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HMG-CoA Reductase Inhibitor

Aka: HMG-CoA Reductase Inhibitor, 3-Hydroxy-3-Methyl-Glutaryl Coenzyme A Reductase, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Statin, Lovastatin, Simvastatin, Pravastatin, Atorvastatin, Fluvastatin, Rosuvastatin, Zocor, Lipitor, Crestor
  1. See Also
    1. Hyperlipidemia
    2. Statin-Induced Myopathy
  2. Indications
    1. See Hyperlipidemia Management for formal criteria
    2. Coronary Artery Disease
    3. Diabetes Mellitus
      1. Age over 40 years old, comorbidities or long diabetes duration (20 years for DM 1, 10 years for DM 2)
    4. Chronic Kidney Disease
    5. Cerebrovascular Accident
    6. Peripheral Vascular Disease
    7. Hyperlipidemia
      1. Most Statins are approved down to age 10 years (age 8 years for Pravastatin)
      2. If used in children and teens, LDL Cholesterol above 190 is an indication for Statins (esp. with premature CAD FHx)
  3. Mechanism: Effects
    1. Lipid-related effects
      1. LDL decreased (20-40%)
      2. HDL Increased (5-15%)
      3. Triglycerides decreased
        1. Atorvastatin (40%)
        2. Simvastatin (30%)
        3. Other Statins (10-20%)
    2. Statin Benefit increases with 10 year ASCVD Risk
      1. ASCVD Risk 7.5%: NNT 40 to prevent one ASCVD event with moderate-dose Statin (NNT 26 if high-dose Statin)
      2. ASCVD Risk 10%: NNT 33 to prevent one ASCVD event with moderate-dose Statin (NNT 20 if high-dose Statin)
      3. ASCVD Risk 15%: NNT 20 to prevent one ASCVD event with moderate-dose Statin (NNT 13 if high-dose Statin)
      4. ASCVD Risk 20%: NNT 15 to prevent one ASCVD event with moderate-dose Statin (NNT 10 if high-dose Statin)
      5. ASCVD Risk 25%: NNT 12 to prevent one ASCVD event with moderate-dose Statin (NNT 8 if high-dose Statin)
      6. Grundy (2016) Pharmaceutical Journal
        1. http://www.pharmaceutical-journal.com/research/review-article/primary-prevention-of-cardiovascular-disease-with-statins-assessing-the-evidence-base-behind-clinical-guidance/20200568.article
    3. Other effects (related to decreased coronary events)
      1. Antiproliferation effect on Smooth Muscle Cells
      2. Antioxidant and anti-inflammatory effects
    4. Outcomes: Primary Prevention
      1. NNT taken four years to prevent one coronary event: 81
      2. NNT taken four years to prevent one cerebrovascular event: 81
    5. Outcomes: Secondaary Prevention
      1. NNT taken five years to prevent one death: 50
      2. NNT taken two years to prevent one fatal MI: 77
  4. Contraindications
    1. Drug Interactions (see below): Myopathy or hepatitis
    2. Pregnancy (Teratogen)
      1. Spontaneous Abortion and Stillbirth risk
      2. Birth defects in animal studies, but observational studies do not show increased risk
      3. In 2021, FDA allows for Statin use in high risk cardiovascular risks in pregnancy
        1. https://www.fda.gov/safety/medical-product-safety-information/statins-drug-safety-communication-fda-requests-removal-strongest-warning-against-using-cholesterol
        2. May consider use in prior MI, CVA or Homozygous familial Hypercholesterolemia
      4. Ensure reliable Contraception
      5. Stop Statin at least 1-2 months before planned pregnancy
      6. Do NOT use in Lactation (small amounts pass into Breast Milk)
    3. Acute Liver Failure or decompensated Cirrhosis
      1. As of 2012 Statins are considered safe in other chronic stable liver disease
        1. Chalasani (2004) Gastroenterology 126(5): 1287-92 [PubMed]
        2. Vuppalanchi (2005) Am J Med Sci 329(2):62-5 [PubMed]
      2. Beneficial in non-Alcoholic Steatohepatitis (NASH)
        1. Lowers cardiovascular risk
        2. Transaminases frequently improve on Statins
        3. Rallidis (2004) Atherosclerosis 174(1): 193-6 [PubMed]
  5. Efficacy
    1. Findings
      1. Reduces Myocardial Infarction risk (30%)
        1. Reduces need for Angioplasty (47 vs 20)
        2. Associated with regression on angiogram
        3. Prevents one cardiovascular event in 5 years for 20 with CV disease and 50 at high risk for CV disease
      2. Reduces coronary death rate (42%)
      3. Reduces Cerebrovascular Accident risk (30%)
      4. Conflicting evidence on reducing Dementia risk
        1. Recent prospective articles do not suggest benefit
        2. Rea (2005) Arch Neurol 62:1047-51 [PubMed]
      5. Reduces C-Reactive Protein
        1. Inflammatory factors related to ACS pathogenesis
        2. May explain benefit to normolipidemic patients
      6. In age over 75 years without significant CAD risk, starting Statin may increase mortality without a decrease in CV risk
        1. Han (2017) JAMA Intern Med +PMID:28531241 [PubMed]
    2. References
