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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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alpha-Substituted malonester amides: tools to define the relationship between ACAT inhibition and adrenal toxicity.

We prepared a series of alpha-substituted malonester amides that were evaluated for their ability to inhibit acyl-CoA:cholesterol O-acyl transferase activity in vitro and to lower plasma total cholesterol levels in a variety of cholesterol-fed animal models. Compounds of this series were also useful in examining the relationship between adrenal toxicity and ACAT inhibition. One compound from this series, 9f, was a potent inhibitor of ACAT in both the microsomal and cellular assays. It was also bioavailable as determined by both a bioassay and a HPLC-UV assay. This compound was evaluated in both guinea pig and dog models of adrenal toxicity and compared to tetrazole amide 15. In the most sensitive species, the dog, both of these compounds achieved good plasma levels; however, compound 9f caused adrenal necrosis, whereas compound 15 had no effect on the adrenal gland. This adds to the growing body of evidence that the adrenal toxicity observed with ACAT inhibitors may not be mechanism related.[1]

References

  1. alpha-Substituted malonester amides: tools to define the relationship between ACAT inhibition and adrenal toxicity. Sliskovic, D.R., Picard, J.A., O'Brien, P.M., Liao, P., Roark, W.H., Roth, B.D., Anderson, M.A., Mueller, S.B., Bocan, T.M., Bousley, R.F., Hamelehle, K.L., Homan, R., Reindel, J.F., Stanfield, R.L., Turluck, D., Krause, B.R. J. Med. Chem. (1998) [Pubmed]
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