Monoclonal antibody against IL-5 receptor alpha (afucosylated IgG1) that depletes eosinophils via ADCC and blocks IL-5 signaling to reduce eosinophilic inflammation.
Afucosylated humanized IgG1 monoclonal antibody targeting IL-5 receptor alpha that blocks IL-5 signaling and engages FcγRIIIa to drive potent ADCC, depleting IL-5Rα–expressing eosinophils and basophils to reduce eosinophilic inflammation.
YES
DIRECT
Benralizumab binds IL-5Rα on target cells and engages FcγRIIIa on NK cells, triggering potent ADCC (and related effector functions), leading to apoptosis/depletion of IL-5Rα-expressing eosinophils and basophils.
Monoclonal antibody against IL-5 receptor alpha (afucosylated IgG1) that depletes eosinophils via ADCC and blocks IL-5 signaling to reduce eosinophilic inflammation.
Afucosylated humanized IgG1 monoclonal antibody targeting IL-5 receptor alpha that blocks IL-5 signaling and engages FcγRIIIa to drive potent ADCC, depleting IL-5Rα–expressing eosinophils and basophils to reduce eosinophilic inflammation.
NO
INDIRECT
Benralizumab uses its afucosylated Fc to engage FcγRIIIa (CD16a) on NK cells and trigger ADCC against IL-5Rα–expressing eosinophils/basophils; CD16a-expressing cells are effectors, not killed by the drug.
Autologous, gene-modified Tmod logic-gated CAR T-cell therapy with an MSLN-targeting activating receptor and an HLA-A*02–specific inhibitory receptor, designed to selectively kill mesothelin-positive tumor cells with loss of HLA-A*02 while sparing normal tissues.
Autologous, gene‑modified logic‑gated CAR T cells with an MSLN‑targeting activating CAR and an HLA‑A*02–specific inhibitory receptor (Tmod) that enable killing of mesothelin‑positive tumor cells that have lost HLA‑A*02 while sparing HLA‑A*02–positive normal tissues; includes B2M shRNA to modulate HLA class I on the engineered T cells. Anti‑tumor effect via redirected T‑cell cytotoxicity (perforin/granzyme, cytokines).
YES
DIRECT
MSLN-positive tumor cells lacking HLA-A*02 are recognized by the activating anti-mesothelin CAR and are lysed by the engineered T cells via perforin/granzyme-mediated cytotoxicity (with cytokine effects). The HLA-A*02–specific inhibitory receptor blocks killing of HLA-A*02–positive cells.
Autologous, gene-modified Tmod logic-gated CAR T-cell therapy with an MSLN-targeting activating receptor and an HLA-A*02–specific inhibitory receptor, designed to selectively kill mesothelin-positive tumor cells with loss of HLA-A*02 while sparing normal tissues.
Autologous, gene‑modified logic‑gated CAR T cells with an MSLN‑targeting activating CAR and an HLA‑A*02–specific inhibitory receptor (Tmod) that enable killing of mesothelin‑positive tumor cells that have lost HLA‑A*02 while sparing HLA‑A*02–positive normal tissues; includes B2M shRNA to modulate HLA class I on the engineered T cells. Anti‑tumor effect via redirected T‑cell cytotoxicity (perforin/granzyme, cytokines).
NO
INDIRECT
HLA-A*02 engagement of the Tmod inhibitory receptor prevents CAR T activation; cytotoxicity is directed only to mesothelin-positive cells lacking HLA-A*02 via T-cell perforin/granzyme pathways.
Investigational intravenous immunotherapy; specific target/mechanism not specified in the registry (administered every 2 weeks, the day after toripalimab).
SMET12 is a bispecific anti-EGFR/CD3 T-cell engager antibody that binds EGFR on tumor cells and CD3 on T cells, crosslinking and activating cytotoxic T lymphocytes to redirect them to EGFR-expressing tumor cells and induce targeted T-cell-mediated killing.
NO
INDIRECT
SMET12 engages CD3 on T cells and EGFR on tumor cells to activate T-cell cytotoxicity (perforin/granzyme) against EGFR-expressing tumor cells; CD3ε-expressing T cells are not killed.