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.
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A4146 CEP-337791 CitationSummary: JAK2 inhibitor,highly selective -
A8199 PD153035 hydrochloride1 CitationTarget: EGFRSummary: Potent EGFR inhibitor -
A4145 TG101209Summary: JAK2/3 inhibitor -
A8197 Compound 561 CitationTarget: EGFRSummary: REGFR inhibitor -
A4144 AZ 960Target: JAKSummary: JAKs inhibitor -
A5455 AEE788 (NVP-AEE788)Summary: EGFR/HER-2/VEGFR inhibitor -
A4143 CYT3871 CitationSummary: JAK-1/-2 inhibitor,ATP competitive -
A4139 AG-4903 CitationTarget: EGFR|JAKSummary: JAK2/EGFR inhibitor -
A4141 Baricitinib (LY3009104, INCB028050)2 CitationSummary: JAK1/JAK2 inhibitor,selective orally bioavailable -
N1843 CryptotanshinoneSummary: STAT3/AChE inhibitor
