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Rosuvastatin: a new inhibitor of HMG-coA reductase for the treatment of dyslipidemia.
Expert Rev Cardiovasc Ther. 2003 Nov; 1(4):495-505.ER

Abstract

Rosuvastatin (Crestor, AstraZeneca) is a synthetic statin that represents an advance on the pharmacologic and clinical properties of other agents in this class. Relative to other statins, rosuvastatin possesses a greater number of binding interactions with HMG-CoA reductase and has a high affinity for the active site of the enzyme. Rosuvastatin is relatively hydrophilic and is selectively taken up by, and active in, hepatic cells. Rosuvastatin has the longest terminal half-life of the statins and is only minimally metabolized by the cytochrome P450 (CYP 450) enzyme system with no significant involvement of the 3A4 enzyme. Consistent with this finding is the absence of clinically significant drug interactions between rosuvastatin and other drugs known to inhibit CYP 450 enzymes. In patients with hypercholesterolemia, rosuvastatin 10-40 mg has been shown to reduce low-density lipoprotein cholesterol (LDL-C) levels by 52-63%, as well as increase high-density lipoprotein cholesterol (HDL-C) levels by up to 14% and reduce triglycerides (TG) by up to 28%. Studies have shown that rosuvastatin is superior to atorvastatin, simvastatin and pravastatin in reducing LDL-C and favorably modifying other components of the atherogenic lipid profile. The significant decreases in LDL-C with rosuvastatin treatment should help to improve attainment of lipid goals and reduce the requirement for dose titration. In addition, the effects of rosuvastatin on HDL-C and TG levels will be of benefit in treating patients with abnormalities such as mixed dyslipidemia and the metabolic syndrome. Rosuvastatin is well tolerated, with a safety profile comparable with that of other currently available statins.

Authors+Show Affiliations

Preventive Cardiology Center, Northwestern University, The Feinberg School of Medicine, Chicago, IL 60611, USA. r-rosenson@northwestern.edu

Pub Type(s)

Comparative Study
Journal Article
Review

Language

eng

PubMed ID

15030249

Citation

Rosenson, Robert S.. "Rosuvastatin: a New Inhibitor of HMG-coA Reductase for the Treatment of Dyslipidemia." Expert Review of Cardiovascular Therapy, vol. 1, no. 4, 2003, pp. 495-505.
Rosenson RS. Rosuvastatin: a new inhibitor of HMG-coA reductase for the treatment of dyslipidemia. Expert Rev Cardiovasc Ther. 2003;1(4):495-505.
Rosenson, R. S. (2003). Rosuvastatin: a new inhibitor of HMG-coA reductase for the treatment of dyslipidemia. Expert Review of Cardiovascular Therapy, 1(4), 495-505.
Rosenson RS. Rosuvastatin: a New Inhibitor of HMG-coA Reductase for the Treatment of Dyslipidemia. Expert Rev Cardiovasc Ther. 2003;1(4):495-505. PubMed PMID: 15030249.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Rosuvastatin: a new inhibitor of HMG-coA reductase for the treatment of dyslipidemia. A1 - Rosenson,Robert S, PY - 2004/3/20/pubmed PY - 2004/5/12/medline PY - 2004/3/20/entrez SP - 495 EP - 505 JF - Expert review of cardiovascular therapy JO - Expert Rev Cardiovasc Ther VL - 1 IS - 4 N2 - Rosuvastatin (Crestor, AstraZeneca) is a synthetic statin that represents an advance on the pharmacologic and clinical properties of other agents in this class. Relative to other statins, rosuvastatin possesses a greater number of binding interactions with HMG-CoA reductase and has a high affinity for the active site of the enzyme. Rosuvastatin is relatively hydrophilic and is selectively taken up by, and active in, hepatic cells. Rosuvastatin has the longest terminal half-life of the statins and is only minimally metabolized by the cytochrome P450 (CYP 450) enzyme system with no significant involvement of the 3A4 enzyme. Consistent with this finding is the absence of clinically significant drug interactions between rosuvastatin and other drugs known to inhibit CYP 450 enzymes. In patients with hypercholesterolemia, rosuvastatin 10-40 mg has been shown to reduce low-density lipoprotein cholesterol (LDL-C) levels by 52-63%, as well as increase high-density lipoprotein cholesterol (HDL-C) levels by up to 14% and reduce triglycerides (TG) by up to 28%. Studies have shown that rosuvastatin is superior to atorvastatin, simvastatin and pravastatin in reducing LDL-C and favorably modifying other components of the atherogenic lipid profile. The significant decreases in LDL-C with rosuvastatin treatment should help to improve attainment of lipid goals and reduce the requirement for dose titration. In addition, the effects of rosuvastatin on HDL-C and TG levels will be of benefit in treating patients with abnormalities such as mixed dyslipidemia and the metabolic syndrome. Rosuvastatin is well tolerated, with a safety profile comparable with that of other currently available statins. SN - 1477-9072 UR - https://www.unboundmedicine.com/medline/citation/15030249/Rosuvastatin:_a_new_inhibitor_of_HMG_coA_reductase_for_the_treatment_of_dyslipidemia_ L2 - https://www.tandfonline.com/doi/full/10.1586/14779072.1.4.495 DB - PRIME DP - Unbound Medicine ER -