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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Thomas, Douglas D. / Turk, Boris / Wittinghofer, Alfred


IMPACT FACTOR 2018: 3.014
5-year IMPACT FACTOR: 3.162

CiteScore 2018: 3.09

SCImago Journal Rank (SJR) 2018: 1.482
Source Normalized Impact per Paper (SNIP) 2018: 0.820

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1437-4315
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Volume 392, Issue 3

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PETIR-001, a dual inhibitor of dipeptidyl peptidase IV (DP IV) and aminopeptidase N (APN), ameliorates experimental autoimmune encephalomyelitis in SJL/J mice

Dirk Reinhold
  • Institute of Molecular and Clinical Immunology, Otto von Guericke University Magdeburg, D-39120 Magdeburg, Germany
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/ Ute Bank / Dominik Entz
  • Institute of Molecular and Clinical Immunology, Otto von Guericke University Magdeburg, D-39120 Magdeburg, Germany
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/ Alexander Goihl
  • Institute of Molecular and Clinical Immunology, Otto von Guericke University Magdeburg, D-39120 Magdeburg, Germany
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/ Diana Stoye
  • Institute of Molecular and Clinical Immunology, Otto von Guericke University Magdeburg, D-39120 Magdeburg, Germany
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/ Sabine Wrenger
  • Institute of Molecular and Clinical Immunology, Otto von Guericke University Magdeburg, D-39120 Magdeburg, Germany
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/ Stefan Brocke
  • Departments of Pharmacology and Immunology, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030-6125, USA
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/ Anja Thielitz
  • University Clinic of Dermatology and Venereology, Otto von Guericke University Magdeburg, D-39120 Magdeburg, Germany
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/ Sofia Stefin / Karsten Nordhoff / Anke Heimburg / Michael Täger / Siegfried Ansorge
Published Online: 2011-06-18 | DOI: https://doi.org/10.1515/bc.2011.024

Abstract

Cellular dipeptidyl peptidase IV (DP IV, CD26) and amino-peptidase N (APN, CD13) play regulatory roles in T cell activation and represent potential targets for treatment of inflammatory disorders. We have developed a novel therapeutic strategy, ‘peptidase-targeted Immunoregulation’ (PETIR™), which simultaneously targets both cellular DP IV and APN via selective binding sites different from the active sites with a single inhibitor. To prove the therapeutic concept of PETIR™ in autoimmunity of the central nervous system (CNS), we evaluated the effect of a single substance, PETIR-001, in an animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE) in SJL/J mice. Administration of PETIR-001 significantly delayed and decreased clinical signs of active EAE, when given in a therapeutic manner intraperitoneally from day 15 to day 24 after induction of EAE. Both the acute phase and the first relapse of EAE were markedly inhibited. Importantly, a similar therapeutic benefit was obtained after oral administration of PETIR-001 from day 12 to day 21 after disease induction. Our results demonstrate that PETIR-001 exhibits a therapeutic effect on EAE in SJL/J mice. Thus, PETIR™ represents a novel and efficient therapeutic approach for immunotherapy of CNS inflammation.

Keywords: experimental autoimmune encephalomyelitis; multiple sclerosis; peptidase inhibitors; PETIR™; T cell activation

About the article

Corresponding author


Received: 2010-06-24

Accepted: 2010-11-02

Published Online: 2011-06-18

Published in Print: 2011-03-01


Citation Information: Biological Chemistry, Volume 392, Issue 3, Pages 233–237, ISSN (Online) 1437-4315, ISSN (Print) 1431-6730, DOI: https://doi.org/10.1515/bc.2011.024.

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