      1. (1994) Lancet 344(8934):1383-9 [PubMed]
      2. (1997) FDC Reports 59(46):T&G6
      3. (2004) Lancet 363:757-67 [PubMed]
      4. Jick (2000) Lancet 356:1627-31 [PubMed]
      5. Jukema (1995) Circulation 91:2528-40 [PubMed]
      6. Ridker (2001) N Engl J Med 344:1959-65 [PubMed]
      7. Sacks (1996) N Engl J Med 335:1001-9 [PubMed]
  6. Precautions
    1. Do not stop Statins abruptly (worse CAD outcomes)
    2. Elderly (even over age 80) benefit from continued Statin use for CAD prevention
  7. Adverse Effects
    1. See Statin-Induced Myopathy
    2. Mild Gastrointestinal upset
    3. Rash
    4. Insomnia (seen more with lipophilic agents)
      1. May be reduced with Pravastatin or Fluvastatin
    5. Lupus-Like Syndrome
    6. Peripheral Neuropathy
    7. Concurrent use with Coumadin increases bleeding risk
    8. Cataract development
      1. Controversial - some early reports demonstrate Statin users might present 2-3 years earlier than their peers with Cataracts
      2. Fong (2012) Am J Ophthalmol 153(2):222-8 [PubMed]
    9. Cognitive Impairment
      1. Uncommon, and reversible on stopping Statin
      2. Subjective patient reports but not found in initial studies
      3. Statins may also protect cognitive function by affecting atherosclerosis
      4. Consider a water soluble Statin (e.g. Pravastatin) that does not cross blood-brain barrier
      5. Wagstaff (2003) Pharmacotherapy 23(7):871-80 [PubMed]
    10. Diabetes Mellitus
      1. Statins (especially at high dose) are associated with an increase in Hemoglobin A1C
        1. Affects 1-3 patients in 1000 who might be raised from Metabolic Syndrome to meeting criteria for Diabetes Mellitus
        2. Dormuth (2014) BMJ 348:g3244 [PubMed]
        3. Sattar (2010) Lancet 375(9716): 735-42 [PubMed]
    11. Liver Function Abnormalities (1-2% Incidence)
      1. AST and ALT may be increased 2-3x normal
        1. These effects are typically transient
        2. Serious liver injury is rare and idiosyncratic
        3. Liver failure occurs in 1 patient in one million on Statins
          1. Same Incidence in those not on a Statin
      2. FDA No longer recommends routine monitoring of Liver Function Tests as of 2012
        1. Obtain baseline Liver Function Test and then as clinically indicated
      3. Statins are safe in chronic stable liver disease
        1. Statins may actually improve Liver Function Tests (and lower CV risk) in NASH
  8. Adverse Effects: Compliance and Tolerance
    1. Discontinuation rate with Statins: 15%
    2. Discontinuation rate with other medications: 35%
  9. Pharmacokinetics
    1. First-pass metabolism in all Statins except Pravastatin
    2. Protein binding
      1. Most Statins are 90% Protein bound
      2. Pravastatin is 50% Protein bound
    3. Cytochrome P450 Metabolism
      1. CYP3A4 isoenzyme metabolizes most Statins (except Rosuvastatin and Pravastatin)
      2. CYP2C9 isoenzyme metabolizes Fluvastatin
      3. Pravastatin is not metabolized by P450 system
        1. Safer to use in combination with other drugs
    4. Renal elimination occurs most with Pravastatin
  10. Dosing
    1. Specific LDL and HDL targets have been replaced with high-intensity Statin if 10 year cardiovascular risk >20%
    2. High intensity Statin (age <75 years with 10 year cardiovascular risk >20%)
      1. Atorvastatin 40-80 mg orally daily
      2. Rosuvastatin 20-40 mg orally daily
    3. Low intensity Statin (age >75 years, or Statin intolerant)
      1. Atorvastatin 10-20 mg orally daily
      2. Rosuvastatin 25-10 mg orally daily
      3. Simvastatin 20-40 mg orally daily
      4. Pravastatin 40-80 mg orally daily
      5. Lovastatin 40 mg orally daily
  11. Preparations (from least to most potent)
    1. Fluvastatin (Lescol, generic)
      1. Dose 20 mg lowers LDL 17% (recommended starting dose)
      2. Dose 40 mg lowers LDL 23%
      3. Dose 80 mg lowers LDL 33%
    2. Pravastatin (Pravachol, generic)
      1. Dose 10 mg lowers LDL 19%
      2. Dose 20 mg lowers LDL 24% (recommended starting dose)
      3. Dose 40 mg lowers LDL 34%
      4. Dose 80 mg lowers LDL 40%
    3. Lovastatin (Mevacor, generic)
      1. Starting Dose: 20 mg qd
      2. Dose 20 mg lowers LDL 29% (recommended starting dose)
      3. Dose 40 mg lowers LDL 31%
      4. Dose 80 mg lowers LDL 48%
    4. Cerivastatin (Baycol, not available in US)
      1. Cerivastatin recalled in United States (August 2001)
      2. Dose 0.2 mg lowers LDL 25% (start if Renal Failure)
      3. Dose 0.3 mg lowers LDL 30% (recommended start dose)
      4. Dose 0.4 mg lowers LDL 36%
      5. Dose 0.8 mg lowers LDL 44%
    5. Simvastatin (Zocor, generic)
      1. Dose 10 mg lowers LDL 28%
      2. Dose 20 mg lowers LDL 35% (recommended starting dose)
