Reparixin

  • CAT Number: I002912
  • CAS Number: 266359-83-5
  • Molecular Formula: C14H21NO3S
  • Molecular Weight: 283.39
  • Purity: ≥95%
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Reparixin(Cat No.:I002912), also known as Repertaxin or DF 1681Y, is a highly potent and specific inhibitor of CXCR1, a chemokine receptor involved in immune cell migration. It has an IC50 of 1 nM, effectively inhibiting CXCL8-induced PMN (polymorphonuclear leukocyte) migration. Reparixin also inhibits chemotaxis in rodent PMNs induced by CXCL1 and CXCL2. Furthermore, it demonstrates inhibitory effects on human PMN responses to CXCL1, which interacts with CXCR2, with an IC50 of 400 nM. Reparixin’s ability to modulate chemokine receptor activity makes it a potential therapeutic candidate for inflammatory conditions.

Catalog Number I002912
CAS Number 266359-83-5
Molecular Formula

C14H21NO3S

Purity 95%
Target CXCR
Solubility 10 mM in DMSO
Storage Room Temperature
IC50 5.6 nM/80 nM (for CXCR1 weight and cells expressing Ile43Val CXCR1 mutant respectively)
IUPAC Name (2R)-2-[4-(2-methylpropyl)phenyl]-N-methylsulfonylpropanamide
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)/t11-/m1/s1
InChIKey KQDRVXQXKZXMHP-LLVKDONJSA-N
SMILES CC(C)CC1=CC=C(C=C1)C(C)C(=O)NS(=O)(=O)C
Reference

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<br>[1]. Moriconi A, Cesta MC, Cervellera MN, Design of noncompetitive interleukin-8 inhibitors acting on CXCR1 and CXCR2. J Med Chem. 2007 Aug 23;50(17):3984-4002.
<br>[2]. Gorio A, Madaschi L, Zadra G, Reparixin, an inhibitor of CXCR2 function, attenuates inflammatory responses and promotes recovery of functionafter traumatic lesion to the spinal cord. J Pharmacol Exp Ther. 2007 Sep;322(3):973-81.
<br>[3]. Kim HY, Choi JH, Kang YJ, Reparixin, an inhibitor of CXCR1 and CXCR2 receptor activation, attenuates blood pressure and hypertension-related mediators expression in spontaneously hypertensive rats. Biol Pharm Bull. 2011;34(1):120-7.
<br>[4]. Sousa LF, Coelho FM, Rodrigues DH, Blockade of CXCR1/2 chemokine receptors protects against brain damage in ischemic stroke in mice. Clinics (Sao Paulo). 2013;68(3):391-4.
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