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HDAC inhibitors and NO donors have both demonstrated independently broad therapeutic potential in a variety of diseases. Borretto et al. presented the topic of NO-HDAC dual inhibitors for the first time in 2013 as an attractive new topic. Here we collected the general structure of all synthesized NO-HDAC dual inhibitors, lead compounds, synthesis methods and biological features of the most potent dual NO-HDAC inhibitor in each category with the intention of assisting in the synthesis and optimization of new drug-like compounds for diverse diseases. Based on studies done so far, NO-HDAC dual inhibitors have displayed satisfactory results against wound healing (3), heart hypertrophy (3), inflammatory, cardiovascular, neuromuscular illnesses (11a-11e) and cancer (6a-6o, 9a-9d, 10a-10d, 16 and 17). NO-HDAC dual inhibitors can have high therapeutic potential for various diseases due to their new properties, NO properties, HDAC inhibitor properties and also due to the effects of NO on HDAC enzymes.

Experimental cardiomyopathy in terms of heart hypertrophy and noninflammatory myocardial lesions was induced in rabbit by i.v. administration of anthracycline antibiotic daunorubicin during 2 to 12 weeks. The animals showed a high rate of unexpected mortality in comparison with controls. This mortality was evaluated from the point of view of the unexpected death as a forensic pathologic term.

1. 1. Four fatal cases of unexplained hypertrophy and dilatation of the heart during the third decade of life are presented. None of the usual causes of hypertrophy were present. 2. 2. The onset of illness differed in individual cases and was not at first recognized as heart disease. 3. 3. Electrocardiograms at first were normal. When changes occurred, the abnormalities suggested only nonspecific myocardial damage. 4. 4. The possible etiologic factors are discussed, but it is not concluded which, if any, were responsible for the cardiac hypertrophy. 5. 5. There is no certainty that the causes of heart disease in the four cases were related.