      3. Dose 40 mg lowers LDL 40% (maximum dose recommended in U.S. as of 2011)
      4. Dose 80 mg lowers LDL 48% (dose no longer recommended due to complications)
    6. Atorvastatin (Lipitor, generic)
      1. Dose 10 mg lowers LDL 38% (recommended starting dose)
      2. Dose 20 mg lowers LDL 46%
      3. Dose 40 mg lowers LDL 51%
      4. Dose 80 mg lowers LDL 54%
      5. Triglycerides lowered 40%
    7. Rosuvastatin (Crestor, generic but still >$200/month as of summer 2016)
      1. Dose 5 mg lowers LDL 45%
      2. Dose 10 mg lowers LDL: 52%
      3. Dose 20 mg lowers LDL 55%
      4. Dose 40 mg lowers LDL: 63%
      5. Indications to start at lower dose (5 mg)
        1. Asians
          1. Higher drug levels leads to higher toxicity risk
        2. Renal Insufficiency (max 10 mg if CrCl < 30 ml/min)
        3. Hypothyroidism (uncontrolled)
        4. Age over 65 years
        5. Cyclosporine use (max dose 5 mg daily)
        6. Concurrent Gemfibrozil (max dose 10 mg daily)
  12. Management: Statin choices if special concerns
    1. Preferred agents if risk of Drug Interactions
      1. Pravastatin (no CYP 450 METABOLISM)
      2. Fluvastatin
    2. Preferred agents if Renal Function impaired
      1. Atorvastatin
      2. Fluvastatin
      3. Avoid Pravastatin if Creatinine Clearance <60 ml/min
        1. If used, start dosing at 10 mg and titrate slowly
  13. Monitoring: Liver transaminase testing (AST,ALT)
    1. Protocols below are no longer routinely indicated as of March 2012
      1. FDA recommends only obtaining baseline Liver Function Test and then as clinically indicated
      2. Statins are contraindicated in Acute Liver Failure or decompensated Cirrhosis
      3. Statins should be discontinued if symptoms of liver injury and elevated Serum Bilirubin
    2. No history of liver disease (old pre-2012 guidelines, listed for historical purposes only)
      1. Stop Statin if >3x over baseline
      2. Liver Transaminase testing (AST, ALT) schedule
        1. Baseline
        2. Obtain only as clinically indicated
        3. Previously was routinely scheduled at week 6, month 3 and then every 6-12 months
    3. Chronic Liver Disease history (old pre-2012 guidelines, listed for historical purposes only)
      1. Start with lower initial Statin dose
      2. Stop Statin if transaminase >2x over baseline
      3. Liver Transaminase testing (AST or ALT) schedule (adjust per clinical discretion, FDA does not mandate any schedule as of 2012)
        1. Baseline
        2. Two weeks
        3. One month
        4. Two months
        5. Three months
  14. Drug Interactions (See Contraindications above)
    1. CYP3A4 Inhibitors
      1. Azole Antifungals (Intraconazole, Ketoconazole - 10-20 fold increase in Statin serum levels)
        1. Increased risk of Statin Myopathy (esp. with age >65, Obesity, renal or liver Impairment)
        2. Avoid with Lovastatin or Simvastatin
        3. Avoid with Atorvastatin over 20 mg daily
        4. Fluconazole is less risky, especially with single dose, but Exercise caution with prolonged course
      2. Calcium Channel Blocker
        1. Diltiazem (limit to 240 mg daily)
          1. Avoid with Lovastatin over 20 mg daily
          2. Avoid with Simvastatin over 10 mg daily
          3. Remain alert for Statin Myopathy with Atorvastatin
        2. Verapamil (6-10 fold increase in Statin serum levels)
          1. Avoid with Lovastatin over 40 mg daily
          2. Avoid with Simvastatin over 10 mg daily
          3. Remain alert for Statin Myopathy with Atorvastatin
        3. Amlodipine (Norvasc)
          1. Avoid with Simvastatin over 20 mg daily
      3. Grapefruit juice increases some Statin levels
        1. Drugs most affected: Simvastatin,Lovastatin
          1. Avoid with any Grapefruit juice (or minimal use)
        2. Drugs affected moderately: Atorvastatin
          1. Limit Grapefruit juice to 8-16 ounces daily (effects more likely to manifest at 32 ounces)
          2. Limit juice timing to opposite Statin dose
            1. Take juice at night, if Statin taken in morning
        3. Drugs not affected: Pravachol, Crestor, Lescol
        4. References
          1. (2016) Presc Lett 23(3):18
          2. Reamy (2007) Am Fam Physician 76:190-1 [PubMed]
    2. CYP3A4/oragnic anion transporting polypeptide inhibitors
      1. Cyclosporine (10-20 fold increase in Statin serum levels)
        1. Avoid with Atorvastatin over 10 mg daily
        2. Avoid with Lovastatin over 20 mg daily
        3. Avoid with Rosuvastatin over 5 mg daily
        4. Avoid with pitavastatin, Pravastatin
        5. Avoid with Fluvastatin
      2. Macrolides (Erythromycin, Clarithromycin - 6-10 fold increase in Statin serum levels)
