PeptideDB

(Rac)-Reparixin

CAS: 957407-64-6 F: C14H21NO3S W: 283.39

(Rac)-Reparixin is the inactive isomer of Reparixin (HY-15251), and can be used as an experimental control. Reparixin is
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This product is for research use only, not for human use. We do not sell to patients.

Bioactivity (Rac)-Reparixin is the inactive isomer of Reparixin (HY-15251), and can be used as an experimental control. Reparixin is a non-competitive allosteric inhibitor of the chemokine receptors CXCR1 and CXCR2 activation with IC50s of 1 and 100 nM, respectively.
Name (Rac)-Reparixin
CAS 957407-64-6
Formula C14H21NO3S
Molar Mass 283.39
Transport Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Reference [1]. Sousa LF, et al. Blockade of CXCR1/2 chemokine receptors protects against brain damage in ischemic stroke in mice. Clinics (Sao Paulo). 2013;68(3):391-4. [2]. Bertini R, 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 Aug 10;101(32):11791-6. [3]. Krishnamurthy A, et al. Identification of a novel chemokine-dependent molecular mechanism underlying rheumatoid arthritis-associated autoantibody-mediated bone loss. Ann Rheum Dis. 2016 Apr;75(4):721-9. [4]. Crespo J, et al. Human Naive T Cells Express Functional CXCL8 and Promote Tumorigenesis. J Immunol. 2018 Jul 15;201(2):814-820. [5]. Moriconi A, et al. Design of noncompetitive interleukin-8 inhibitors acting on CXCR1 and CXCR2. J Med Chem. 2007 Aug 23;50(17):3984-4002. [6]. Bertini R, et al. Receptor binding mode and pharmacological characterization of a potent and selective dual CXCR1/CXCR2non-competitive allosteric inhibitor. Br J Pharmacol. 2012 Jan;165(2):436-54. [7]. Kim HY, et al. 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.