Abstract: The present invention provides for methods of treating and preventing cardiac hypertrophy. Class II HDACs, which are known to participate in regulation of chromatin structure and gene expression, have been shown to have beneficial effects on cardiac hypertrophy. Surprisingly, the present invention demonstrates that HDAC inhibitors inhibit cardiac hypertrophy by inhibiting fetal cardiac gene expression and interfering with sarcomeric organization.

Abstract: The present invention provides the (R)-(+) enoximone sulfoxide enantiomer, as well as pharmaceutical formulations of the purified (R)-(+) sulfoxide enantiomer. Also provided are methods of treating diseases in which inhibition of PDE-III may be beneficial.

Abstract: The present invention provides the (S)-(?) enoximone sulfoxide enantiomer, as well as pharmaceutical formulations of the purified (S)-(?) sulfoxide enantiomer. Also provided are methods of treating diseases in which inhibition of PDE-III may be beneficial.

Abstract: The present invention provides for methods of treating and preventing cardiac hypertrophy. Class II HDACs, which are known to participate in regulation of chromatin structure and gene expression, have been shown to have beneficial effects on cardiac hypertrophy. Surprisingly, the present invention demonstrates that HDAC inhibitors inhibit cardiac hypertrophy by inhibiting fetal cardiac gene expression and interfering with sarcomeric organization.

Abstract: The present invention provides formulations of the drug enoximone that include 40% to 80% non-ionic surfactant. Also provided a methods of treating heart failure and cardiac hypetrophy with these formulations.

Abstract: The invention provides methods of diagnosing myocardial failure in a human. The methods comprise obtaining a sample of myocardial tissue from a ventricle of the heart of the human. In one method, the expression of ?-myosin heavy chain (?-MHC), ?-myosin heavy chain (?-MHC), or both in the sample is quantitated, and it is determined by statistical analysis if the expression of ?-MHC, ?-MHC, or both in the sample is significantly different than their expression in normal human ventricular myocardial tissue. A second method comprises quantitating the expression of ?1-thyroid hormone receptor (?1-THR), ?2-THR, ?1-THR+?1-THR, or combinations thereof in the sample, and determining by statistical analysis if the expression of ?1-THR, ?2-THR, or ?1-THR+?1-THR in the sample is significantly different than their expression in normal human ventricular myocardial tissue. The invention also provides kits for diagnosing myocardial failure by these methods.

Abstract: The present invention provides for methods of treating and preventing cardiac hypertrophy. Class II HDACs, which are known to participate in regulation of chromatin structure and gene expression, have been shown to have beneficial effects on cardiac hypertrophy. Surprisingly, the present invention demonstrates that HDAC inhibitors inhibit cardiac hypertrophy by inhibiting fetal cardiac gene expression and interfering with sarcomeric organization.

Abstract: The present invention provides for methods of treating and preventing cardiac hypertrophy. Class II HDACs, which are known to participate in regulation of chromatin structure and gene expression, have been shown to have beneficial effects on cardiac hypertrophy. Surprisingly, the present invention demonstrates that HDAC inhibitors inhibit cardiac hypertrophy by inhibiting fetal cardiac gene expression and interfering with sarcomeric organization.

Abstract: The present invention provides for methods of treating and preventing cardiac hypertrophy. Class II HDACs, which are known to participate in regulation of chromatin structure and gene expression, have been shown to have beneficial effects on cardiac hypertrophy. Surprisingly, the present invention demonstrates that HDAC inhibitors inhibit cardiac hypertrophy by inhibiting fetal cardiac gene expression and interfering with sarcomeric organization.

Abstract: The present invention provides for methods of treating and preventing cardiac hypertrophy. Class II HDACs, which are known to participate in regulation of chromatin structure and gene expression, have been shown to have beneficial effects on cardiac hypertrophy. Surprisingly, the present invention demonstrates that HDAC inhibitors inhibit cardiac hypertrophy by inhibiting fetal cardiac gene expression and interfering with sarcomeric organization.