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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B1130 GLPG06341 CitationTarget: JAKSummary: JAK1 inhibitor -
A4517 ZM 449829Summary: JAK3 inhibitor -
B1105 AZD-9291 mesylateSummary: third generation EGFRm inhibitor, oral and irreversible -
A4516 TCS 21311Summary: JAK3 inhibitor -
B1104 AZD-92911 CitationTarget: EGFRSummary: Mutated forms EGFR inhibitor -
A4515 SD 1008Summary: Inhibitor of JAK2/STAT3 signaling pathway,apoptosis inducer -
B1103 Mutant EGFR inhibitorSummary: Selective Mutated EGFR inhibitor -
A4514 NSC 33994Summary: Selective JAK2 inhibitor -
B1020 AST-1306 TsOHSummary: ErbB2 and EGFR inhibitor -
A4513 Lestaurtinib1 CitationSummary: JAK2/FLT3/TrkA inhibitor
