Sustained release of a p38 inhibitor from non-inflammatory microspheres inhibits cardiac dysfunction. Sy, J. C., Seshadri, G., Yang, S. C., Brown, M., Oh, T., Dikalov, S., Murthy, N., & Davis, M. E. Nat Mater, 7(11):863–8, 2008.
doi  abstract   bibtex   
Cardiac dysfunction following acute myocardial infarction is a major cause of death in the world and there is a compelling need for new therapeutic strategies. In this report we demonstrate that a direct cardiac injection of drug-loaded microparticles, formulated from the polymer poly(cyclohexane-1,4-diylacetone dimethylene ketal) (PCADK), improves cardiac function following myocardial infarction. Drug-delivery vehicles have great potential to improve the treatment of cardiac dysfunction by sustaining high concentrations of therapeutics within the damaged myocardium. PCADK is unique among currently used polymers in drug delivery in that its hydrolysis generates neutral degradation products. We show here that PCADK causes minimal tissue inflammatory response, thus enabling PCADK for the treatment of inflammatory diseases, such as cardiac dysfunction. PCADK holds great promise for treating myocardial infarction and other inflammatory diseases given its neutral, biocompatible degradation products and its ability to deliver a wide range of therapeutics.
@article{sy_sustained_2008,
	title = {Sustained release of a p38 inhibitor from non-inflammatory microspheres inhibits cardiac dysfunction},
	volume = {7},
	issn = {1476-1122 (Print) 1476-1122},
	doi = {10.1038/nmat2299},
	abstract = {Cardiac dysfunction following acute myocardial infarction is a major cause of death in the world and there is a compelling need for new therapeutic strategies. In this report we demonstrate that a direct cardiac injection of drug-loaded microparticles, formulated from the polymer poly(cyclohexane-1,4-diylacetone dimethylene ketal) (PCADK), improves cardiac function following myocardial infarction. Drug-delivery vehicles have great potential to improve the treatment of cardiac dysfunction by sustaining high concentrations of therapeutics within the damaged myocardium. PCADK is unique among currently used polymers in drug delivery in that its hydrolysis generates neutral degradation products. We show here that PCADK causes minimal tissue inflammatory response, thus enabling PCADK for the treatment of inflammatory diseases, such as cardiac dysfunction. PCADK holds great promise for treating myocardial infarction and other inflammatory diseases given its neutral, biocompatible degradation products and its ability to deliver a wide range of therapeutics.},
	number = {11},
	journal = {Nat Mater},
	author = {Sy, J. C. and Seshadri, G. and Yang, S. C. and Brown, M. and Oh, T. and Dikalov, S. and Murthy, N. and Davis, M. E.},
	year = {2008},
	keywords = {Animals Cell Line Delayed-Action Preparations Imidazoles/*administration \& dosage Macrophage Activation/drug effects Male Mice Mice, Inbred C57BL Microspheres Myocardial Infarction/*drug therapy/physiopathology Phosphorylation Polymers Protein Kinase Inhibitors/*administration \& dosage Pyrimidines/*administration \& dosage Rats Rats, Sprague-Dawley Superoxides/metabolism Tumor Necrosis Factor-alpha/biosynthesis p38 Mitogen-Activated Protein Kinases/*antagonists \& inhibitors},
	pages = {863--8},
}

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