        1. Avoid while on Lovastatin and Simvastatin (or stop Statin while on Macrolide)
        2. Avoid with pitavastatin over 1 mg daily
        3. Avoid with Atorvastatin over 20 mg daily
        4. Azithromycin appears to be safe with Statins
      3. Protease inibitors (Atazanavir, Ritonavir, Lopinavir/Ritonavir)
        1. Avoid with Lovastatin, pitavastatin, and Simvastatin
        2. Avoid with Atorvastatin over 20 mg daily
        3. Avoid with Rosuvastatin over 10 mg daily
    3. CYP3A4/CYP2C9 Inhibitor
      1. Amiodarone
        1. Increased risk of Statin Myopathy (esp. with age >65, Obesity, renal or liver Impairment)
        2. Avoid with Lovastatin over 40 mg daily
        3. Avoid with Simvastatin over 20 mg daily
        4. Caution with Fluvastatin and Atorvastatin (consider dose adjustment)
      2. Warfarin (Increased INR and bleeding risk)
        1. Highest risk: Fluvastatin, Lovastatin, Rosuvastatin, Simvastatin
        2. Lowest risk: Atorvastatin, Pravastatin
    4. CYP2C9, CYP2C19/oragnic anion transporting polypeptide inhibitors
      1. Gemfibrozil (2-3 fold increase in Statin serum levels, >13 fold increase in Rhabdomyolysis risk)
        1. Avoid with Simvastatin over 10 mg daily
        2. Avoid with Rosuvastatin over 10 mg daily
        3. Avoid with Lovastatin over 20 mg daily
        4. Avoid with Pravastatin
        5. Caution with Fluvastatin or pitavastatin
    5. CYP2C9 Inhibitor
      1. Fluconazole (Diflucan)
        1. Caution with Fluvastatin
    6. Other interactions
      1. Mibefradil (Posicor)
      2. Niacin
      3. Alcohol
        1. Increases risk of liver enzyme elevations
  15. Resources
    1. FDA Safety information on Statins (March 2012)
      1. http://www.fda.gov/Drugs/DrugSafety/ucm293101.htm
  16. References
    1. (2017) Presc Lett 24(11): 62
    2. (2012) Presc Lett 19(5): 25
    3. Carpenter (2019) Am Fam Physician 99(9):558-64 [PubMed]
    4. Chong (2001) Am J Med 111:390-400 [PubMed]
    5. Crouch (2001) Am Fam Physician 63(2):309-20 [PubMed]
    6. Gillett (2011) Am Fam Physician 83(6): 711-6 [PubMed]
    7. Jones (1998) Am J Cardiol 81:582-7 [PubMed]
    8. Sasaki (1998) Clin Ther 20:539-48 [PubMed]
Medication Costs
Lovastatin (on 6/18/2017 at Walmart.com)
Lovastatin 10mg #30 tablets for $4.00 $0.13 each
Lovastatin 10mg #90 tablets for $10.00 $0.11 each
Lovastatin 20mg #30 tablets for $4.00 $0.13 each
Lovastatin 20mg #90 tablets for $10.00 $0.11 each
lovastatin (on 5/17/2017 at Medicaid.Gov Pharmacy Drug pricing)
LOVASTATIN 10 MG TABLET Generic $0.06 each
LOVASTATIN 20 MG TABLET Generic $0.06 each
LOVASTATIN 40 MG TABLET Generic $0.07 each
simvastatin (on 5/17/2017 at Medicaid.Gov Pharmacy Drug pricing)
SIMVASTATIN 10 MG TABLET Generic $0.02 each
SIMVASTATIN 20 MG TABLET Generic $0.02 each
SIMVASTATIN 40 MG TABLET Generic $0.04 each
SIMVASTATIN 5 MG TABLET Generic $0.05 each
SIMVASTATIN 80 MG TABLET Generic $0.08 each
pravastatin (on 5/17/2017 at Medicaid.Gov Pharmacy Drug pricing)
PRAVASTATIN SODIUM 10 MG TAB Generic $0.19 each
PRAVASTATIN SODIUM 20 MG TAB Generic $0.13 each
PRAVASTATIN SODIUM 40 MG TAB Generic $0.18 each
PRAVASTATIN SODIUM 80 MG TAB Generic $0.32 each
atorvastatin (on 5/17/2017 at Medicaid.Gov Pharmacy Drug pricing)
ATORVASTATIN 10 MG TABLET Generic $0.10 each
ATORVASTATIN 20 MG TABLET Generic $0.11 each
ATORVASTATIN 40 MG TABLET Generic $0.12 each
ATORVASTATIN 80 MG TABLET Generic $0.15 each
fluvastatin (on 4/19/2017 at Medicaid.Gov Pharmacy Drug pricing)
FLUVASTATIN ER 80 MG TABLET Generic $5.00 each
FLUVASTATIN SODIUM 20 MG CAP Generic $3.67 each
FLUVASTATIN SODIUM 40 MG CAP Generic $3.54 each
rosuvastatin (on 5/17/2017 at Medicaid.Gov Pharmacy Drug pricing)
ROSUVASTATIN CALCIUM 10 MG TAB Generic $0.18 each
ROSUVASTATIN CALCIUM 20 MG TAB Generic $0.18 each
ROSUVASTATIN CALCIUM 40 MG TAB Generic $0.19 each
ROSUVASTATIN CALCIUM 5 MG TAB Generic $0.19 each
zocor (on 6/8/2017 at Medicaid.Gov Pharmacy Drug pricing)
ZOCOR 40 MG TABLET Generic $0.04 each
lipitor (on 6/1/2017 at Medicaid.Gov Pharmacy Drug pricing)
LIPITOR 10 MG TABLET Generic $0.10 each
LIPITOR 20 MG TABLET Generic $0.11 each
LIPITOR 40 MG TABLET Generic $0.12 each
LIPITOR 80 MG TABLET Generic $0.15 each
crestor (on 4/19/2017 at Medicaid.Gov Pharmacy Drug pricing)
CRESTOR 10 MG TABLET Generic $0.18 each
CRESTOR 20 MG TABLET Generic $0.18 each
CRESTOR 40 MG TABLET Generic $0.19 each
CRESTOR 5 MG TABLET Generic $0.19 each
FPNotebook does not benefit financially from showing this medication data or their pharmacy links. This information is provided only to help medical providers and their patients see relative costs. Insurance plans negotiate lower medication prices with suppliers. Prices shown here are out of pocket, non-negotiated rates. See Needy Meds for financial assistance information.

