1. GPCR/G Protein
    Immunology/Inflammation
  2. CXCR

Reparixin (Synonyms: Repertaxin; DF 1681Y)

Cat. No.: HY-15251 Purity: 99.88% ee.: 100.00%
Handling Instructions

Reparixin 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).

For research use only. We do not sell to patients.

Reparixin Chemical Structure

Reparixin Chemical Structure

CAS No. : 266359-83-5

Size Price Stock Quantity
10 mM * 1 mL in DMSO USD 168 In-stock
Estimated Time of Arrival: December 31
2 mg USD 108 In-stock
Estimated Time of Arrival: December 31
5 mg USD 228 In-stock
Estimated Time of Arrival: December 31
10 mg USD 384 In-stock
Estimated Time of Arrival: December 31
25 mg USD 840 In-stock
Estimated Time of Arrival: December 31
50 mg USD 1080 In-stock
Estimated Time of Arrival: December 31
100 mg USD 1320 In-stock
Estimated Time of Arrival: December 31
200 mg USD 2040 In-stock
Estimated Time of Arrival: December 31
500 mg   Get quote  
1 g   Get quote  

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Customer Review

Other Forms of Reparixin:

    Reparixin purchased from MCE. Usage Cited in: J Gastroenterol Hepatol. 2017 May 8.

    The effects of TRAF2 overexpression with or without Reparixin (100 nM), or BAY 11-7082 (30 μM) on the migration and invasion of AGS cell are examined by transwell assay.

    Reparixin purchased from MCE. Usage Cited in: Oncogenesis. 2016 Jun 13;5(6):e234.

    The effects of Reparixin (100 nM) on the migration of OLFM4-depleted gastric cancer cells are detected by transwell assay.

    Reparixin purchased from MCE. Usage Cited in: Oncotarget. 2017 Jul 21;8(36):60210-60222.

    Migration assay of MDA-MB-231 cells treated 0.1 uM of Reparixin in CM from fibroblasts or macrophages with TCM of MDA-MB-231 cells using the Oris Cell migration kit.
    • Biological Activity

    • Protocol

    • Technical Information

    • Purity & Documentation

    • References

    Description

    Reparixin 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).

    IC50 & Target

    IC50: 5.6/80 nM (CXCR1wt/CXCR1Ile43Val, in L1.2 cell)[1]

    In Vitro

    Reparixin is a potent functional inhibitor of CXCL8-induced biological activities on human PMNs with a marked selectivity (around 400-fold) for CXCR1, as shown in specific experiments on CXCR1/L1.2 and CXCR2/L1.2 transfected cells and on human PMNs. The efficacy of Reparixin is significantly lower in L1.2 cells expressing Ile43Val CXCR1 mutant (IC50 values of 5.6 nM and 80 nM for CXCR1 wt and CXCR1 Ile43Val, respectively)[1]. Reparixin is a non-competitive allosteric inhibitor of IL-8 receptors with a 400-fold higher efficacy in inhibiting CXCR1 activity than CXCR2[2].

    In Vivo

    Reparixin is an inhibitor of CXCL8 receptor CXCR1 and CXCR2 activation, has been shown to attenuate inflammatory responses in various injury models. Spontaneously hypertensive rats (SHR) are administered a subcutaneous injection of Reparixin (5 mg/kg) daily for 3 weeks. Reparixin effectively decreases systolic blood pressure and increased the blood flow[3]. Reparixin reduces the levels of IL-1β in the brain after middle cerebral artery occlusion/reperfusion (MCAo) in mice. Bars represent levels of IL-1β (pg/100 mg) measured by ELISA in the brain tissues of mice subjected or not (SHAM) to MCAo and pretreated with vehicle or Reparixin (30 mg/kg, s.c.)[4].

    Clinical Trial
    Solvent & Solubility
    In Vitro: 

    DMSO : ≥ 500 mg/mL (1764.35 mM)

    *"≥" means soluble, but saturation unknown.

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 3.5287 mL 17.6435 mL 35.2871 mL
    5 mM 0.7057 mL 3.5287 mL 7.0574 mL
    10 mM 0.3529 mL 1.7644 mL 3.5287 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Reparixin is prepare in vehicle (sterile saline)[5].

    • 2.

      Reparixin is prepared in PBS[6].

    References
    Cell Assay
    [1]

    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-1μM) 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[1].

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

    Animal Administration
    [3][4]

    Rats[3]
    The Reparixin-treated group contained 5 SHR (SHR-R), where equal numbers of normal saline-treated SHR (SHR-N) and WKY (WKY-N) served as controls. Eighteen-week-old SHR received a subcutaneous injection of Reparixin (5 mg/kg) once per day for 3 weeks. Reparixin effects on blood flow, blood pressure and body weight are measured before treatment and then weekly until 1 week after the final injection. The effect of Reparixin on the expression of hypertension-related mediators in thoracic aortas, as well as nitric oxide (NO) plasma levels, is examined 1 week after the final injection. At the end of the 4 week period, both control and Reparixin-treated rats are anesthetized via intraperitoneal injection of thiopental (50 mg/kg), and blood and tissue samples are collected.
    Mice[4]
    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.

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

    References
    Molecular Weight

    283.39

    Formula

    C₁₄H₂₁NO₃S

    CAS No.

    266359-83-5

    SMILES

    CS(=O)(NC([[email protected]@H](C1=CC=C(CC(C)C)C=C1)C)=O)=O

    Storage
    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Shipping

    Room temperature in continental US; may vary elsewhere

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    Inquiry Information

    Product Name:
    Reparixin
    Cat. No.:
    HY-15251
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    Reparixin

    Cat. No.: HY-15251