JAK-IN-23

• CAT Number: I042829
• CAS Number: 3031837-35-8
• Molecular Formula: C23H22Cl2N4O
• Molecular Weight: 441.35
• Purity: ≥95%
• Synonyms: 2,6-dichloro-4-[2-methyl-1-(1-methylpiperidin-4-yl)imidazo[4,5-c]quinolin-8-yl]phenol
• InChI: InChI=1S/C23H22Cl2N4O/c1-13-27-21-12-26-20-4-3-14(15-10-18(24)23(30)19(25)11-15)9-17(20)22(21)29(13)16-5-7-28(2)8-6-16/h3-4,9-12,16,30H,5-8H2,1-2H3
• InChIKey: JEESDVDVWGRNFE-UHFFFAOYSA-N
• SMILES: CC1=NC2=CN=C3C=CC(=CC3=C2N1C4CCN(CC4)C)C5=CC(=C(C(=C5)Cl)O)Cl

JAK-IN-23 is an orally active double inhibitor of JAK/STAT and NF-κB. JAK-IN-23 can inhibit JAK1/2/3 with IC50 values of 8.9 nM, 15 nM and 46.2 nM, respectively. JAK-IN-23 has potent inhibitory activities against interferon-stimulated genes (ISG) and NF-κB pathways with IC50 values of 3.3 nM and 150.7 nM, respectively. JAK-IN-23 has great anti-inflammatory that decreases the release of various proinflammatory factors. JAK-IN-23 can be used for the research of inflammatory bowel disease (IBD)[1].
JAK-IN-23 inhibits JAK1/2/3 with IC50 values of 8.9 nM, 15 nM and 46.2 nM, respectively[1].
JAK-IN-23 shows potent inhibitory activities against ISG and NF-KB with IC50 values of 3.3 nM and 150.7 nM, respectively[1].
WB— JAK-IN-23 (0.33μM, 1μM, 3μM; 24 h) can simultaneously block JAK-STAT1/3 and NF-κB proinflammatory signaling pathways in THP1-dual cells[1].
JAK-IN-23 (0.003-3 μM; 24 h) decreases the release of various proinflammatory factors, including IL-6, IL-8, IL-1β in THP1-dual cells stimulated by LPS[1].
JAK-IN-23 (0.11-3 μM; 24 h) decreases the release of various proinflammatory factors, including TNF-α, IL-12, IL-10 and IFNγ in LPS-induced peripheral blood mononuclear cells (PBMCs)[1].
JAK-IN-23 (1 μM) inhibits the expression of a variety of inflammation-related genes induced by LPS, including IL-1B, TNF, IL12B, and IL-23A and has inhibitory effects on the expression of genes involved in the unfolded protein response that was induced by LPS (1 μg/mL)[1].
JAK-IN-23 (1-5 mg/kg, oral) produces a strong anti-inflammatory activity in both dextran sulfate sodium (DSS) – and 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced acute enteritis models and restores the structural composition of gut microbiota[1].

Reference

[1]. Xuewu Liang, et al. Discovery of Novel Imidazo[4,5- c]quinoline Derivatives to Treat Inflammatory Bowel Disease (IBD) by Inhibiting Multiple Proinflammatory Signaling Pathways and Restoring Intestinal Homeostasis. J Med Chem. 2022 Sep 2.
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