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.
- A4193 SMI-4aTarget: PimSummary: Potent Pim inhibitor
- A4152 BMS-911543Target: JAKSummary: JAK2 inhibitor,selective small molecule
- A3221 Bardoxolone methylTarget: Nrf2Summary: IKK inhibitor, potent antioxidant inflammation modulator
- A3222 Baricitinib phosphateSummary: JAK1/JAK2 inhibitor
- A3256 BMS-690514Summary: HER/EGFR inhibitor
- A3320 CO-1686 (AVL-301)1 CitationTarget: EGFRSummary: EGFR inhibitor
- A3337 CX-6258Summary: Pan-Pim kinases Inhibitor
- A3339 CYT387 sulfate saltSummary: JAK1/JAK2 inhibitor
- A3397 Erlotinib4 CitationSummary: EGFR tyrosine kinase inhibitor
- A3433 Gefitinib hydrochlorideTarget: EGFRSummary: Potent EGFR inhibitor