NEW ORLEANS, Dec. 8 /PRNewswire-FirstCall/ -- Cell Therapeutics, Inc. ("CTI") (Nasdaq and MTA: CTIC) announced today an abstract to be published online at the journal Blood website by M. Hacker, et al. demonstrating significant reduction in cardiac cell toxicity with pixantrone compared to currently marketed anthracyclines. The authors conclude that the reduction is due to pixantrone's inability to generate toxic drug iron complexes and reduced propensity to generate oxygen free radicals. Pixantrone was specifically designed to have a higher affinity and avidity for the topisomerase II enzyme, which is the common target for this class of anti-cancer agents, while reducing oxygen-free radicals and preventing the formation of toxic drug metal complexes, which are the primary culprit that leads to dose-related irreversible heart damage associated with standard anthracyclines.
"This study adds to the growing scientific evidence which is central to the mechanistic basis for the relatively low incidence of cardiac events observed in our pixantrone clinical trials compared to the expected incidence of events had other anthracyclines been used. The ability to reintroduce an effective anthracycline like agent to patients who are no longer eligible to receive further standard anthracycline therapy due to potential irreversible heart damage addresses a major and growing unmet medical need," Jack Singer, M.D., Chief Medical Officer of Cell Therapeutics, Inc.
About the Study
To validate the proposed mechanisms underlying the observed differences in cardiotoxicity, researchers used established spectrophotometric techniques to quantify iron and drug interactions that are thought to be mechanistic for chronic doxorubicin cardiotoxicity. When adding increasing amounts of iron to drug solutions, they observed that doxorubicin and mitoxantrone underwent changes in visible range absorbance patterns, which is characteristic 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.
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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This press release includes forward-looking statements that involve a number of risks and uncertainties, the outcome of which could materially and/or adversely affect actual future results and the trading price of the securities of CTI. Specifically, the risks and uncertainties that could affect the development of pixantrone include risks associated with preclinical and clinical developments in the biopharmaceutical industry in general, and with pixantrone in particular, including, without limitation, the potential failure of pixantrone to prove safe and effective for the treatment of relapsed or refractory, aggressive non-Hodgkin's lymphoma as determined by the U.S. Food and Drug Administration, the potential failure of pixantrone to significantly reduce cardiac cell toxicity compared to currently marketed anthracyclines, the potential failure of pixantrone to reintroduce an effective anthracycline like agent in patients, CTI's ability to continue to raise capital as needed to fund its operations, competitive factors, technological developments, costs of developing, producing and selling pixantrone, and the risk factors listed or described from time to time in CTI's filings with the Securities and Exchange Commission including, without limitation, CTI's most recent filings on Forms 10-K, 10-Q and 8-K. Except as may be required by law, CTI does not intend to update or alter its forward-looking statements whether as a result of new information, future events, or otherwise.
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SOURCE Cell Therapeutics, Inc.
|SOURCE Cell Therapeutics, Inc.|
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