Lovastatin (C0024027)

Definition (NCI) A lactone metabolite isolated from the fungus Aspergillus terreus with cholesterol-lowering and potential antineoplastic activities. Lovastatin is hydrolyzed to the active beta-hydroxyacid form, which competitively inhibits 3-hydroxyl-3-methylgutarylcoenzyme A (HMG-CoA) reductase, an enzyme involved in cholesterol biosynthesis. In addition, this agent may induce tumor cell apoptosis and inhibit tumor cell invasiveness, possibly by inhibiting protein farnesylation and protein geranylgeranylation, and may arrest cells in the G1 phase of the cell cycle. The latter effect sensitizes tumor cells to the cytotoxic effects of ionizing radiation.
Definition (NCI_NCI-GLOSS) A drug used to lower the amount of cholesterol in the blood. It is also being studied in the prevention and treatment of some types of cancer. Lovastatin is a type of HMG-CoA reductase inhibitor (statin).
Definition (MSH) A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.
Definition (CSP) HMG coA reductase inhibitor which inhibits cholesterol biosynthesis and thus lowers blood cholesterol levels; also blocks isoprenylation of protein CAAX motifs.
Definition (PDQ) A lactone metabolite isolated from the fungus Aspergillus terreus with cholesterol-lowering activity and potential antineoplastic activity. Lovastatin is hydrolyszed to the active beta-hydroxyacid form, which competitively inhibits 3-hydroxyl-3-methylgutarylcoenzyme A (HMG-CoA) reductase, an enzyme involved in the cholesterol biosynthesis. In addition, this agent may inhibit tumor cell proliferation and reduce tumor cell invasiveness, thereby decreasing tumor metastatic potential; induce tumor cell apoptosis, possibly by inhibiting protein geranylgeranylation and; arrest cells in the G1 phase of the cell cycle, an effect that sensitizes tumor cells to the cytotoxic effects of ionizing radiation. Check for "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=41658&idtype=1" active clinical trials or "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=41658&idtype=1&closed=1" closed clinical trials using this agent. ("http://nciterms.nci.nih.gov:80/NCIBrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&code=C620" NCI Thesaurus)
Concepts Pharmacologic Substance (T121) , Organic Chemical (T109)
MSH D008148
SnomedCT 74205000, 386024001, 96303004
LNC LP171620-0
English 6 Methylcompactin, 6-Methylcompactin, Mevinolin, Butanoic acid, 2-methyl-, 1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-(2-(tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl)ethyl)-1-naphthalenyl ester, (1S-(1alpha(R*),3alpha,7beta,8beta(2S*,4S*),8abeta))-, Monacolin K, (2S)-2-Methylbutanoic Acid, (1S,3R,7S,8S,8aR)-1,2,3,7,8,8a-Hexahydro-3,7-dimethyl-8-[2-[(2R,4R)-tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl]ethyl]-1-naphthalenyl Ester, lovastatin, Lovastatin, mevinolin, lovastatin (medication), HMG-CoA reductase inhibitors lovastatin, LOVASTATIN, Lovastatin [Chemical/Ingredient], lovastatins, monacolin k, Lovastatin (product), Lovastatin (substance), Lovastatin -RETIRED-
Swedish Lovastatin
Czech lovastatin
Finnish Lovastatiini
Russian MEVINOLIN, LOVASTATIN, ЛОВАСТАТИН, МЕВИНОЛИН
Japanese メビノリン, ロバスタチン
Polish Lovastatin, Lowastatyna
Spanish lovastatina-RETIRADO- (concepto no activo), lovastatina-RETIRADO-, lovastatina (producto), lovastatina (sustancia), lovastatina, mevinolina, monacolina K, Lovastatina, Mevinolina
French Lovastatine
German Lovastatin, Mevinolin
Italian Lovastatina
Portuguese Lovastatina, Mevinolina
Sources
Derived from the NIH UMLS (Unified Medical Language System)


