BERKELEY HEIGHTS, N.J., March 27, 2013 (GLOBE NEWSWIRE) -- Cyclacel Pharmaceuticals, Inc. (Nasdaq:CYCC) (Nasdaq:CYCCP) ("Cyclacel" or the "Company") announced today its financial results and business highlights for the fourth quarter and full year 2012. The Company's net loss applicable to common stockholders for the fourth quarter of 2012 was $4.9 million, or $0.59 per basic and diluted share, compared to a net loss applicable to common stockholders of $3.8 million, or $0.50 per basic and diluted share, for the fourth quarter of 2011. For the year ended December 31, 2012, the Company reported a net loss applicable to common stockholders of $13.9 million, or $1.68 per basic and diluted share, compared to a net loss of $16.0 million or $2.22 per basic and diluted share, for the year ended December 31, 2011. As of December 31, 2012, cash and cash equivalents totaled $16.4 million.
"In 2012 we continued to make progress with the SEAMLESS Phase 3 study of sapacitabine in Acute Myeloid Leukemia (AML). At a year-end review the independent committee overseeing SEAMLESS identified no safety or efficacy concerns and recommended that the study should continue as planned," said Spiro Rombotis, President and Chief Executive Officer of Cyclacel. "Sapacitabine's potential in other indications continues to evolve. Recent data from a Phase 2 study demonstrated that sapacitabine nearly doubled expected survival of patients with myelodysplastic syndromes (MDS) after treatment failure of hypomethylating agents. In a Phase 1 study, sapacitabine, in combination with Cyclacel's seliciclib, showed antitumor activity in cancer patients found to be carriers of BRCA mutations. We plan to report updated data from both on-going studies as soon as mature follow-up is reached. We have broadened sapacitabine's patent estate with certain claims supporting market exclusivity to 2030. We continue to prudently manage our cash needs and have received an aggregate of $4.4 million through our Aspire Capital agreement and a government grant of $1.9 million supporting development of CYC065, our second-generation cyclin dependent kinase (CDK) inhibitor."
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