1. Metabolic Enzyme/Protease PI3K/Akt/mTOR Epigenetics Immunology/Inflammation NF-κB Apoptosis
  2. Lactate Dehydrogenase AMPK FOXO Interleukin Related Reactive Oxygen Species (ROS) TNF Receptor Bcl-2 Family Caspase Apoptosis
  3. FuBIG

FuBIG 是一种亚氨基胍类衍生物,具有神经保护作用。 FuBIGL 抑制 L-LDH 激活,减少乳酸生成。FuBIGL 对炎症神经细胞具有保护作用,上调 AMPKpAMPKFOXO3 表达,激活细胞中的 AMPK 通路。FuBIG 通过减少促炎细胞因子 (IL-6IL-1βTNF-α) 并增加抗炎细胞因子 IL-10,发挥抗炎作用。FuBIG 维持细胞线粒体膜电位,缓解线粒体功能障碍,降低 ROS 生成,缓解氧化应激。FuBIG 上调 Bcl-2、下调 BaxCaspase-3,抑制细胞凋亡 (apoptosis)。FuBIG 改善糖尿病小鼠的代谢紊乱,降低 LDL-CALTAST 水平,同时升高 HDL-C。FuBIG 可用于糖尿病神经炎症的研究。

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FuBIG

FuBIG Chemical Structure

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Customer Review

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

FuBIG is an iminoguanidine derivative with neuroprotective effects. FuBIGL inhibits L-LDH activation and reduces lactate production. FuBIGL exerts protective effects on inflammatory nerve cells, upregulates the expressions of AMPK, pAMPK and FOXO3, and activates the AMPK pathway in cells. FuBIG exerts anti-inflammatory effects by reducing pro-inflammatory cytokines (IL-6, IL-1β, TNF-α) and increasing the anti-inflammatory cytokine IL-10. FuBIG maintains mitochondrial membrane potential, alleviates mitochondrial dysfunction, reduces ROS production, and relieves oxidative stress. FuBIG upregulates Bcl-2, downregulates Bax and Caspase-3, and inhibits cell apoptosis (apoptosis). FuBIG improves metabolic disorders in diabetic mice, decreases the levels of LDL-C, ALT and AST, and increases HDL-C level simultaneously. FuBIG can be used in the research of diabetic neuroinflammation[1].

体外研究
(In Vitro)

FuBIG (3d) (0.3 mM; 48 h) 可强效降低 LPS (HY-D1056) 诱导的 SH-SY5Y 和 THLE-2 细胞中 L-LDH 的过度激活,使其活性恢复至接近基础水平,降低乳酸积累[1]
FuBIG (0-1600 μM; 48 h) 对 LPS 诱导的 SH-SY5Y 细胞和 BV2 细胞死亡具有保护作用 (SH-SY5Y 细胞的 EC50 = 222.3 μM,BV2 细胞的 EC50 = 198.1 μM),在 1 mM 浓度下细胞存活率维持在 85%以上[1]
FuBIG (0.3 mM; 12-24 h) 可通过 OCT1 转运进入 THLE-2 细胞[1]
FuBIG (0.3 mM; 48 h) 通过上调 AMPK、pAMPK 和 FOXO3 蛋白表达,激活 LPS 诱导的 BV2 细胞中的 AMPK 通路[1]
FuBIG (0.3 mM; 48 h) 可通过减少促炎细胞因子 (IL-6、IL-1β、TNF-α) 并增加抗炎细胞因子 IL-10,在 LPS 诱导的 BV2 细胞中发挥抗炎作用[1]
FuBIG (0.3 mM; 48 h) 可在 LPS 诱导的 BV2 细胞中维持线粒体膜电位,缓解 LPS 诱导的线粒体功能障碍,降低细胞 ROS 生成,缓解氧化应激[1]
FuBIG (0.3 mM; 48 h) 可通过上调抗凋亡蛋白 Bcl-2、下调促凋亡蛋白 Bax、Caspase-3 及活化型 Caspase-3,抑制 LPS 诱导的 SH-SY5Y 细胞凋亡[1]

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

Cell Viability Assay[1]

Cell Line: LPS-induced SH-SY5Y human neuroblastoma cells, BV2 mouse microglial cells
Concentration: 1 mM/ (50, 100, 200, 400, 800, and
1600 μM)
Incubation Time: 48 h
Result: Maintained >85% cell viability in LPS-induced SH-SY5Y and BV2 cells at 1 mM.
Achieved an EC50 of 222.3 μM in LPS-induced SH-SY5Y cells.
Achieved an EC50 of 198.1 μM in LPS-induced BV2 cells.

Western Blot Analysis[1]

Cell Line: LPS-induced BV2 mouse microglial cells
Concentration: 0.3 mM
Incubation Time: 48 h
Result: Upregulated AMPK protein expression to levels comparable to metformin-treated cells.
Upregulated pAMPK protein expression to levels comparable to metformin-treated cells.
Upregulated FOXO3 protein expression to levels comparable to metformin-treated cells.\nReduced IL-6 protein expression and fluorescence intensity.
Reduced IL-1β protein expression.
Reduced TNF-α protein expression.
Increased IL-10 protein expression.

Western Blot Analysis[1]

Cell Line: LPS-induced SH-SY5Y human neuroblastoma cells
Concentration: 0.3 mM
Incubation Time: 48 h
Result: Upregulated anti-apoptotic protein Bcl-2 expression.
Downregulated pro-apoptotic protein Bax expression.
Downregulated pro-apoptotic protein Caspase-3 expression.
Downregulated pro-apoptotic protein Cleaved Caspase-3 expression and fluorescence intensity.
药代动力学
(Parmacokinetics)
Species Dose Route AUC0-t AUC0-∞ Cmax Tmax T1/2
Rat[1] 10 mg/kg i.v. 226.29 mg·h/L 228.79 mg·h/L 87.55 mg/L 0.083 h 4.106 h
体内研究
(In Vivo)

FuBIG (10 mg/kg; 静脉注射;每日给药;持续 21 天) 可改善糖尿病小鼠中与糖尿病相关的代谢异常,包括体重过度增加、空腹血糖升高、糖耐量受损、血脂异常及肝损伤,可使空腹血糖降低 19.7%,口服葡萄糖耐量试验曲线下面积降低 24.2%[1]

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

Animal Model: C57BL/6J (female, 5-week-old, high-fat diet + streptozotocin-induced type 2 diabetes)[1]
Dosage: 10 mg/kg
Administration: i.v.; daily; 21 days
Result: Limited diabetic mice weight gain to 5.57 g.
Reduced fasting blood glucose by 19.7% (from 21.927 to 17.566 mmol/L).
Reduced the area under the oral glucose tolerance test curve by 24.2% (2542 min mmol/L vs.
3353 min mmol/L in untreated diabetic mice).
Increased serum HDL-C to 1.12 mmol/L.
Decreased serum LDL-C to 0.98 mmol/L.
Reduced serum AST to 109.50 U/L.
Reduced serum ALT to 65.67 U/L.
分子量

236.23

Formula

C8H12N8O

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
  • 摩尔计算器

  • 稀释计算器

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量   浓度   体积   分子量 *
= × ×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

浓度 (start) × 体积 (start) = 浓度 (final) × 体积 (final)
× = ×
C1   V1   C2   V2
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.

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