Reparixin (Repertaxin)

For research use only. Not for use in humans.

Catalog No.S8640

1 publication

Reparixin (Repertaxin) Chemical Structure

Molecular Weight(MW): 283.39

Reparixin(Repertaxin) is a inhibitor of human CXCR1/R2 and rat CXCR2 receptor activation. It also inhibits human CXCL8 receptor activation.

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Selleck's Reparixin (Repertaxin) has been cited by 1 publication

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Biological Activity

Description Reparixin(Repertaxin) is a inhibitor of human CXCR1/R2 and rat CXCR2 receptor activation. It also inhibits human CXCL8 receptor activation.
CXCR1 [1]
CXCR2 [1]
CXCL8 [1]
In vitro

Reparixin is a non-competitive allosteric blocker of CXCR1 and CXCR2 receptor activation, which inhibits intracellular signal pathways without affecting receptor bindings. Reparixin potently and selectively inhibits a wide range of biological activities that are induced by CXCL8 such as leukocytes recruitment and functional inflammatory reactions. However, reparixin does not affect CXCR1/CXCR2 activation induced by other chemotactic factors, C5a, fMLP, CXCL12 or several other agonists of GPCRs. Reparixin can regulate the production of angiotensin II receptors, which may influence Ang II-induced hypertension[1]. Reparixin specifically blocks CXCR1/2-mediated mouse and human neutrophil migration in vitro without affecting other receptors. Reparixin inhibits CXCL8-induced neutrophil activation through human CXCR1 and human CXCR2 and blocks phosphorylation of downstream signalling molecules. Reparixin prevents the increase of intracellular free calcium, elastase release and production of reactive oxygen intermediates, but leaves phagocytosis of Escherichia coli bacteria unaffected[2].

Methods Test Index PMID
Western blot
IL-8 / STAT3 / p-STAT3 / AKT / p-AKT; 

PubMed: 30397072     

CAA1 cells were treated with different doses of reparixin for 24 h, and anti-IL-8 neutralizing antibody was used as a positive control. Cell lysates were prepared and utilized to assess the level of the indicated proteins using specific antibodies. The numbers below the bands indicate the corresponding protein expression levels relative to GAPDH. The levels of phosphorylated proteins were normalized against the total amounts of the respective nonphosphorylated proteins.

CXCR1 / CACR2 / Bcl-2 / Bax / Cyclin D1 / VEGF / MMP-2 / MMP-9 / TIMP-2 / E-cadherin / p-ERK / ERK ; 

PubMed: 26847910     

MKN45 cells were treated with repertaxin (25 μg/ml) alone, 5-FU (10 μg/ml) alone, or combined repertaxin and 5-FU for 48 h. Cell lysates (50 μg) were fractionated by SDS-PAGE and subject to western blot analysis; GAPDH was used as a loading control. 

30397072 26847910
p-FAK / p-AKT / FOXO3A ; 

PubMed: 20051626     

Using immunofluorescence staining on CXCR1+ cells, we confirmed that repertaxin treatment caused a disappearance of phospho-FAK (membranous staining in red) and phospho-AKT expression (cytoplasmic staining in red). Immunofluorescence staining with anti-FOXO3A revealed a cytoplasmic location of FOXO3A (red) in the untreated cells, whereas repertaxin treatment induced a relocalization of FOXO3A to the nucleus. In contrast, cells with PTEN deletion or FAK overexpression displayed a high level of phospho-FAK, phospho-AKT, and cytoplasmic FOXO3A expression in both the repertaxin-treated and untreated cells. In all samples, nuclei were counterstained with DAPI (blue). Scale bar: 50 μm.

In vivo Reparixin, an inhibitor of CXCL8 receptor CXCR1 and CXCR2 activation, attenuates inflammatory responses in various injury models. Reparixin effectively decreases systolic blood pressure and increases the blood flow. The thoracic aorta wall thickness is significantly decreased in SHR-R (the reparixin-treated group) compared to SHR-N (normal saline-treated SHR)[1]. (SHR: Spontaneously hypertensive rats)


Cell Research:


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  • Cell lines: HUVECs
  • Concentrations: 1 μM
  • Incubation Time: 30 min
  • Method:

    HUVECs are pretreated without or with reparixin (1 μM) for 30 min. Cells were then treated with or without Ang II (100 nmol/l) or CXCL8 (100 ng/ml) for 2 h. After total RNA is isolated, real-time PCR was performed.

    (Only for Reference)
Animal Research:


- Collapse
  • Animal Models: SHR rats
  • Formulation: saline
  • Dosages: 5 mg/kg
  • Administration: s.c.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 56 mg/mL (197.6 mM)
Ethanol 56 mg/mL (197.6 mM)
Water Insoluble

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 283.39


CAS No. 266359-83-5
Storage powder
in solvent
Synonyms N/A
Smiles CC(C)CC1=CC=C(C=C1)C(C)C(=O)N[S](C)(=O)=O

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Frequently Asked Questions

  • Question 1:

    Do you have the information of the half life time of reparixin Catalog No.S8640 in rats?

  • Answer:

    The following paper indicated the half-life of this compound in rats is 0.5h (

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID