Second-Generation Non-Covalent NAAA Inhibitors are Protective in a Model of Multiple Sclerosis

  • Angew Chem Int Ed Engl. 2016 Sep 5;55(37):11193-11197. doi: 10.1002/anie.201603746.
Marco Migliore Dr   #  1 Silvia Pontis Dr   #  1 Angel Luis Fuentes de Arriba  1 Natalia Realini  1 Esther Torrente  1 Andrea Armirotti  1 Elisa Romeo  1 Simona Di Martino  1 Debora Russo  1 Daniela Pizzirani  1 Maria Summa  1 Massimiliano Lanfranco  1 Giuliana Ottonello  1 Perrine Busquet  1 Kwang-Mook Jung  2 Miguel Garcia-Guzman  3 Roger Heim  3 Rita Scarpelli  1 Daniele Piomelli  1  2
Affiliations
  • 1. Department of Drug Discovery and Development, Fondazione Istituto Italiano di Tecnologia, via Morego 30, 16163 Genoa, Italy.
  • 2. Departments of Anatomy and Neurobiology, Pharmacology and Biological Chemistry, University of California, Irvine, CA 92697-4625, USA.
  • 3. Anteana Therapeutics, 11189 Sorrento Valley Road, Suite 104, San Diego CA 92121, USA.
  • # Contributed equally.
Abstract

Palmitoylethanolamide (PEA) and oleoylethanolamide (OEA) are endogenous lipid mediators that suppress inflammation. Their actions are terminated by the intracellular cysteine amidase, N-acylethanolamine acid amidase (NAAA). Even though NAAA may offer a new target for anti-inflammatory therapy, the lipid-like structures and reactive warheads of current NAAA inhibitors limit the use of these agents as oral drugs. A series of novel benzothiazole-piperazine derivatives that inhibit NAAA in a potent and selective manner by a non-covalent mechanism are described. A prototype member of this class (8) displays high oral bioavailability, access to the central nervous system (CNS), and strong activity in a mouse model of multiple sclerosis (MS). This compound exemplifies a second generation of non-covalent NAAA inhibitors that may be useful in the treatment of MS and Other chronic CNS disorders.

Keywords
N-acylethanolamine acid amidase; cysteine hydrolase; fatty acylethanolamides; multiple sclerosis; neuroinflammation.
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