Hydroxymethylglutaryl coenzyme reductase

C. R. Sirtori, Tissue Selectivity of Hydroxymethylglutaryl Coenzyme A (HMG CoA) Reductase Inhibitors , Pharmacol. Ther. 1993, 60, 431-459. 

Chen, G.Z., Foster, L. and Bennett, J.L. (1991) Purification and characterization of 3-hydroxymethylglutaryl-coenzyme A reductase of Schistosoma mansoni regulation of parasite enzyme activity differs from mammalian host. Experimental Parasitology 73, 82-92. 

Garnett WR. Interactions with hydroxymethylglutaryl-coenzyme a reductase inhibitors. Am J Health Syst Pharm 1995 52(15) 1639 15. 

Landesman KA, Stozek M, Freeman NJ. Rhabdomyolysis associated with the combined use of hydroxymethylglutaryl-coenzyme A reductase inhibitors with gemfibrozil and macrolide antibiotics. Conn Med 1999 63(8) 455-7. 

Jamal SM, EisenbergMJ, Christopoulos S. Rhab-domyolysis associated with hydroxymethylglutaryl-coenzyme A reductase inhibitors. Am Heart J. 2004 147 956-965. 

P.-T. Ho and S. Chung, Synthesis of 2,4-dideoxy-D-eryi/tro-hexopyranose. An intermediate for synthesis of the lactone moiety of inhibitors of hydroxymethylglutaryl-coenzyme A reductase, Carbohydr. Res., 125 (1984) 318-322. 

Hakamada-Taguchi R, UeharaY Kuribayashi K, etal. Inhibition of hydroxymethylglutaryl-coenzyme a reductase reduces Th I development and promotes Th2 development, Circ Res 2003 93 948-956. 

Alberts, A.W., Chen, J., Kuron, G., Hunt, V., Huff, J., Hoffman, C., Rothrock, J., Lopez, M., Joshua, H., Harris, E., Patchett, A., Monaghan, R., et al. (1980). Mevinolin a highly potent competitive inhibitor of hydroxymethylglutaryl-coenzyme A reductase and a cholesterol-lowering agent. Proc Natl Acad Sci USA 77 3957-3961. 

Fig. 6), led to the discovery of the mevalonate pathway leading to IPP 7 and DMAPP 8 (Fig. 1). In this pathway, isoprene units are derived, like fatty acids, from acetyl-coenzyme A 1. The key intermediate is mevalonate 4, which results from the reduction of hydroxymethylglutaryl-coenzyme A 3 catalyzed by the HMG-CoA reductase, and represents the committed step of the pathway. Confirmation of this pathway was obtained for the biosynthesis of plant sterols, triterpenes, and sesquiterpenes. 

Einarson TR, Metge CJ, Iskedjian M, Mukherjee J. An examination of the effect of cytochrome P450 drug interactions of hydroxymethylglutaryl-coenzyme A reductase... 

The interruption of enterohepatic recirculation of bile acids by the resins effectively lowers plasma cholesterol levels since cholesterol must now be diverted to de novo synthesis of bile acids. In addition, intestinal absorption of dietary cholesterol, normally facilitated by bile acids, is also reduced due to their excretion. Two significant compensatory mechanisms are called into action increased activity of hydroxymethylglutaryl coenzyme A reductase (HMG CoA reductase), which is the rate-controlling enzyme in the hepatic synthesis of cholesterol (see Fig. 11-4 and discussion to follow), and an increase in the number of LDL receptors. The latter mechanism offered the first meaningful treatment of heterozygous FH. Homozygous FH patients lacking LDL receptors, of course, do not respond. 

M. J. Kaufman, Applications of oxygen polarography to drug stability testing and formulation development Solution-phase oxidation of hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, Pharm. Res. 7, 289-292(1990). 

Reductase, hydroxymethylglutaryl coenzyme A (reduced nicotinamide adenine dinucleotide phosphate) XXII-2... 

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