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Sunesis Pharmaceuticals Presents Nonclinical Data on SNS-595 at the Annual Meeting of the American Association for Cancer Research
Date:4/14/2008

ble G2 arrest and rapid apoptosis. SNS-595's targeted DNA-topoisomerase II interactions may contribute to the broad therapeutic window observed in patients treated with SNS-595.

In a translational research study designed to evaluate SNS-595's activity in primary patient samples of breast and ovarian cancers and acute myeloid leukemia against other agents, SNS-595 demonstrated potent activity and compared favorably with doxorubicin, etoposide and platinum therapy at clinically relevant concentrations. SNS-595 is not a P-glycoprotein substrate and its activity is independent of the p53 family. This finding is noteworthy, as high or increased expression of P-glycoprotein is a common form of drug resistance. In addition, the activity of many cancer agents requires functional p53 family members, and p53 mutations or deletions are also a frequent cause of drug resistance. Based on these findings, evidence from prior nonclinical studies in drug-resistant tumor models and the objective clinical responses observed to date among patients who have failed prior anthracycline-based therapies, SNS-595 may be active in settings where other topoisomerase poisons are no longer effective. These findings support the ongoing clinical trials in AML and ovarian cancer, and indicate that SNS-595 may also be well-suited to the treatment of breast cancer.

In a third set of studies reported today, Sunesis researchers profiled the potential relationship between SNS-595 activity and DNA repair pathways. Since SNS-595 causes double-strand breaks, the integrity of DNA repair pathways could impact cell sensitivity to SNS-595. Identification of the role of various DNA repair pathways may contribute to the identification of biomarkers for patient stratification. Researchers found that the DNA damage induced by SNS-595 is repaired by homologous recombination repair (HRR), and that cells deficient in HRR have greater sensitivity to SNS-595. Breast and ovarian cancers with BRCA mutations
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SOURCE Sunesis Pharmaceuticals, Inc.
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