ReparixinInhibitor of CXCL8 receptor and CXCR1/CXCR2 activation CAS# 266359-83-5 |
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Quality Control & MSDS
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| Cas No. | 266359-83-5 | SDF | Download SDF |
| PubChem ID | 6433115 | Appearance | Powder |
| Formula | C14H21NO3S | M.Wt | 283.39 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | Repertaxin; DF 1681Y | ||
| Solubility | DMSO : ≥ 100 mg/mL (352.87 mM) H2O : < 0.1 mg/mL (insoluble) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | 2-[4-(2-methylpropyl)phenyl]-N-methylsulfonylpropanamide | ||
| SMILES | CC(C)CC1=CC=C(C=C1)C(C)C(=O)NS(=O)(=O)C | ||
| Standard InChIKey | KQDRVXQXKZXMHP-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C14H21NO3S/c1-10(2)9-12-5-7-13(8-6-12)11(3)14(16)15-19(4,17)18/h5-8,10-11H,9H2,1-4H3,(H,15,16) | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| 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).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]. References: | |||||
| Kinase experiment [1]: | |
| Binding assays | Isolated PMNs (107×mL) were resuspended in RPMI 1640 and incubated at 37℃ for 15 min in the presence of repertaxin (1 mM) or vehicle. After incubation cells were resuspended (2×107/mL) in binding medium (RPMI 1640 containing 10 mg/ml BSA, 20 mM HEPES, and 0.02% NaN3) in the presence of repertaxin or vehicle. Aliquots of 0.2 nM of [125I]CXCL8 and serial dilutions of unlabeled CXCL8 were added to 106 cells in 100 μL of binding medium and incubated at room temperature for 1 hr under gentle agitation. Unbound radioactivity was separated from cell-bound radioactivity by centrifugation through anoil gradient (80% silicon and 20% paraffin) on a microcentrifuge. Nonspecific binding was determined by a 200-fold molar excess of unlabeled CXCL8. Scatchard analysis was performed with the LIGAND program. |
| Cell experiment [1]: | |
| Cell lines | Human polymorphonuclear cells (PMN) and monocytes and rodent peritoneal PMN. |
| Preparation method | Soluble in DMSO. General tips for obtaining a higher concentration: Please warm the tube at 37℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months. |
| Reacting condition | 45 min (human PMN), 1 h (rodent PMN), or 2 h (monocytes). |
| Applications | Repertaxin inhibits human PMN migration induced by CXCL8 and CXCL1 with IC50 values of 1 nM and 400 nM respectively, which are mediated by CXCR1 and CXCR2, respectively. Repertaxin also inhibits rodent PMN chemotaxis induced by CXCL1 and CXCL2. |
| Animal experiment [1]: | |
| Animal models | Rat model of liver postischaemia RI. |
| Dosage form | 3, 15, or 30 mg/kg; 15 min before reperfusion (i.v.) and 2 h after reperfusion (s.c.). |
| Application | Repertaxin (15 mg/kg) inhibits PMN recruitment into reperfused livers by 90% and significantly reducesliver damage. |
| Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
| References: [1]. Bertini R, Allegretti M, Bizzarri C, et al. Noncompetitive allosteric inhibitors of the inflammatory chemokine receptors CXCR1 and CXCR2: prevention of reperfusion injury. Proc Natl Acad Sci U S A, 2004, 101(32): 11791-11796. | |
Reparixin Dilution Calculator
Reparixin Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.5287 mL | 17.6435 mL | 35.2871 mL | 70.5741 mL | 88.2177 mL |
| 5 mM | 0.7057 mL | 3.5287 mL | 7.0574 mL | 14.1148 mL | 17.6435 mL |
| 10 mM | 0.3529 mL | 1.7644 mL | 3.5287 mL | 7.0574 mL | 8.8218 mL |
| 50 mM | 0.0706 mL | 0.3529 mL | 0.7057 mL | 1.4115 mL | 1.7644 mL |
| 100 mM | 0.0353 mL | 0.1764 mL | 0.3529 mL | 0.7057 mL | 0.8822 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Reparixin is a non-competitive allosteric inhibitor of CXCR1/2.
CXCR is a 7-transmembrane G protein-coupled receptor. CXCR plays a critical role in the development of different models of ALI Following engagement of this receptor, the Gbg-complex dissociates from the Gai-subunit and can activate phosphoinositide-3 kinase, different subtypes of phospholipase C and P-Rex-1. The downstream effectors of these molecules initiate a broad range of functional responses, including arrest from rolling, cytoskeletal rearrangement, cell polarization, chemotaxis, degranulation and respiratory burst.
