Pharmacological reversal of a pain phenotype in iPSC-derived sensory neurons and patients with inherited erythromelalgia

Author:

Cao Lishuang1,McDonnell Aoibhinn1,Nitzsche Anja1,Alexandrou Aristos1,Saintot Pierre-Philippe1,Loucif Alexandre J.C.1,Brown Adam R.1,Young Gareth1,Mis Malgorzata2,Randall Andrew3,Waxman Stephen G.4,Stanley Philip1,Kirby Simon1,Tarabar Sanela5,Gutteridge Alex1,Butt Richard1,McKernan Ruth M.1,Whiting Paul1,Ali Zahid1,Bilsland James1,Stevens Edward B.1

Affiliation:

1. Pfizer Neuroscience and Pain Research Unit, The Portway Building, Granta Park, Cambridge CB21 6GS, UK.

2. University of Bristol, School of Physiology, Pharmacology, and Neuroscience, Bristol BS8 1TD, UK.

3. Hatherly College of Life and Environmental Sciences, University of Exeter, Prince of Wales Road, Exeter EX4 4PS, UK.

4. Yale Center for Neuroscience and Regeneration Research, Veterans Affairs Medical Center, 950 Campbell Avenue, Building 34,West Haven, CT 06516, USA.

5. Pfizer, 1 Howe Street, New Haven, CT 06511, USA.

Abstract

A selective Nav1.7 sodium channel blocker reduced hyperexcitability of iPSC-derived sensory neurons and alleviated pain in a subpopulation of patients with an inherited pain disorder.

Funder

Pfizer Inc.

Innovative Medicines Initiative Joint Undertaking

European Union's Seventh Framework Programme

European Federation of Pharmaceutical Industries and Association (EFPIA)

Biotechnology and Biological Sciences Research Council (BBSRC)

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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