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.
- A4092 CUDC-1011 CitationTarget: Histone Deacetylases (HDACs)|EGFR|ErbBSummary: Multitargeted HDAC inhibitor
- A4139 AG-4903 CitationTarget: EGFR|JAKSummary: JAK2/EGFR inhibitor
- A4150 WHI-P154Target: VEGFR|Src|EGFR|JAKSummary: JAK3 inhibitor
- A3320 CO-1686 (AVL-301)1 CitationTarget: EGFRSummary: EGFR inhibitor
- A3433 Gefitinib hydrochlorideTarget: EGFRSummary: Potent EGFR inhibitor
- B5836 AZ5104Target: EGFRSummary: EGFR inhibitor
- B1104 AZD-92911 CitationTarget: EGFRSummary: Mutated forms EGFR inhibitor
- A3967 Lapatinib DitosylateTarget: EGFR|ErbB-2Summary: EGFR/HER2 inhibitor,potent and selective
- A8219 Gefitinib (ZD1839)3 CitationTarget: EGFRSummary: Selective EGFR inhibitor
- A8247 Afatinib (BIBW2992)1 CitationTarget: EGFRSummary: Irreversible EGFR/HER2 inhibitor