BERKELEY HEIGHTS, N.J. and DUNDEE, UK, Aug. 12, 2013 (GLOBE NEWSWIRE) -- Cyclacel Pharmaceuticals, Inc. (Nasdaq:CYCC) (Nasdaq:CYCCP) (Cyclacel or the Company), today announced that scientists at Newcastle University have been awarded £1 million (approximately $1.5 million) by the UK's Medical Research Council for a clinical trial to evaluate whether seliciclib, Cyclacel's oral cyclin dependent kinase (CDK) inhibitor currently in clinical development to treat certain cancers, can be repurposed to treat rheumatoid arthritis (RA) in patients who do not respond to existing treatments. Seliciclib may work for RA by targeting proliferating fibroblasts, a different type of approach than conventional RA therapies, and could therefore succeed where these treatments have failed.
"Repurposing of drugs is a powerful way of bridging the gap between early stage research and development of new treatments," said Professor John Isaacs, Director of the Institute of Cellular Medicine at Newcastle University and lead investigator. "Compared with traditional drug discovery approaches, this is a considerably quicker route to the clinic because it leapfrogs the early stages of drug development. If our trial with seliciclib proves successful, it could dramatically improve treatment outcomes for patients with rheumatoid arthritis."
Over the past 20 years, improved treatment strategies and better drugs have resulted in greatly improved outcomes for patients. Currently available drugs for RA, called disease-modifying antirheumatic drugs (DMARDs), slow or halt the progress of the disease by reducing joint inflammation or neutralizing immune cells. However, many patients still do not recover and about one in ten do not respond at all to conventional treatments.Scientists believe that another type of cell, fibroblasts, may be responsible and may be limiting response to conventional treatments. In RA these cells divide uncontrollably and produce chemicals that eat into cartilage and bone and cause inflammation. Using Seliciclib to Target Fibroblasts The Newcastle team, with collaborators at the Universities of Birmingham and Glasgow, believe that seliciclib may reduce or stop abnormal fibroblast activity. Seliciclib has been previously shown to selectively inhibit enzyme targets which are central to the process of cell division and cell cycle control thereby inhibiting cellular proliferation.
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