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Apremilast, a novel PDE4 inhibitor, inhibits spontaneous production of tumour necrosis factor-alpha from human rheumatoid synovial cells and ameliorates experimental arthritis

Fiona E McCann1*, Andrew C Palfreeman1, Melanie Andrews12, Dany P Perocheau1, Julia J Inglis13, Peter Schafer4, Marc Feldmann1, Richard O Williams1 and Fionula M Brennan1

Author Affiliations

1 The Kennedy Institute of Rheumatology, Imperial College London, 65 Aspenlea Road, London, W6 8LH, UK

2 Institute for Molecular Bioscience, University of Queensland, Bldg 80 Services Road, Brisbane, QLD 4072, Australia

3 Pharmacology & Anaesthesiology Unit, School of Medicine & Pharmacology, University of Western Australia, 35 Stirling Highway, Crawley, WA 6009, Australia

4 Translational Development, Celgene Corporation, 86 Morris Avenue, Summit, NJ, 07901, USA

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Arthritis Research & Therapy 2010, 12:R107  doi:10.1186/ar3041

Published: 2 June 2010

Additional files

Additional file 1:

Supplementary figure S1. Apremilast has no effect on cell viability in human cells. (a) Human monocytes and (b) rheumatoid arthritis (RA) synovial membrane cells were cultured with increasing concentrations of apremilast or rolipram as in Figure 1. After supernatants were collected for cytokine analysis, 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) was added at a final concentration of 0.5 ng/ml for six hours. A 100 μl sample of 10% SDS in 0.01 M HCl was then added overnight before the plate was read on a spectrophotometer at 620 nm. None of the culture conditions assayed altered cell viability relative to cells alone.

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