2. GPCR/G Protein
  3. Leukotriene Receptor
  4. Boc-Phe-Leu-Phe-Leu-Phe

Boc-Phe-Leu-Phe-Leu-Phe  (Synonyms: L-BOC2)

目录号: HY-P3318 纯度: 98.03%
COA 产品使用指南 技术支持

Boc-Phe-Leu-Phe-Leu-Phe (Boc-FLFLF) 是一种 N-甲酰肽受体 (FPR) 抑制剂。Boc-Phe-Leu-Phe-Leu-Phe 消除 FMLP 诱导的肽类白三烯释放。Boc-Phe-Leu-Phe-Leu-Phe 在三维纤维蛋白凝胶中分别抑制增生性糖尿病视网膜病变 (PDR) 玻璃体和血管内皮生长因子 (VEGF) 介导的人脐静脉内皮细胞 (HUVEC) 球体出芽。Boc-Phe-Leu-Phe-Leu-Phe 可抑制 Ac2-26 (HY-P1098) 的抗炎和抗纤维化作用。Boc-Phe-Leu-Phe-Leu-Phe 可用于炎症的研究。

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Custom Peptide Synthesis

Boc-Phe-Leu-Phe-Leu-Phe

Boc-Phe-Leu-Phe-Leu-Phe Chemical Structure

CAS No. : 73572-58-4

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规格 价格 是否有货 数量
1 mg ￥320
In-stock
5 mg ￥720
In-stock
10 mg ￥1160
In-stock
25 mg ￥2320
In-stock
50 mg ￥3720
In-stock
100 mg ￥5960
In-stock
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500 mg   询价  

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Other Forms of Boc-Phe-Leu-Phe-Leu-Phe:

Boc-Phe-Leu-Phe-Leu-Phe 相关抗体

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LTB4 LTC4/CysLT2 LTD4/CysLT1 LTE4

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Boc-Phe-Leu-Phe-Leu-Phe (Boc-FLFLF) is a N-formyl peptide receptors (FPR) inhibitor. Boc-Phe-Leu-Phe-Leu-Phe abolishes the FMLP-induced release of peptide leukotrienes. Boc-Phe-Leu-Phe-Leu-Phe inhibits the sprouting of human umbilical vein endothelial cell (HUVEC) spheroids mediated by proliferative diabetic retinopathy (PDR) vitreous and vascular endothelial growth factor (VEGF) respectively in a three-dimensional fibrin gel. Boc-Phe-Leu-Phe-Leu-Phe inhibits the anti-inflammatory and antifibrotic effects of Ac2-26 (HY-P1098). Boc-Phe-Leu-Phe-Leu-Phe can be used for the study of immunology[1][2][3][4][5].

体外研究
(In Vitro)

Boc-Phe-Leu-Phe-Leu-Phe (0-50 μg/mL) 抑制 PDR 玻璃体诱导的 HUVEC 球体在三维纤维蛋白凝胶中的出芽[1]。
Boc-Phe-Leu-Phe-Leu-Phe (0-120 μM，24 小时) 以剂量依赖方式抑制 VEGF 介导的 HUVEC 球体出芽[2]。
Boc-Phe-Leu-Phe-Leu-Phe (100 ng/mL, 24 h) 抑制 Ac2-26 (HY-P1098) 在 LPS (HY-D1056) 诱导的 RAW264.7 细胞中降低 TGF-β1、IL-1β 和 IL-6 表达的能力[4]。
Boc-Phe-Leu-Phe-Leu-Phe (100 ng/mL, 24 h) 阻断 Ac2-26 对 LPS 诱导的肝星状细胞 (HSCs) 中 α-SMA、胶原 I、CTGF 和 β-catenin 表达的抑制作用[4]。
Boc-Phe-Leu-Phe-Leu-Phe (10 µM) 阻断 Ac2-26 对 A549 细胞中 AnxA1 蛋白表达、磷酸化 NF-κB p65 水平、IκB-α 降解以及 IL-8 产生的抑制作用[5]。

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

Boc-Phe-Leu-Phe-Leu-Phe 相关抗体:

Real Time qPCR[4]

Cell Line: LPS (HY-D1056)-induced RAW264.7 cells
Concentration: 100 ng/mL
Incubation Time: 24 h
Result: Reduced the expression of TGF-β1, IL-1β, and IL-6.

