266359-83-5

Usage

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 
• 51146-57-7 (R)-ibuprofene 
• 51146-56-6 (S)-ibuprofen 
• 15687-27-1 ibuprofen 

Relevant academic research and scientific papers

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

A new and efficient method for the facile synthesis of N-acyl sulfonamides under Lewis acid catalysis

The N-acylation of sulfonamides with carboxylic acid anhydrides in the presence of Lewis acids is described. Several Lewis acids such as BF3·Et2O, ZnCl2, MoCl5, TiCl4, B(C6F5)su

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.

Predicting human serum albumin affinity of interleukin-8 (CXCL8) inhibitors by 3D-QSPR approach

A novel class of 2-(R)-phenylpropionamides has been recently reported to inhibit in vitro and in vivo interleukin-8 (CXCL8)-induced biological activities. These CXCL8 inhibitors are derivatives of phenylpropionic nonsteroidal antiinflammatory drugs (NSAID