Reperixin, specifically blocks CXCR1/2-mediated mouse and human neutrophil migration in vitro without affecting other receptors. Reparixin reduces ligand binding to human CXCR1 and CXCR2, calcium influx and downstream signalling in response to human CXCL8 and neutrophil recruitment into the liver in a mouse model of ischaemia-reperfusion injury. Reparixin reduced neutrophil recruitment and liver damage by approximately 30% and 80% in a model of ischaemiareperfusion injury.[1,2]
Reparixin reduced oligodendrocyte apoptosis, migration to the injury site of neutrophils and ED-1-positive cells. The best beneficial outcome of reparixin treatment will require 7-day administration either by i.p. route (15 mg/kg) or subcutaneous infusion via osmotic pumps (10 mg/kg), reaching a steady blood level of 8 μg/ml. Methylprednisolone are used as a reference drug, and such treatment reduced cytokine production but failed to affect the rate of hind limb recovery. [1,2]
References:
[1] A Zarbock, M Allegretti and K Ley. Therapeutic inhibition of CXCR2 by Reparixin attenuates acute lung injury in mice. British Journal of Pharmacology (2008) 155, 357–364.
[2] Alfredo Gorio, Laura Madaschi, Giorgia Zadra et al. Reparixin, an Inhibitor of CXCR2 Function, Attenuates Inflammatory Responses and Promotes Recovery of Function after Traumatic Lesion to the Spinal Cord. doi:10.1124/jpet.107.123679.
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Reparixin attenuates neuronal injury in experimental Klebsiella pneumoniae meningoencephalitis through dual effects on neuroprotection and neuroinflammation.[Pubmed:26245311]
Neuropathol Appl Neurobiol. 2016 Jun;42(4):326-43.
AIMS: Bacterial meningitis causes high mortality and brain damage. The host immune response is associated with brain injury. Chemokine (C-X-C motif) (CXC) chemokines are neutrophil chemoattractants. This study focused on the beneficial effects of intracerebroventricular administration of Reparixin, an inhibitor of chemokine (C-X-C motif) receptor (CXCR)1/2, to rats at 2 h following experimental Klebsiella pneumoniae meningoencephalitis. METHODS: We used a previously established meningoencephalitis animal model in which Sprague-Dawley rats were infected by K. pneumoniae. Sham and infected animals were treated with vehicle or Reparixin and sacrificed at various time points. Leukocyte infiltration into cerebrospinal fluid (CSF) and brain as well as gene and protein expression of chemokines and receptors, and neuronal apoptosis were examined. Primary cultures of neuron/glia were infected with K. pneumoniae as an in vitro model of meningoencephalitis. RESULTS: Levels of chemokine (C-X-C motif) ligand (CXCL)2 in CSF time-dependently increased markedly as early as 2 h, and peaked at 8 h following infection and were much higher than those in serum collected simultaneously. Reparixin significantly reduced leukocyte infiltration into CSF and brain tissues, clinical illness, and brain cell apoptosis at 24 h. Reparixin reduced the elevated CSF concentrations of chemokines [CXCL1, CXCL2, chemokine (C-C motif) ligand (CCL)2 and CCL5] and proinflammatory cytokines. Reparixin also reduced the expression of mRNA of various chemokines, chemokine receptors and proinflammatory cytokines in infected brain tissues. Using primary cultures that are devoid of leukocytes, we further observed that Reparixin attenuated the neuronal, but not microglial cell death after infection. CONCLUSIONS: Reparixin not only reduces amplified inflammation, but also provides direct neuroprotective effects in K. pneumoniae meningoencephalitis.
Simultaneous quantification of reparixin and paclitaxel in plasma and urine using ultra performance liquid chromatography-tandem mass spectroscopy (UHPLC-MS/MS): Application to a preclinical pharmacokinetic study in rats.[Pubmed:28187377]
J Chromatogr B Analyt Technol Biomed Life Sci. 2017 Mar 1;1046:165-171.
