Boc-Phe-Leu-Phe-Leu-Phe
Based on 1 Customer Validation
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.
For research use only. We do not sell to patients.
- Purity: 98.10%
- CAS No.: 73572-58-4
- Formula: C44H59N5O8
- Molecular Weight:785.97
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Storage:
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)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
All Leukotriene Receptor Isoforms
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Biological Activity
Boc-Phe-Leu-Phe-Leu-Phe (0-50 μg/mL) inhibits the sprouting of HUVEC spheroids induced by PDR vitreous in a three-dimensional fibrin gel[1].
Boc-Phe-Leu-Phe-Leu-Phe (0-120 μM, 24 h) inhibits the sprouting of HUVEC spheroids mediated by VEGF in a dose-dependent manner[2].
Boc-Phe-Leu-Phe-Leu-Phe (100 ng/mL, 24 h) inhibits the ability of Ac2-26 (HY-P1098) to reduce the expression of TGF-β1, IL-1β, and IL-6 in LPS (HY-D1056)-induced RAW264.7 cells[4].
Boc-Phe-Leu-Phe-Leu-Phe (100 ng/mL, 24 h) blocks the inhibitory effect of Ac2-26 on the expression of α-SMA, collagen I, CTGF, and β-catenin in LPS-induced hepatic stellate cells (HSCs)[4].
Boc-Phe-Leu-Phe-Leu-Phe (10 µM) blocks the inhibitory effect of Ac2-26 on the increase of AnxA1 protein expression, phosphorylated NF-κB p65 levels, IκB-α degradation, and IL-8 production in A549 cells[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:LPS (HY-D1056)-induced RAW264.7 cells
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Concentration:100 ng/mL
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Incubation Time:24 h
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Result:Reduced the expression of TGF-β1, IL-1β, and IL-6.
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Cell Line:LPS (HY-D1056)-induced RAW264.7 cells
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Concentration:100 ng/mL
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Incubation Time:24 h
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Result:Reduced the expression of α-SMA, collagen I, CTGF, and β-catenin.
Boc-Phe-Leu-Phe-Leu-Phe (50 µg per rat, intraperitoneal injection 30 min before surgery, single dose) reverses the protective effects of Ac2-26 in rats with ischemia-reperfusion-induced acute lung injury[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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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]
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Dosage:1 mg/kg
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Administration:Intraperitoneal injection, twice weekly for 4/8 weeks
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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.
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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]
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Dosage:50 µg per rat
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Administration:Intraperitoneal injection 30 min before surgery for a single dose
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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.
Chemical Information
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CAS No. 73572-58-4
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Appearance Solid
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Molecular Weight 785.97
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Formula C44H59N5O8
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Color White to off-white
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Synonyms
L-BOC2
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Sequence
{Boc}-Phe-Leu-Phe-Leu-Phe
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Sequence Shortening
{Boc}-FLFLF
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
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)
Purity & Documentation
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Data Sheet (279 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Rezzola S, et al. Inflammation and N-formyl peptide receptors mediate the angiogenic activity of human vitreous humour in proliferative diabetic retinopathy. Diabetologia. 2017 Apr;60(4):719-728. [Content Brief]
[2]. Nawaz MI, et al. D-Peptide analogues of Boc-Phe-Leu-Phe-Leu-Phe-COOH induce neovascularization via endothelial N-formyl peptide receptor 3. Angiogenesis. 2020 Aug;23(3):357-369. [Content Brief]
[3]. Lefer AM, Roth DM, Kugler JL, Smith JB. Modulation of receptor mediated leukotriene release in the perfused heart. Gen Pharmacol. 1986;17(4):437-40. [Content Brief]
[4]. Fan JH, et al. Mechanism of annexin A1/N-formylpeptide receptor regulation of macrophage function to inhibit hepatic stellate cell activation through Wnt/β-catenin pathway. World J Gastroenterol. 2023 Jun 14;29(22):3422-3439. [Content Brief]
[5]. Liao WI, et al. Ac2-26, an Annexin A1 Peptide, Attenuates Ischemia-Reperfusion-Induced Acute Lung Injury. Int J Mol Sci. 2017 Aug 15;18(8):1771. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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