Preclinical evaluation of potential nilotinib cardiotoxicity

Leukemia Research

Volumn 35, Issue 5, 2011, Pages 631-637

  Wolf, Armin ^a   Couttet, Philippe ^a   Dong, Min ^a   Grenet, Olivier ^a   Heron, Marcia ^a   Junker, Ursula ^a   Ledieu, David ^a   Mahl, Andreas ^a   Marrer, Estelle ^a   Persohn, Elke ^a   Pognan, Francois ^a   Zhou, Wei ^a   Tsao, Jeffrey ^b   Roman, Danielle ^a  

^a NOVARTIS PHARMA AG   (Switzerland)

^b NOVARTIS INSTITUTES FOR BIOMEDICAL RESEARCH   (United States)

Author keywords

ABL1; Cardiotoxicity; Chronic myeloid leukemia; Left ventricular function; Nilotinib; Tyrosine kinase inhibitor

Indexed keywords

NILOTINIB;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CARDIOTOXICITY; CELL VIABILITY; CONCENTRATION RESPONSE; CONTROLLED STUDY; CYTOTOXICITY; DRUG DOSE COMPARISON; ENDOPLASMIC RETICULUM STRESS; ENZYME ACTIVITY; GENE EXPRESSION PROFILING; HEART FUNCTION; HEART WEIGHT; HISTOPATHOLOGY; MALE; NONHUMAN; NUCLEAR MAGNETIC RESONANCE IMAGING; PRIORITY JOURNAL; RAT; TOXICOKINETICS;

ANIMALS; ANIMALS, NEWBORN; CARDIOTOXINS; CELLS, CULTURED; DOSE-RESPONSE RELATIONSHIP, DRUG; DRUG EVALUATION, PRECLINICAL; HEART; HEART VENTRICLES; MALE; MYOCYTES, CARDIAC; PYRIMIDINES; RANDOM ALLOCATION; RATS; RATS, SPRAGUE-DAWLEY; RATS, WISTAR; VENTRICULAR FUNCTION;

EID: 79954621834     PISSN: 01452126     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.leukres.2010.11.001     Document Type: Article

References (23)

1. Weisberg E., Manley P.W., Breitenstein W., et al. Characterization of AMN107, a selective inhibitor of native and mutant bcr-abl. Cancer Cell 2005, 7:129-141.
2. Weisberg E., Manley P., Mestan J., et al. AMN107 (nilotinib): a novel and selective inhibitor of BCR-ABL. Br J Cancer 2006, 94:1765-1769.
3. Golemovic M., Verstovsek S., Giles F., et al. AMN107, a novel aminopyrimidine inhibitor of bcr-abl, has in vitro activity against imatinib-resistant chronic myeloid leukemia. Clin Cancer Res 2005, 11:4941-4947.
4. TASIGNA® (nilotinib) capsules prescribing information 2007-2009, Novartis Pharmaceuticals Corporation, East Hanover, NJ.
5. Force T., Krause D.S., Van Etten R.A. Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition. Nat Rev Cancer 2007, 7:332-344.
6. Wolf A., Couttet P., Dong M., et al. Imatinib does not induce cardiotoxicity at clinically relevant concentrations in preclinical studies. Leuk Res 2010.
7. Kerkela R., Grazette L., Yacobi R., et al. Cardiotoxicity of the cancer therapeutic agent imatinib mesylate. Nat Med 2006, 12:908-916.
8. Toraason M., Luken M.E., Breitenstein M., Krueger J.A., Biagini R.E. Comparative toxicity of allylamine and acrolein in cultured myocytes and fibroblasts from neonatal rat heart. Toxicology 1989, 56:107-117.
9. Atallah E., Durand J.B., Kantarjian H., Cortes J. Congestive heart failure is a rare event in patients receiving imatinib therapy. Blood 2007, 110:1233-1237.
10. Sprycel (dasatinib) [package insert] 2009, Bristol-Myers Squibb Company, Princeton, NJ.
11. Freebern W.J., Fang H.S., Slade M.D., et al. In vitro cardiotoxicity potential comparative assessments of chronic myelogenous leukemia tyrosine kinase inhibitor therapies: dasatinib, imatinib and nilotinib. Blood 2007, 110:217b-218b. [ASH abstract 4582].
12. Tanaka C., Yin O.Q., Sethuraman V., et al. Clinical pharmacokinetics of the BCR-ABL tyrosine kinase inhibitor nilotinib. Clin Pharmacol Ther 2010, 87:197-203.
13. Bartlett J.D., Luethy J.D., Carlson S.G., Sollott S.J., Holbrook N.J. Calcium ionophore A23187 induces expression of the growth arrest and DNA damage inducible CCAAT/enhancer-binding protein (C/EBP)-related gene, gadd153. Ca2+ increases transcriptional activity and mRNA stability. J Biol Chem 1992, 267:20465-20470.
14. Chen Q., Yu K., Holbrook N.J., Stevens J.L. Activation of the growth arrest and DNA damage-inducible gene gadd 153 by nephrotoxic cysteine conjugates and dithiothreitol. J Biol Chem 1992, 267:8207-8212.
15. Price B.D., Calderwood S.K. Gadd45 and Gadd153 messenger RNA levels are increased during hypoxia and after exposure of cells to agents which elevate the levels of the glucose-regulated proteins. Cancer Res 1992, 52:3814-3817.
16. Wang X.Z., Lawson B., Brewer J.W., et al. Signals from the stressed endoplasmic reticulum induce C/EBP-homologous protein (CHOP/GADD153). Mol Cell Biol 1996, 16:4273-4280.
17. Greaves P. Cardiovascular system, heart and pericardium. Histopathology of preclinical toxicity studies 2007, 277-278. Elsevier, San Diego, CA. 3rd ed. P. Greaves (Ed.).
18. Ruben Z., Arceo R.J., Bishop S.P., et al. Non-proliferative lesions of the heart and vasculature in rats. Toxicologic pathology. Guides for toxicologic pathology 2000, TTP/ARP/AFIP, Washington.
19. Dixon D., Heider K., Elwell M.R. Incidence of nonneoplastic lesions in historical control male and female Fisher-344 rats from 90-day toxicity studies. Toxicol. Pathol. 1995, 23:338-348.
20. Li F., Wang X., Capasso J.M., Gerdes A.M. Rapid transition of cardiac myocytes from hyperplasia to hypertrophy during postnatal development. J Mol Cell Cardiol 1996, 28:1737-1746.
21. Lorell B.H., Carabello B.A. Left ventricular hypertrophy: pathogenesis, detection, and prognosis. Circulation 2000, 102:470-479.
22. Gerdes A.M., Kellerman S.E., Moore J.A., et al. Structural remodeling of cardiac myocytes in patients with ischemic cardiomyopathy. Circulation 1992, 86:426-430.
23. Hew K.W., Keller K.A. Postnatal anatomical and functional development of the heart: a species comparison. Birth Defects Res B: Dev Reprod Toxicol 2003, 68:309-320.