266359-83-5

Basic information

• Product Name: Repertaxin
• Synonyms: Reparixin;Repertaxin;DF 1681Y;(R)-(-)-N-2-[(4-Isobutylphenyl)propionyl]methanesulfonamide;Repertaxin(R-configuration, free base form)
• CAS NO: 266359-83-5
• Molecular Formula: C14H21NO3S
• Molecular Weight: 283.38644
• Mol File: 266359-83-5.mol
• Article Data: 4

Chemical Properties

• Melting Point: 103-105℃
• Appearance: /
• Density: 1.137g/cm³
• Refractive Index: 1.524
• Storage Temp.: Sealed in dry,Room Temperature
• Solubility: Soluble in DMSO (up to 100 mg/ml) or in Ethanol (up to 25 mg/ml)
• PKA: 4.28±0.40(Predicted)
• Stability: Stable for 1 year from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20°C for up to 3 months.
• CAS DataBase Reference: Repertaxin(CAS DataBase Reference)
• NIST Chemistry Reference: Repertaxin(266359-83-5)
• EPA Substance Registry System: Repertaxin(266359-83-5)

Safety Data

• Hazardous Substances Data: 266359-83-5(Hazardous Substances Data)

Usage

Description

Reparixin is a noncompetitive allosteric inhibitor of IL-8 (CXCL8) activation of CXCR1 and CXCR2 chemokine receptors, with IC50 values of 1 and 100 nM, respectively. It is characterized by its ability to block IL-8 signaling activities, such as leukocyte recruitment, without affecting receptor activation induced by other CXCR1 and CXCR2 agonists.

Uses

Used in Solid Organ Transplant:
Reparixin is used as a prevention agent for delayed graft function in solid organ transplant, acting as a CXCL8 inhibitor.
Used in Inflammation and Hypertension:
Reparixin is used as an inhibitor of CXCR1 and CXCR2 chemokine receptors for blocking leukocyte recruitment and IL-8 signaling, which helps in reducing blood pressure and attenuating inflammatory responses in spontaneously hypertensive rats.
Used in Spinal Cord Injury Recovery:
Reparixin is used as a therapeutic agent to promote recovery of function after traumatic lesions to the spinal cord by attenuating inflammatory responses.
Used in Cancer Stem Cell Depletion:
Reparixin is used as a CXCR1 blocker in vitro to deplete cancer stem cell populations in human breast cancer cell lines, potentially contributing to cancer treatment strategies.

References

1) Bertini?et al.?(2004),?Non-competitive allosteric inhibitors of the inflammatory cytokine receptors CXCR1 and CXCR2: prevention of reperfusion injury; Proc. Natl. Acad. Sci. USA,?101?11791 2) Kim?et al. (2011),?Reparixin, an inhibitor of CXCR1 and CXCR2 receptor activation, attenuates blood pressure and hypertension-related mediators expression in spontaneously hypertensive rats; Biol. Pharm. Bull.,?34?120 3) Gorio?et al.?(2007),?Reparixin, an inhibitor of CXCR2 function, attenuates inflammatory responses and promotes recovery of function after traumatic lesion to the spinal cord; J. Pharmacol. Exp. Ther.,?322?973 4) Ginestier?et al.?(2010),?CXCR1 blockade selectively targets human breast cancer stem cells in vitro and in xenografts; J. Clin. Invest.,?120?485

InChI:InChI=1/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)

Upstream product

• 3144-09-0 methanesulfonamide 
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• 51146-56-6 (S)-ibuprofen 
• 51146-57-7 (R)-ibuprofene 

Relevant articles and documents

Modified acidic nonsteroidal anti-inflammatory drugs as dual inhibitors of mPGES-1 and 5-LOX

mPGES-1 is a promising target for development of new anti-inflammatory drugs. We aimed to create mPGES-1 inhibitors by modifying the structure of NSAIDs by replacing the carboxylic acid functionality by sulfonamide moieties. Compounds were also tested for

2-Arylpropionic CXC chemokine receptor 1 (CXCR1) ligands as novel noncompetitive CXCL8 inhibitors

The CXC chemokine CXCL8/IL-8 plays a major role in the activation and recruitment of polymorphonuclear (PMN) cells at inflammatory sites. CXCL8 activates PMNs by binding the seven-transmembrane (7-TM) G-protein-coupled receptors CXC chemokine receptor 1 (CXCR1) and CXC chemokine receptor 2 (CXCR2). (R)-Ketoprofen (1) was previously reported to be a potent and specific noncompetitive inhibitor of CXCLS-induced human PMNs chemotaxis. We report here molecular modeling studies showing a putative interaction site of 1 in the TM region of CXCR1. The binding model was confirmed by alanine scanning mutagenesis and photoaffinity labeling experiments. The molecular model driven medicinal chemistry optimization of 1 led to a new class of potent and specific inhibitors of CXCL8 biological activity. Among these, repertaxin (13) was selected as a clinical candidate drug for prevention of post-ischemia reperfusion injury.