signaling and mediating ADCC to deplete OX40+ T cells, thereby reducing T-cell activation, survival, and memory and attenuating type 2 inflammation.
Human afucosylated IgG1 monoclonal antibody targeting OX40 (TNFRSF4) on activated T cells; blocks OX40–OX40L co-stimulatory signaling and leverages enhanced ADCC to deplete OX40+ effector/memory T cells, reducing T-cell activation, survival, and type 2 inflammatory responses.
YES
DIRECT
Afucosylated IgG1 binding to OX40 recruits FcγRIIIa-expressing effectors (e.g., NK cells) to mediate ADCC, with possible ADCP, depleting OX40+ T cells.