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pubmed-article:20122731pubmed:abstractTextCytotoxic concentrations of imatinib mesylate (10-50 microM) were required to trigger markers of apoptosis and endoplasmic reticulum stress response in neonatal rat ventricular myocytes and fibroblasts, with no significant differences observed between c-Abl silenced and nonsilenced cells. In mice, oral or intraperitoneal imatinib treatment did not induce cardiovascular pathology or heart failure. In rats, high doses of oral imatinib did result in some cardiac hypertrophy. Multi-organ toxicities may have increased the cardiac workload and contributed to the cardiac hypertrophy observed in rats only. These data suggest that imatinib is not cardiotoxic at clinically relevant concentrations (5 microM).lld:pubmed
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pubmed-article:20122731pubmed:copyrightInfoCopyright 2010 Elsevier Ltd. All rights reserved.lld:pubmed
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pubmed-article:20122731pubmed:articleTitleImatinib does not induce cardiotoxicity at clinically relevant concentrations in preclinical studies.lld:pubmed
pubmed-article:20122731pubmed:affiliationPreclinical Safety, Novartis Institutes for Biomedical Research, CH-4009 Basel, Switzerland.lld:pubmed
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