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.
- A3012 Ruxolitinib (INCB018424)4 CitationTarget: JAKSummary: JAK inhibitor
- A3433 Gefitinib hydrochlorideTarget: EGFRSummary: Potent EGFR inhibitor
- A8322 Neratinib (HKI-272)1 CitationTarget: EGFRSummary: HER2/EGFR inhibitor,potent and irreversible
- A4512 Cucurbitacin ITarget: STAT|JAKSummary: STAT3/JAK2 signaling inhibitor
- A8219 Gefitinib (ZD1839)3 CitationTarget: EGFRSummary: Selective EGFR inhibitor
- A2412 CP-724714Target: VEGFR|PDGFR|Bcr-Abl|Src|EGFR|c-MET|Insulin Receptors|IRG-1RSummary: HER2 inhibitor,potent and selective
- A2822 AC480 (BMS-599626)Target: EGFRSummary: HER1/2 inhibitor,selective and efficacious