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.
- A1393 WZ8040Target: EGFRSummary: EGFR T790M inhibitor,irreversible amd potent
- A2822 AC480 (BMS-599626)Target: EGFRSummary: HER1/2 inhibitor,selective and efficacious
- A1845 Canertinib (CI-1033)Summary: HER family tyrosine kinase inhibitor
- A5424 FludarabineSummary: DNA synthsis inhibitor
- A5455 AEE788 (NVP-AEE788)Summary: EGFR/HER-2/VEGFR inhibitor
- A2024 PD168393Target: PDGFR|FGFR|EGFR|PKC|insulinSummary: EGFR inhibitor
- A2224 Stattic5 CitationTarget: STATSummary: STAT3 inhibitor,small-molecule and potent
- A1173 AG-18Summary: EGFR/PDGFR inhibitor
- A2689 ButeinTarget: Src|STAT|EGFR|Angiotensin-Converting Enzymes (ACEs)|5-Lipoxygenases|PTK|enoyl-acyl-carrier protein reductaseSummary: Protein kinase inhibitor
- A1367 ALK-IN-1Summary: Anaplastic lymphoma kinase (ALK) inhibitor