Simvastatin (C0074554)

Definition (CHV) a kind of cholesterol- lowering drug
Definition (CHV) a kind of cholesterol- lowering drug
Definition (NCI) A lipid-lowering agent derived synthetically from a fermentation product of the fungus Aspergillus terreus. Hydrolyzed in vivo to an active metabolite, simvastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. This agent lowers plasma cholesterol and lipoprotein levels, and modulates immune responses by suppressing MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. (NCI04)
Definition (CSP) a derivative of lovastatin and inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG coA reductase), a rate limiting enzyme in the biosynthesis of cholesterol.
Definition (MSH) A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.
Definition (PDQ) A lipid-lowering agent derived synthetically from a fermentation product of the fungus Aspergillus terreus. Hydrolyzed in vivo to an active metabolite, simvastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. This agent lowers plasma cholesterol and lipoprotein levels, and modulates immune responses by suppressing MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. Check for "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=455226&idtype=1" active clinical trials or "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=455226&idtype=1&closed=1" closed clinical trials using this agent. ("http://nciterms.nci.nih.gov:80/NCIBrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&code=C29454" NCI Thesaurus)
Concepts Pharmacologic Substance (T121) , Organic Chemical (T109)
MSH D019821
SnomedCT 387584000, 96304005
LNC LP171640-8
English synvinolin, Simvastatin, Synvinolin, [1S-[1alpha,3alpha,7beta,8beta(2S*,4S*),8abeta]]-1,2,3,7,8,8a-Hexahydro-3,7-dimethyl-8-[2-(tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl)ethyl]-1-naphthalenyl 2,2-dimethylbutanoate, simvastatin, HMG-CoA reductase inhibitors simvastatin, simvastatin (medication), SIMVASTATIN, Simvastatin [Chemical/Ingredient], simvastatin product, Velastatin, Simvastatin (product), Simvastatin (substance)
German Synvinolin, Simvastatin
Swedish Simvastatin
Czech simvastatin
Finnish Simvastatiini
Russian SIMVASTATIN, СИМВАСТАТИН
Japanese シンバスタチン
Italian Sinvinolina, Simvastatina
Polish Symwastatyna
Portuguese Simvastatina, Sinvastatina
Spanish simvastatina (producto), simvastatina (sustancia), simvastatina, simvastatin, Simvastatina
French Simvastatine
Sources
Derived from the NIH UMLS (Unified Medical Language System)


