JAK/STAT Signaling
Various ligands including cytokines (e.g. interferons and interleukins), hormones (e.g. erythropoietin and growth hormone) and their cell surface receptors activate JAK proteins, which autophosphorylate, and then phosphorylate the receptor. Subsequently, JAKs phosphorylate a specific tyrosine residue on the STAT protein, promoting dimerization via SH2 domains. The activated STATs form homo-/heterodimers and translocate to the nucleus to trigger target gene transcription. In addition, suppressors of cytokine signaling (SOCS) family inhibit receptor signaling via homologous or heterologous feedback regulation. Dysregulation in JAK/STAT signaling is associated with diseases such as atherosclerosis, immunodeficiencies and cancer.
- A8317 Fludarabine Phosphate (Fludara)2 CitationTarget: STATSummary: Inhibits STAT1 activation and DNA synthesis
- A8319 Dacomitinib (PF299804, PF299)Target: ErbBSummary: HER inhibitor
- A8322 Neratinib (HKI-272)1 CitationTarget: EGFRSummary: HER2/EGFR inhibitor,potent and irreversible
- A8338 NSC 748595 CitationTarget: STATSummary: Stat3 inhibitor
- A8357 AG-1478Target: EGFRSummary: EGFR inhibitor,potent and selective
- A8365 Varlitinib (ARRY334543)Summary: ErbB inhibitor
- A8366 ARRY-380Target: HER2Summary: Tyrosine kinase HER2 and p95-HER2 inhibitor
- A8367 AST-1306Summary: EGFR/HER2 inhibitor
- A8375 AZD8931 (Sapitinib)Target: EGFR|ErbBSummary: ErbB inhibitor
- B6116 GLPG0634 analogueSummary: JAK1 inhibitor, potent and selective