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.
- A8219 Gefitinib (ZD1839)3 CitationTarget: EGFRSummary: Selective EGFR inhibitor
- A8247 Afatinib (BIBW2992)1 CitationTarget: EGFRSummary: Irreversible EGFR/HER2 inhibitor
- A2412 CP-724714Target: VEGFR|PDGFR|Bcr-Abl|Src|EGFR|c-MET|Insulin Receptors|IRG-1RSummary: HER2 inhibitor,potent and selective
- A1393 WZ8040Target: EGFRSummary: EGFR T790M inhibitor,irreversible amd potent
- A2822 AC480 (BMS-599626)Target: EGFRSummary: HER1/2 inhibitor,selective and efficacious
- A8357 AG-1478Target: EGFRSummary: EGFR inhibitor,potent and selective
- A8375 AZD8931 (Sapitinib)Target: EGFR|ErbBSummary: ErbB inhibitor
- B5836 AZ5104Target: EGFRSummary: EGFR inhibitor
- B1104 AZD-92911 CitationTarget: EGFRSummary: Mutated forms EGFR inhibitor
- A4139 AG-4903 CitationTarget: EGFR|JAKSummary: JAK2/EGFR inhibitor