fluvastatin (C0082608)

Definition (NCI) A synthetic lipid-lowering agent with antilipidemic and potential antineoplastic properties. Fluvastatin competitively inhibits hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. This agent lowers plasma cholesterol and lipoprotein levels, and modulates immune responses through the suppression of MHC II (major histocompatibility complex II) on interferon gamma-stimulated antigen-presenting cells such as human vascular endothelial cells. Due to its anti-inflammatory effects mediated by alterations of lipid metabolism, fluvastatin may possess chemopreventive and therapeutic antineoplastic properties.
Concepts Pharmacologic Substance (T121) , Organic Chemical (T109)
MSH C065180
SnomedCT 387585004, 96307003
LNC LP171399-1
English 7-(3-(4-fluorophenyl)-1-(1-methylethyl)-1H-indol-2-yl)-3,5-dihydroxy-6-heptenoate, fluindostatin, fluvastatin, fluvastatin (medication), HMG-CoA reductase inhibitors fluvastatin, fluvastatin [Chemical/Ingredient], FLUVASTATIN, Fluvastatin, Fluvastatin (product), Fluvastatin (substance)
Spanish fluvastatina (producto), fluvastatina (sustancia), fluvastatina
Sources
Derived from the NIH UMLS (Unified Medical Language System)


Pravastatin (C0085542)

Definition (NCI) A synthetic lipid-lowering agent. Pravastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. Pravastatin lowers plasma cholesterol and lipoprotein levels, and modulates immune responses by suppressing MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. (NCI04)
Definition (NCI_NCI-GLOSS) The active ingredient in a drug used to lower the amount of cholesterol in the blood and to prevent stroke and heart attack. It is also being studied in the treatment of cancer and other conditions. Pravastatin blocks an enzyme that helps make cholesterol in the body. It may also make tumor cells more sensitive to anticancer drugs. It is a type of HMG-CoA reductase inhibitor, a type of statin, and a type of chemosensitizer.
Definition (MSH) An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES).
Definition (PDQ) A synthetic lipid-lowering agent. Pravastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. Pravastatin lowers plasma cholesterol and lipoprotein levels, and modulates immune responses by suppressing MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. Check for "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=424450&idtype=1" active clinical trials or "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=424450&idtype=1&closed=1" closed clinical trials using this agent. ("http://nciterms.nci.nih.gov:80/NCIBrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&code=C29375" NCI Thesaurus)
Concepts Pharmacologic Substance (T121) , Organic Chemical (T109)
MSH D017035
SnomedCT 96305006, 373566006
LNC LP171630-9
English Eptastatin, Pravastatin, 1-Naphthaleneheptanoic acid, 1,2,6,7,8,8a-hexahydro-beta,delta,6-trihydroxy-2-methyl-8-(2-methyl-1-oxobutoxy)-, (1S-(1alpha(betaS*,deltaS*),2alpha,6alpha,8beta(R*),8aalpha))-, HMG-CoA reductase inhibitors pravastatin, pravastatin (medication), Pravastatin [Chemical/Ingredient], [1S-[1alpha(betaS*,deltaS*),2alpha,6alpha,8beta(R*),8aalpha]]-1,2,6,7,8,8a-Hexahydro-beta,!d,6-trihydroxy-2-methyl-8-(2-methyl-1-oxobutoxy)-1-naphthaleneheptanoic Acid, pravastatin, PRAVASTATIN, Pravastatin (product), Pravastatin (substance), PRAV
Swedish Pravastatin
Czech eptastatin, pravastatin
Finnish Pravastatiini
Russian EPTASTATIN, PRAVASTATIN, ПРАВАСТАТИН, ЭПТАСТАТИН
Italian Eptastatina, Pravastatina
Polish Prawastatyna, Eptastatyna
Japanese エプタスタチン, プラバスタチン
Spanish pravastatina (producto), pravastatina (sustancia), pravastatina, pravastatin, Eptastatin, Pravastatina
French Eptastatine, Pravastatine
German Eptastatin, Pravastatin
Portuguese Eptastatina, Pravastatina
Sources
Derived from the NIH UMLS (Unified Medical Language System)


atorvastatin (C0286651)

