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Reparixin

Catalog No. T4163   CAS 266359-83-5
Synonyms: DF 1681Y, Repertaxin

Reparixin (Repertaxin) is a potent inhibitor of both CXCL8 receptors CXCR1/2, it inhibits weakly CXCR2-mediated cell migration (IC50=100 nM), whereas it strongly blocks CXCR1-mediated chemotaxis (IC50=1 nM).

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Reparixin Chemical Structure
Reparixin, CAS 266359-83-5
Pack Size Availability Price/USD Quantity
1 mg In stock $ 48.00
2 mg In stock $ 72.00
5 mg In stock $ 122.00
10 mg In stock $ 197.00
25 mg In stock $ 413.00
50 mg In stock $ 618.00
100 mg In stock $ 879.00
500 mg In stock $ 1,750.00
1 mL * 10 mM (in DMSO) In stock $ 113.00
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Purity: 99.89%
Purity: 99.73%
Purity: 98%
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Biological Description
Chemical Properties
Storage & Solubility Information
Description Reparixin (Repertaxin) is a potent inhibitor of both CXCL8 receptors CXCR1/2, it inhibits weakly CXCR2-mediated cell migration (IC50=100 nM), whereas it strongly blocks CXCR1-mediated chemotaxis (IC50=1 nM).
Targets&IC50 CXCR1:1 nM, CXCR2:100 nM
Cell Research L1.2 Cell suspension (1.5-3×106 cells/mL) is incubated at 37°C for 15 min in the presence of vehicle or of Reparixin (1 nM-1 μM) and next seeded in triplicates in the upper compartment of the chemotactic chamber. Different agonists are seeded in the lower compartment of the chamber at the following concentrations: 1 nM CXCL8, 0.03 nM fMLP, 10 nM CXCL1, 2.5 nM CCL2, 30 nM C5a. The chemotactic chamber is incubated at 37°C in air with 5% CO2 for 45 min (human PMNs) or 2 h (monocytes). At the end of incubation, the filter is removed, fixed, and stained and five oil immersion fields at high magnification (100×) are counted for each migration well after sample coding. L1.2 migration is evaluated using 5 μM pore size Transwell filters.
Animal Research C57BL/6J mice (8-10 weeks old/20-25 g) are used. The subcutaneous administration of Reparixin (30 mg/kg) is performed 60 minutes before cerebral ischemia induction. The animals are divided into the following three experimental groups: Sham (i.e., the group in which the arteries are visualized, but there is no occlusion of the middle cerebral artery), Vehicle (i.e., the group pre-treated with the vehicle, phosphate buffer solution, 60 minutes before MCAo) and Reparixin (i.e., the group pre-treated with the drug 60 minutes before MCAo). To evaluate neurological signs secondary to MCAo, the animals are assessed with the SHIRPA battery 24 h after reperfusion.
Synonyms DF 1681Y, Repertaxin
Molecular Weight 283.39
Formula C14H21NO3S
CAS No. 266359-83-5

Storage

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

DMSO: 500 mg/mL

TargetMolReferences and Literature

1. Moriconi A, et al. Design of noncompetitive interleukin-8 inhibitors acting on CXCR1 and CXCR2. J Med Chem. 2007 Aug 23;50(17):3984-4002. 2. Bertini R, et al. Receptor binding mode and pharmacological characterization of a potent and selective dual CXCR1/CXCR2non-competitive allosteric inhibitor. Br J Pharmacol. 2012 Jan;165(2):436-54. 3. Kim HY, et al. Reparixin, an inhibitor of CXCR1 and CXCR2 receptor activation, attenuates blood pressure and hypertension-related mediators expression in spontaneously hypertensive rats. Biol Pharm Bull. 2011;34(1):120-7. 4. Sousa LF, et al. Blockade of CXCR1/2 chemokine receptors protects against brain damage in ischemic stroke in mice. Clinicals (Sao Paulo). 2013;68(3):391-4. 5. Krishnamurthy A, et al. Identification of a novel chemokine-dependent molecular mechanism underlying rheumatoid arthritis-associated autoantibody-mediated bone loss. Ann Rheum Dis. 2016 Apr;75(4):721-9. 6. Crespo J, et al. Human Naive T Cells Express Functional CXCL8 and Promote Tumorigenesis. J Immunol. 2018 Jul 15;201(2):814-820. 7. Shi Y, Yu J, Zhang Y, et al. RhTyrRS (Y341A), a novel human tyrosyl-tRNA synthetase mutant, stimulates thrombopoiesis through activation of the VEGF-R II/NF-κB pathway[J]. Biochemical Pharmacology. 2019, 169: 113634.

TargetMolCitations

1. Shi Y, Yu J, Zhang Y, et al. RhTyrRS (Y341A), a novel human tyrosyl-tRNA synthetase mutant, stimulates thrombopoiesis through activation of the VEGF-R II/NF-κB pathway. Biochemical Pharmacology. 2019, 169: 113634. 2. Ma Y T, Zheng L, Zhao C W, et al.Interferon-α induces differentiation of cancer stem cells and immunosuppression in hepatocellular carcinoma by upregulating CXCL8 secretion.Cytokine.2024, 177: 156555.

Related compound libraries

This product is contained In the following compound libraries:
Anti-Cancer Drug Library Anti-Cancer Clinical Compound Library Anti-Aging Compound Library Anti-Cancer Compound Library GPCR Compound Library Orally Active Compound Library Immuno-Oncology Compound Library Drug Repurposing Compound Library ReFRAME Related Library NO PAINS Compound Library

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Keywords

Reparixin 266359-83-5 Autophagy GPCR/G Protein Immunology/Inflammation CXCR DF 1681Y Inhibitor CXC chemokine receptors inhibit Repertaxin inhibitor

 

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