Rabbit polyclonal anti-thymocyte globulin that depletes T cells to prevent rejection and GVHD.
Rabbit polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, producing immunosuppression to prevent rejection and GVHD.
YES
DIRECT
Polyclonal anti-thymocyte IgG binds CD28 on T cells and depletes them via complement-dependent cytotoxicity, Fc-mediated ADCC, and apoptosis.
Off-the-shelf, allogeneic iPSC-derived HER2-directed CAR T-cell therapy designed to kill HER2 (ERBB2)-expressing tumor cells.
Off-the-shelf, allogeneic iPSC-derived HER2-directed CAR T cells that recognize HER2 (ERBB2) via a 1XX CAR, triggering T-cell activation and cytotoxic killing of HER2+ tumor cells. Engineered features include CXCR2 to enhance trafficking, a TGFβ signal-redirection receptor to counter immunosuppression, CD38 knockout for persistence, an IL-7/IL-7R fusion to support T-cell stemness, TCR removal to reduce GVHD risk, and a high-affinity non-cleavable CD16a to enable antibody-dependent cellular cytotoxicity when a compatible therapeutic antibody is administered.
NO
INDIRECT
FT825 kills HER2-expressing cells via CAR-mediated T-cell cytotoxicity. TGF-beta 3 only engages the engineered TGF-beta signal-redirection receptor to enhance activation and resistance to suppression; it is not a killing target.
Off-the-shelf, allogeneic iPSC-derived HER2-directed CAR T-cell therapy designed to kill HER2 (ERBB2)-expressing tumor cells.
Off-the-shelf, allogeneic iPSC-derived HER2-directed CAR T cells that recognize HER2 (ERBB2) via a 1XX CAR, triggering T-cell activation and cytotoxic killing of HER2+ tumor cells. Engineered features include CXCR2 to enhance trafficking, a TGFβ signal-redirection receptor to counter immunosuppression, CD38 knockout for persistence, an IL-7/IL-7R fusion to support T-cell stemness, TCR removal to reduce GVHD risk, and a high-affinity non-cleavable CD16a to enable antibody-dependent cellular cytotoxicity when a compatible therapeutic antibody is administered.
NO
INDIRECT
IL-8 is not a killing target. CXCR2 on FT825 uses IL-8 as a chemotactic cue to enhance trafficking; cytotoxicity occurs when the CAR T cells recognize HER2 (or via CD16a-mediated ADCC with a therapeutic antibody), not by binding IL-8.
Chimeric IgG1 monoclonal antibody against EGFR (ERBB1); blocks EGFR signaling and induces ADCC.
Chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR (ERBB1), blocking ligand binding, receptor activation and dimerization to inhibit downstream signaling and tumor cell proliferation; its Fc region also engages immune effector cells to mediate ADCC against EGFR-expressing cells.
YES
DIRECT
IgG1 Fc engages FcγR-bearing immune cells (e.g., NK cells) to mediate ADCC, with some complement-dependent cytotoxicity; EGFR blockade is antiproliferative but cytolysis occurs via ADCC/CDC against EGFR-expressing cells.
An anti-CD19 IgG monoclonal antibody–drug conjugate (Zynlonta; ADCT-402) that delivers the PBD dimer cytotoxic payload tesirine to CD19-expressing B cells. After binding and internalization, tesirine is released to create DNA interstrand crosslinks, triggering DNA damage responses, cell-cycle arrest, and apoptosis. Administered IV every 21 days for relapsed/refractory B-cell malignancies.
Humanized anti-CD19 monoclonal antibody linked via a cleavable linker to tesirine (a pyrrolobenzodiazepine dimer). After binding CD19 and internalization, the payload is released to form DNA minor-groove interstrand crosslinks (at N2-guanine), inhibiting DNA replication and inducing DNA damage response, cell-cycle arrest, and apoptosis in CD19-expressing B cells.
YES
DIRECT
ADC binds CD19, is internalized, and releases the tesirine (PBD dimer) payload, which forms DNA interstrand crosslinks (N2-guanine), inhibiting replication and triggering DNA damage–mediated cell-cycle arrest and apoptosis in CD19+ cells.