Western Blot Analysis[4]

Cell Line: LPS (HY-D1056)-induced RAW264.7 cells
Concentration: 100 ng/mL
Incubation Time: 24 h
Result: Reduced the expression of α-SMA, collagen I, CTGF, and β-catenin.
体内研究
(In Vivo)

Boc-Phe-Leu-Phe-Leu-Phe (1 mg/kg，腹腔注射，每周两次，持续4-8周) 在 CCl4 诱导肝纤维化的野生型和 AnxA1 敲除小鼠模型中，可逆转 Ac2-26 的抗炎和抗纤维化作用[4]。
Boc-Phe-Leu-Phe-Leu-Phe (50 µg/只，手术前30分钟腹腔注射，单次剂量) 逆转 Ac2-26 在斯普拉格-道利大鼠缺血再灌注诱导的急性肺损伤中的保护作用[5]。

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

Animal Model: Six-to-eight-week-old C57BL/6 wild-type mice and C57BL/6JGpt Anxa1-KO mice (weighing 18-25 g) were given intraperitoneal injection of 20% CCl4 (500 mL) twice weekly to induce liver fibrosis[4]
Dosage: 1 mg/kg
Administration: Intraperitoneal injection, twice weekly for 4/8 weeks
Result: Induced more severe liver lesions in CCl4-induced wild-type and AnxA1 knockout mice compared to Ac2-26 treatment, with lighter liver color, rougher surface, more nodules, and harder texture.
Increased liver inflammation and collagen deposition, as well as elevated expression of α-SMA, collagen I, CTGF, TGF-β1, IL-1β, IL-6, and β-catenin in liver tissues.
Reversed the anti-inflammatory and antifibrotic effects of Ac2-26, with the degree of liver damage and fibrosis similar to that in the CCl4-induced model group without Ac2-26 treatment.
Animal Model: Sprague-Dawley rats (male, 350 ± 20 g) were used to establish an isolated perfused lung model, with ischemia induced by stopping ventilation and perfusion for 40 min, followed by reperfusion for 60 min to induce ischemia-reperfusion lung injury[5]
Dosage: 50 µg per rat
Administration: Intraperitoneal injection 30 min before surgery for a single dose
Result: Abolished the protective effects of Ac2-26 in ischemia-reperfusion-induced acute lung injury in Sprague-Dawley rats, resulting in more severe lung edema, higher pulmonary arterial pressure, and increased protein concentration in bronchoalveolar lavage fluid.
Enhanced neutrophil infiltration, elevated levels of pro-inflammatory cytokines (CINC-1, TNF-α) in bronchoalveolar lavage fluid, and increased oxidative stress (higher protein carbonyl content and MDA level) and apoptosis (more activated caspase-3-immunolabeled cells, lower Bcl-2 expression) in lung tissue.
Aggravated lung tissue damage, with increased lung injury scores, disrupted tight junction proteins (claudin-3, occludin, ZO-1) in alveolar walls, and reversed the inhibition of NF-κB and MAPK pathways activation by Ac2-26.
分子量

785.97

Formula

C44H59N5O8
CAS 号
性状

固体

颜色

White to off-white

Sequence

{Boc}-Phe-Leu-Phe-Leu-Phe
Sequence Shortening

{Boc}-FLFLF
运输条件

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

Sealed storage, away from moisture

Powder -80°C 2 years
-20°C 1 year

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

纯度 & 产品资料
参考文献

Boc-Phe-Leu-Phe-Leu-Phe 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:

Boc-Phe-Leu-Phe-Leu-Phe73572-58-4L-BOC2Leukotriene Receptorleukotrienesvascular endothelial growth factorInhibitorinhibitorinhibit

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