2. PI3K/Akt/mTOR Immunology/Inflammation Anti-infection
  3. PI3K Akt Interleukin Related Bacterial
  4. FHND5032

FHND5032 是一种具有口服活性的 miR-124 诱导剂。FHND5032 显著上调巨噬细胞中 miR-124 的表达。FHND5032 通过抑制 PIK3R2/PI3K/Akt 轴，阻断炎症信号，促进巨噬细胞重编程，并恢复上皮屏障功能。FHND5032 缓解溃疡性结肠炎小鼠的结肠炎并降低炎症负荷。FHND5032 可用于溃疡性结肠炎的研究。

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FHND5032

FHND5032 Chemical Structure

CAS No. : 3076057-63-8

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FHND5032 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

FHND5032 is an orally active miR-124 inducer. FHND5032 significantly upregulates miR-124 expression in macrophages. FHND5032 disrupts inflammatory signaling, promotes macrophage reprogramming, and restores the epithelial barrier function by inhibiting the PIK3R2/PI3K/Akt axis. FHND5032 alleviates colitis and reduces inflammatory burden in ulcerative colitis mice. FHND5032 can be used for the study of ulcerative colitis[1].

体外研究
(In Vitro)

FHND5032 (0-20 μM, 24 h) 通过增强 miR-124 表达，在 THP-1 和 RAW 264.7 细胞中显著发挥抗炎活性[1]。
FHND5032 (≤ 5 μM) 通过靶向 PIK3R2 激活 miR-124-5p 表达，调控 THP-1 和 RAW 264.7 细胞重编程中的 PI3K/Akt 通路[1]。
FHND5032 降低 RAW 264.7 中 M1 标记物 CD86 的表达，同时增加 M2 标记物 CD206 的表达[1]。
FHND5032 促进 Caco-2 细胞中屏障密封蛋白 ZO-1 和 occludin 的表达，以增强紧密连接 (TJ) 组装[1]。

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

FHND5032 相关抗体:

Real Time qPCR[1]

Cell Line: THP-1 and RAW 264.7 cells
Concentration: 5, 10 μM
Incubation Time: /
Result: Upregulated miR-124 levels and induced miR-124 expression, which peaked at a concentration of 5 μM.
Decreased TNF-α, IL-1β, and IL-6 expression in LPS (HY-D1056)- and IFN-γ-stimulated THP-1 cells and LPS stimulated RAW 264.7 cells.
Decreased the expression of PIK3R2
体内研究
(In Vivo)

FHND5032 (25-50 mg/kg，灌胃，每日一次，持续 12 天) 在 Dextran sulfate sodium salt (DSS) (HY-116282C) 诱导的溃疡性结肠炎小鼠模型中缓解结肠炎并降低炎症负荷[1]。

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

Animal Model: DSS-induced female C57BL/6J mice (18-20 g)[1]
Dosage: 25, 50 mg/kg
Administration: i.g. once daily for 12 days
Result: Restrained the body weight loss of DSS-induced colitis mice.
Reduced the hematochezia occurrence during treatment.
Showed longer colon length of mice.
Protected the colonic barrier from pathological damage.
Decreased the local level of UC-associated myeloperoxidase (MPO) in the colon.
Reduced the expression of pro-inflammatory cytokines, including IL-6, TNF-α, and IFN-γ.
Increased the expression of anti-inflammatory cytokines IL-10.
Prevented intestinal damage in UC through elevation of TJ proteins.
Prevented the FITC-dextran leakage.
Inhibited colonic inflammation and repaired the intestinal barrier in colitis mice.
Upregulated the miR-124 expression and decreased PIK3R2 expression.
Attenuated PIK3R2 upregulation and the hyperphosphorylation of PI3K and Akt.
Showed no significant discrepancies in serum physicochemical parameters (alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), and creatinine (Cr)).
Decreased the abundance of Proteobacteria in colitis mice and effectively enhanced the relative abundance of Firmicutes.
Showed no increase on the abundance of Bacteroidota.
分子量

339.70

Formula

C15H9ClF3N3O
CAS 号
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

FHND5032 相关分类

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  • 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:

FHND50323076057-63-8FHND 5032FHND-5032PI3KAktInterleukin RelatedBacterialPhosphoinositide 3-kinasePKBProtein kinase BILmiR-124ulcerative colitis,THP-1 cellsRAW 264.7 cellsInhibitorinhibitorinhibit

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