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.
- A4519 PIM-1 Inhibitor 2Summary: Potent Pim-1 kinase inhibitor
- A4520 R8-T198wtSummary: Pim-1 kinase inhibitor
- A4521 TCS PIM-1 1Summary: Pim-1 kinase inhibitor,ATP-competitve
- A4514 NSC 33994Summary: Selective JAK2 inhibitor
- A3967 Lapatinib DitosylateTarget: EGFR|ErbB-2Summary: EGFR/HER2 inhibitor,potent and selective
- A8218 Lapatinib2 CitationTarget: ErbBSummary: EGFR/HER2 inhibitor,potent,selective and reversible
- A8219 Gefitinib (ZD1839)3 CitationTarget: EGFRSummary: Selective EGFR inhibitor
- A8234 Erlotinib Hydrochloride2 CitationSummary: Selective EGFR inhibitor
- A8247 Afatinib (BIBW2992)1 CitationTarget: EGFRSummary: Irreversible EGFR/HER2 inhibitor
- A1389 WZ4002Summary: Mutant-selective EGFR inhibitor(L858R,T790M), irreversible and potent