A liquid chromatography-tandem mass spectroscopy (LC-MS/MS) assay was developed and validated to simultaneously quantify anticancer drugs Reparixin and paclitaxel in this study. The compounds were extracted from plasma and urine samples by protein precipitation with acetone (supplemented with 0.1% formic acid). Chromatographic separation was achieved using a C18 column, and drug molecules were ionized using dual ion source electrospray and atmospheric pressure chemical ionization (DUIS: ESI-APCI). Reparixin and paclitaxel were quantified using negative and positive multiple reaction monitoring (MRM) mode, respectively. Stable isotope palcitaxel-D5 was used as the internal standard (IS). The assay was validated for specificity, recovery, carryover and sample stability under various storage conditions; it was also successfully applied to measure drug concentrations collected from a pharmacokinetic study in rats. The results confirmed that the assay was accurate and simple in quantifying both Reparixin and paclitaxel in plasma and urine with minimal sample pretreatment.
Reparixin, a CXCR1/2 inhibitor in islet allotransplantation.[Pubmed:27328412]
Islets. 2016 Sep 2;8(5):115-24.
Quality of life in Type 1 diabetic patients may be improved with islet transplantation, but lifelong immunosuppression is required to prevent rejection. Allo-immune response is a key player in graft dysfunction and although the adaptive immune response is well characterized, the effect of the innate immune reaction after transplantation is only recently becoming appreciated. In this study, we address how the innate response affects long-term outcomes in a murine islet allotransplant model. CTLA-4 Ig treatment is known to significantly prolong kidney subcapsular islet allograft survival and enhance glucose tolerance. The combination of CTLA-4 Ig with Reparixin, which blocks against inflammatory neutrophil infiltration, yielded no long-term graft survival in an intrahepatic allotransplant model but had similar long-term graft survival in the kidney subcapsular model. Seven days after transplant, serum blood IFN-gamma levels were significantly lower in the CTLA-4 Ig with Reparixin treatment group compared to controls. IL-12p70 cytokine levels were increased with combination treatment, a positive modulation of the inflammatory response to the allograft. Furthermore, KC GRO, also known as CXCL1, was decreased in serum 7 d after transplant. Histologically, we found that immune cell infiltrate, CD4+ and CD8+ T cell populations along with both CXCR1+ and CXCR2+ cell populations were decreased within the CTLA-4 Ig and Reparixin islet transplant graft. Overall these data provide insight into the down regulation of T-cell recruitment by CTLA-4 Ig and decreased neutrophil activation and recruitment with Reparixin after long-term islet graft survival.
A pilot study on reparixin, a CXCR1/2 antagonist, to assess safety and efficacy in attenuating ischaemia-reperfusion injury and inflammation after on-pump coronary artery bypass graft surgery.[Pubmed:25402332]
Clin Exp Immunol. 2015 Apr;180(1):131-42.
Reparixin, a CXCR 1/2 antagonist, has been shown to mitigate ischaemia-reperfusion injury (IRI) in various organ systems in animals, but data in humans are scarce. The aim of this double-blinded, placebo-controlled pilot study was to evaluate the safety and efficacy of Reparixin to suppress IRI and inflammation in patients undergoing on-pump coronary artery bypass grafting (CABG). Patients received either Reparixin or placebo (n = 16 in each group) after induction of anaesthesia until 8 h after cardiopulmonary bypass (CPB). We compared markers of systemic and pulmonary inflammation, surrogates of myocardial IRI and clinical outcomes using Mann-Whitney U- and Fisher's exact tests. Thirty- and 90-day mortality was 0% in both groups. No side effects were observed in the treatment group. Surgical revision, pleural and pericardial effusion, infection and atrial fibrillation rates were not different between groups. Reparixin significantly reduced the proportion of neutrophil granulocytes in blood at the beginning [49%, interquartile range (IQR) = 45-57 versus 58%, IQR = 53-66, P = 0.035], end (71%, IQR = 67-76 versus 79%, IQR = 71-83, P = 0.023) and 1 h after CPB (73%, IQR = 71-75 versus 77%, IQR = 72-80, P = 0.035). Reparixin patients required a lesser positive fluid balance during surgery (2575 ml, IQR = 2027-3080 versus 3200 ml, IQR = 2928-3778, P = 0.029) and during ICU stay (2603 ml, IQR = 1023-4288 versus 4200 ml, IQR = 2313-8160, P = 0.021). Numerically, more control patients required noradrenaline >/= 0.11 mug/kg/min (50 versus 19%, P = 0.063) and dobutamine (50 versus 25%, P = 0.14). Therefore, administration of Reparixin in CABG patients appears to be feasible and safe. It concurrently attenuated postoperative granulocytosis in peripheral blood.
