Autologous gene-modified T cells engineered to express a mesothelin-directed KIR-based CAR; given as a single IV infusion. The KIR-CAR binds mesothelin on tumor cells to activate the engineered T cells, inducing antigen-specific cytotoxicity and cytokine release against mesothelin-expressing ovarian cancer, cholangiocarcinoma, and mesothelioma.
Autologous T cells engineered with a mesothelin-directed KIR-based CAR (anti-MSLN scFv fused to KIR2DS2 signaling and DAP12). Binding to mesothelin on tumor cells triggers KIR-mediated activation, leading to antigen-specific T-cell cytotoxicity and cytokine release against mesothelin-expressing cancers; KIR-CAR design may reduce T-cell exhaustion and enhance persistence.
YES
DIRECT
Mesothelin-targeted KIR-CAR T cells bind mesothelin on tumor cells, activate, and kill them via perforin/granzyme-mediated cytolysis and death receptor pathways, with cytokine release.
Anti-CD38 IgG1 monoclonal antibody that mediates complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity/phagocytosis, and apoptosis, depleting CD38-positive plasma and immunosuppressive cells.
Anti-CD38 IgG1 monoclonal antibody that binds CD38 on plasma/tumor and immunosuppressive cells, inducing complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity and phagocytosis, and apoptosis, leading to depletion of CD38+ cells.
YES
DIRECT
Binds CD38 on target cells and triggers complement-dependent cytotoxicity, Fc-mediated ADCC and phagocytosis, and can induce apoptosis, leading to depletion of CD38+ cells.
A humanized monoclonal antibody targeting IL-5 receptor alpha (IL-5Rα) on eosinophils and basophils, inducing rapid cytotoxic depletion to reduce eosinophilic airway inflammation in severe asthma; modulates type-2 inflammatory pathways (IL-5, IL-4, IL-13) including the IL-13/FeNO axis, with potential effects on ILC2s, epithelial cells, macrophages, mast cells, and airway smooth muscle, and exploratory restoration of antiviral responses.
Afucosylated humanized monoclonal antibody that binds IL-5 receptor alpha (IL-5Rα) on eosinophils and basophils and engages FcγRIIIa to drive potent ADCC, causing rapid depletion of these cells and consequent suppression of eosinophilic/type‑2 inflammation (IL‑5/IL‑4/IL‑13 pathways) in severe asthma.
YES
DIRECT
Afucosylated anti–IL-5Rα antibody binds CD125 on eosinophils/basophils and engages FcγRIIIa on NK cells to trigger potent ADCC (and some ADCP), leading to apoptosis/lysis of IL-5Rα+ cells.
A humanized monoclonal antibody targeting IL-5 receptor alpha (IL-5Rα) on eosinophils and basophils, inducing rapid cytotoxic depletion to reduce eosinophilic airway inflammation in severe asthma; modulates type-2 inflammatory pathways (IL-5, IL-4, IL-13) including the IL-13/FeNO axis, with potential effects on ILC2s, epithelial cells, macrophages, mast cells, and airway smooth muscle, and exploratory restoration of antiviral responses.
Afucosylated humanized monoclonal antibody that binds IL-5 receptor alpha (IL-5Rα) on eosinophils and basophils and engages FcγRIIIa to drive potent ADCC, causing rapid depletion of these cells and consequent suppression of eosinophilic/type‑2 inflammation (IL‑5/IL‑4/IL‑13 pathways) in severe asthma.
NO
INDIRECT
Benralizumab binds IL-5Rα on eosinophils/basophils and engages FcγRIIIa (CD16a) on NK cells to trigger ADCC, killing IL-5Rα+ cells; CD16a+ effector cells themselves are not killed.
First-generation BCR-ABL tyrosine kinase inhibitor used to suppress leukemic proliferation in CML.
ATP-competitive tyrosine kinase inhibitor targeting BCR-ABL (and also PDGFR and KIT), blocking downstream phosphorylation signaling to suppress proliferation and induce apoptosis of malignant cells (e.g., CML; GIST via KIT).
YES
DIRECT
Imatinib directly inhibits the PDGFRA tyrosine kinase (ATP-competitive), shutting down downstream signaling (e.g., RAS/MAPK, PI3K/AKT), causing growth arrest and apoptosis of PDGFRA-driven cells.