2. Epigenetics Protein Tyrosine Kinase/RTK JAK/STAT Signaling Stem Cell/Wnt Immunology/Inflammation
  3. JAK STAT Interleukin Related
  4. JAK2/STAT3-IN-2

JAK2/STAT3-IN-2 是一种具有口服有效性的 JAK2/STAT3 抑制剂。JAK2/STAT3-IN-2 可抑制 JAK2 和 STAT3 酪氨酸残基的磷酸化，阻断下游信号传导，破坏 STAT3 的二聚化与核转位，并抑制促炎转录活性。JAK2/STAT3-IN-2 可抑制 IL-17A 和 IL-17F 的表达，减少免疫细胞浸润，同时抑制 NO 的生成。JAK2/STAT3-IN-2 在 DSS (HY-116282C) 诱导的溃疡性结肠炎小鼠模型中发挥保护作用。JAK2/STAT3-IN-2 可用于溃疡性结肠炎的研究。

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JAK2/STAT3-IN-2

JAK2/STAT3-IN-2 Chemical Structure

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JAK2/STAT3-IN-2 相关抗体

Top Publications Citing Use of Products

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JAK1 JAK2 JAK3 Tyk2 JAK

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STAT3 STAT5 STAT6 STAT1

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

JAK2/STAT3-IN-2 is an orally active JAK2/STAT3 inhibitor. JAK2/STAT3-IN-2 inhibits the phosphorylation of tyrosine residues in JAK2 and STAT3, blocks downstream signal transduction, disrupts the dimerization and nuclear translocation of STAT3, and suppresses pro-inflammatory transcriptional activity. JAK2/STAT3-IN-2 inhibits the expression of IL-17A and IL-17F, reduces immune cell infiltration, and inhibits the production of NO simultaneously. JAK2/STAT3-IN-2 exerts a protective effect in a mouse model of ulcerative colitis induced by DSS (HY-116282C). JAK2/STAT3-IN-2 can be used for the research of ulcerative colitis[1].

IC50 & Target[1]

JAK2

 

STAT3

 

IL-17A

 

IL-17F

 

体外研究
(In Vitro)

JAK2/STAT3-IN-2 (Compound 4c) (20 μM; 24 h) 可强效抑制 LPS (HY-D1056) 诱导的 RAW264.7 巨噬细胞中 NO 的生成，其 IC50 为 3.56 μM，同时在 20 μM 浓度下仅表现出极微弱的细胞毒性[1]。
JAK2/STAT3-IN-2 (2-8 μM; 24 h) 可显著下调 LPS 诱导的 RAW264.7 巨噬细胞中 TNF-α 和 IL-6 的表达[1]。
JAK2/STAT3-IN-2 (4-8 μM) 可抑制 LPS 诱导的 RAW264.7 巨噬细胞中 IL-17A、IL-17F、JAK2 及 STAT3 的 mRNA 表达，表明其主要通过抑制 JAK2-STAT3 通路发挥抗炎作用[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

JAK2/STAT3-IN-2 相关抗体:

ELISA Assay[1]

Cell Line: RAW264.7 macrophages
Concentration: 2, 4, 8 μM
Incubation Time: 24 h (incubation with LPS)
Result: Significantly downregulated LPS-induced TNF-α and IL-6 expression.
Exhibited superior activity compared to dexamethasone at 4 μM and 8 μM.
体内研究
(In Vivo)

JAK2/STAT3-IN-2 (Compound 4c) (12.5-50 mg/kg；灌胃；每日 1 次；连续 9 天) 对 DSS 诱导的雄性 C57BL/6J 小鼠溃疡性结肠炎具有剂量依赖性保护作用，其中 50 mg/kg 剂量对 IL-17A/IL-17F-JAK2-STAT3 信号通路的抑制作用最强[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6J (6-week-old male, 20 g)[1]
Dosage: 12.5-50 mg/kg
Administration: i.g.; once daily; 9 days
Result: Significantly alleviated DSS-induced body weight loss.
Reduced Disease Activity Index (DAI) scores.
Preserved colon length compared to the DSS model group.
Attenuated bowel wall thickening, reduced inflammatory cell infiltration, and mitigated goblet cell loss compared to the DSS model group.
Upregulated colonic Occludin expression, with the 25 mg/kg dose producing the most significant increase.
Significantly upregulated colonic MUC2 expression at the 50 mg/kg dose.
Significantly downregulated colonic mRNA expression of IL-17A, IL-17F, MMP3, JAK2, and STAT3 compared to the DSS model group.
Exerted the strongest inhibitory effect on JAK2 and STAT3 mRNA expression at the 50 mg/kg dose, surpassing the positive control.
Reduced the relative expression of phosphorylated JAK2/JAK2 and phosphorylated STAT3/STAT3 compared to the DSS model group, with the 50 mg/kg dose showing the most potent inhibition of phosphorylated STAT3/STAT3.
分子量

685.67

Formula

C33H41BrN4O5S
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

JAK2/STAT3-IN-2 相关分类

  • 摩尔计算器

  • 稀释计算器

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

JAK2/STAT3-IN-2JAKSTATInterleukin RelatedJanus kinaseILRAW264.7 macrophagesIL-17FJAK2H9C2 rat cardiomyocytesCaco-2 intestinal epithelial cellsDSS-induced ulcerative colitis mice modelsHepG2 cellsIL-17AJAK2/STAT3 pathwaySTAT3Inhibitorinhibitorinhibit

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