BERKELEY HEIGHTS, N.J., Sept. 19, 2013 (GLOBE NEWSWIRE) -- Cyclacel Pharmaceuticals, Inc. (Nasdaq:CYCC) (Nasdaq:CYCCP) ("Cyclacel" or the "Company") today announced updated data showing that sapacitabine has activity against a majority of ovarian cancer samples taken from patients, including resistant tumors. The data were reported at a poster presentation during the American Association of Cancer Research (AACR) conference "Advances in Ovarian Cancer: from concept to clinic" being held September 18-21, 2013, in Miami, FL.
"We are encouraged by the activity signal of sapacitabine in ovarian cancer samples," said Judy Chiao, M.D., Vice President, Clinical Development and Regulatory Affairs of Cyclacel. "This observation may be directly related to the drug's mechanism which is enhanced in cancer cells with reduced capacity for DNA repair through the homologous recombination repair or HR pathway. In addition to our ongoing Phase 3 registration trial of sapacitabine in acute myeloid leukemia and Phase 2 studies in myelodysplastic syndromes, we are continuing to evaluate sapacitabine as a potential treatment for patients with solid tumors, and in particular those with BRCA-deficient cancers."
Cyclacel collaborators from the Northern Institute for Cancer Research, Newcastle University, UK led by Nicola Curtin, Professor of Experimental Therapeutics and Richard Edmondson, Professor of Gynaecological Oncology reported that CNDAC, the active metabolite of sapacitabine, was active against 75% (30 of 40) of primary ovarian cancer (POC) samples isolated from patients. In contrast cisplatin was active in less than half of the samples. Over half of the cisplatin-resistant samples were sensitive to CNDAC, indicating that sapacitabine has potential utility for treatment of ovarian cancers, including platinum-resistant disease. The majority, but not all, of the samples tested were from high grade serous ovarian cancers.The HR activity of the ovarian samples was determined as HR deficient or HR proficient by a functional assay. Sensitivity to sapacitabine was substantially greater in HR deficient than HR proficient samples (mean GI 50 values of 135 nM versus 477 nM, respectively). This difference suggests that HR status, or other surrogate markers such as BRCA mutation status, could be used to enrich for potential responders in stratified clinical trials of sapacitabine in patients with solid tumors. Sapacitabine activity has been shown to be substantially enhanced in cell lines with defects or mutations in the HR pathway, including mutations in ATM, BRCA1, BRCA2, RAD51 and XRCC3. The reported data further support the potential for sapacitabine to be used as a treatment for HR defective cancers, such as ATM- or BRCA-defective tumors. Clinical trials examining the activity of sapacitabine in ATM-defective CLL, and of sapacitabine in combination with Cyclacel's seliciclib in cancer patients with BRCA1 or BRCA2 mutations, are currently in progress.
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