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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A3433 Gefitinib hydrochlorideTarget: EGFRSummary: Potent EGFR inhibitor -
B7802 APTSTAT3-9RSummary: STAT3 inhibitor -
A4135 Tofacitinib (CP-690550) Citrate2 CitationTarget: JAKSummary: Potent JAK inhibitor -
A3397 Erlotinib4 CitationSummary: EGFR tyrosine kinase inhibitor -
B6175 STA-21Summary: STAT3 inhibitor -
A3320 CO-1686 (AVL-301)1 CitationTarget: EGFRSummary: EGFR inhibitor -
A3937 XL019Target: JAKSummary: JAK2 inhibitor,potent and selective -
B5999 FLLL32Summary: STAT3 inhibitor -
A3256 BMS-690514Summary: HER/EGFR inhibitor -
A3936 WHI-P97Summary: Janus kinase (JAK)-3 inhibitor
