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. SOURCE Cell Therapeutics, Inc.