JAK-IN-23 是 JAK/STAT 和 NF-Κb 的双重抑制剂，具有口服活性。JAK-IN-23 对J AK1/2/3 具有抑制作用，IC50值分别为 8.9 nM、15 nM 和 46.2 nM。JAK-IN-23 对干扰素刺激基因 (ISG) 和 NF-Κb 通路具有较强的抑制活性，IC50值分别为 3.3 nM 和 150.7 nM。JAK-IN-23 具有很强的抗炎作用，可以减少各种促炎因子的释放。JAK-IN-23 可用于炎症性肠病 (IBD) 的研究。

JAK-IN-23 is an orally active double inhibitor of JAK/STAT and NF-κB. JAK-IN-23 can inhibit JAK1/2/3 with IC 50 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 IC 50 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 IC 50 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 IC 50 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]. Western Blot Analysis [1] Cell Line: THP1-Dual Cells Concentration: 0.33μM, 1μM, 3μM Incubation Time: 24 h Result: Inhibited p-STAT1/3 in a dose-dependent manner that was induced by IL-6, as well as inhibited pNF-κB p65 in a dose-dependent manner, but not on MYD88 and p-IKK α/β that was induced by LPS.

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]. Animal Model: DSS-Induced Acute Colitis Mice Model [1] Dosage: 1 mg/kg, 3 mg/kg Administration: oral Result: Significantly decreased the DAI scores (1 and 3 mg/kg). Recovered the length of the colon (3 mg/kg). Significantly reduced the histopathology of ulcerative colitis (1 and 3 mg/kg). Animal Model: The BALB/c mouse inflammatory bowel disease (IBD) model [1] Dosage: 1 mg/kg, 5 mg/kg Administration: oral Result: Significantly improved the survival probability, had low DAI scores and effectively relieved symptoms of colitis in the TNBS-induced IBD mice model (5 mg/kg). Did not improve the survival probability and decreases the DAI score (100 mg/kg).

C23H22Cl2N4O

441.35

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years