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.
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.
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).
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.
A T-cell–engaging bispecific IgG monoclonal antibody (2:1 format) targeting CD20 on B cells and CD3 on T cells; bridges T cells to CD20+ malignant B cells to trigger TCR/CD3 activation, immunologic synapse formation, and cytotoxic killing.
CD20xCD3 bispecific IgG (2:1) that bridges T cells to CD20+ B cells, activating TCR/CD3 signaling and forming an immunologic synapse to drive CTL-mediated killing (perforin/granzyme, apoptosis) of malignant B cells, with associated cytokine release.
Glofitamab bridges T cells to CD20+ cells via CD3 and CD20, triggering TCR activation and CTL-mediated killing through perforin/granzyme-induced apoptosis.
Bispecific anti-HER2 monoclonal antibody that binds two non-overlapping HER2 epitopes to produce dual HER2 signaling blockade, inhibiting HER2-driven pathways such as MAPK and PI3K/AKT in tumor cells.
Bispecific anti-HER2 monoclonal antibody (derived from trastuzumab and pertuzumab) that binds two non-overlapping HER2 epitopes, blocks HER2 heterodimerization and downstream MAPK and PI3K/AKT signaling, and elicits ADCC against HER2-overexpressing tumor cells, leading to inhibited proliferation and apoptosis.
Binds two HER2 epitopes on tumor cells, blocks HER2 dimerization/signaling causing apoptosis, and engages Fc receptors to elicit ADCC against HER2-expressing cells.
Bispecific anti-HER2 monoclonal antibody that binds two non-overlapping HER2 epitopes to produce dual HER2 signaling blockade, inhibiting HER2-driven pathways such as MAPK and PI3K/AKT in tumor cells.
Bispecific anti-HER2 monoclonal antibody (derived from trastuzumab and pertuzumab) that binds two non-overlapping HER2 epitopes, blocks HER2 heterodimerization and downstream MAPK and PI3K/AKT signaling, and elicits ADCC against HER2-overexpressing tumor cells, leading to inhibited proliferation and apoptosis.
Binds HER2 on tumor cells and recruits FcγR+ effector cells to mediate ADCC (and ADCP), while dual-epitope blockade of HER2 signaling promotes apoptosis.