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Inability of Pixantrone to Form Toxic Iron Complexes Results in Significant Reduction in Cardiac Cell Toxicity Compared to Currently Marketed Anthracyclines
Date:12/8/2009

eristic of the drug to iron complex formation, confirming the expected 1:3 Fe(II)-drug ratio for both doxorubicin and mitoxantrone. In contrast, no spectrophotometric changes were observed with iron added to pixantrone, clearly demonstrating that pixantrone does not bind iron. In vitro studies using H2C9 rat myocardial cells indicate that pixantrone (ID50 >50 ug/ml) is far less toxic than doxorubicin (ID50= 1 ug/ml). Moreover, pixantrone does not induce significant reactive oxygen species (ROS) production in the H2C9 cells compared to doxorubicin.

About Pixantrone

Pixantrone (BBR 2778), is a novel topoisomerase II inhibitor with an aza-anthracenedione molecular structure that differentiates it from the anthracyclines and other related chemotherapy agents. Anthracyclines are the cornerstone therapeutic for the treatment of lymphoma, leukemia, and breast cancer. Although they are sufficiently effective to be used as first-line (initial) treatment, they cause cumulative heart damage that may result in congestive heart failure many years later. As a result, there is a lifetime limit of anthracycline doses and most patients who previously have been treated with an anthracycline are not able to receive further anthracycline treatment if their disease returns. It also can be administered through a peripheral vein rather than a central implanted catheter as required for other drugs in this class. Pixantrone has been granted fast track status designation.

About Cell Therapeutics, Inc.

Headquartered in Seattle, CTI is a biopharmaceutical company committed to developing an integrated portfolio of oncology products aimed at making cancer more treatable. For additional information, please visit www.CellTherapeutics.com.

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SOURCE Cell Therapeutics, Inc.
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