Definition (CHV) a kind of cholesterol lowering drug
Definition (NCI) A synthetic lipid-lowering agent. Atorvastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. Atorvastatin also increases the number of LDL receptors on hepatic cell surfaces to enhance uptake and catabolism of LDL and reduces LDL production and the number of LDL particles. This agent lowers plasma cholesterol and lipoprotein levels and modulates immune responses by suppressing MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. (NCI04)
Definition (NCI_NCI-GLOSS) The active ingredient in a drug used to lower the amount of cholesterol in the blood and to prevent stroke, heart attack, and angina (chest pain). It is also being studied in the prevention and treatment of some types of cancer and other conditions. Atorvastatin blocks an enzyme that helps make cholesterol in the body. It also causes an increase in the breakdown of cholesterol. It is a type of HMG-CoA reductase inhibitor and a type of statin.
Definition (CSP) a synthetic lipid-lowering agent; an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase that catalyzes the conversion of HMG-CoA to mevalonate, an early and rate-limiting step in cholesterol biosynthesis.
Definition (PDQ) A synthetic lipid-lowering agent. Atorvastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. Atorvastatin also increases the number of LDL receptors on hepatic cell surfaces to enhance uptake and catabolism of LDL and reduces LDL production and the number of LDL particles. This agent lowers plasma cholesterol and lipoprotein levels and modulates immune responses by suppressing MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. Check for "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=460239&idtype=1" active clinical trials or "http://www.cancer.gov/Search/ClinicalTrialsLink.aspx?id=460239&idtype=1&closed=1" closed clinical trials using this agent. ("http://nciterms.nci.nih.gov:80/NCIBrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&code=C28837" NCI Thesaurus)
Concepts Pharmacologic Substance (T121) , Organic Chemical (T109)
MSH C065179
SnomedCT 391791009, 108600003, 373444002
LNC LP171386-8
English atorvastatin, (betaR,deltaR)-2-(p-Fluorophenyl)-beta,delta-dihydroxy-5-isopropyl-3-phenyl-4-(phenylcarbamoyl)-pyrrole-1-heptanoic Acid, (betaR,deltaR)-2-(4-Fluorophenyl)-beta,delta-dihydroxy-5-(1-methylethyl)-3-phenyl-4-[(phenylamino)carbonyl]-1H-pyrrole-1-heptanoic Acid, atorvastatin [Chemical/Ingredient], liptonorm, ATORVASTATIN, Atorvastatin - chemical (substance), Atorvastatin - chemical, Atorvastatin, Atorvastatin (product), Atorvastatin (substance)
Spanish atorvastatina (producto), atorvastatina (sustancia), atorvastatina
Sources
Derived from the NIH UMLS (Unified Medical Language System)


Hydroxymethylglutaryl-CoA Reductase Inhibitors (C0360714)

Definition (CHV) cholesterol lowering drug
Definition (MEDLINEPLUS)

Statins are drugs used to lower cholesterol. Your body needs some cholesterol to work properly. But if you have too much in your blood, it can stick to the walls of your arteries, narrowing or even blocking them.

If diet and exercise don't reduce your cholesterol levels, you may need to take medicine. Often, this medicine is a statin. Statins interfere with the production of cholesterol in your liver. They lower bad cholesterol levels and raise good cholesterol levels and can slow the formation of plaques in your arteries.

Statins are relatively safe for most people. But they are not recommended for pregnant patients or those with active or chronic liver disease. They can also cause serious muscle problems. Some statins also interact adversely with other drugs. You may have fewer side effects with one statin drug than another.

Researchers are also studying the use of statins for other conditions.

Food and Drug Administration
Definition (NCI_NCI-GLOSS) Any of a group of drugs that lower the amount of cholesterol and certain fats in the blood. Statins inhibit a key enzyme that helps make cholesterol. Statin drugs are being studied in the prevention and treatment of cancer.
Definition (NCI) Any substance that inhibits HMG-CoA reductase, a key enzyme in cholesterol synthesis. Inhibition of HMG-CoA reductase acts to lower plasma cholesterol and lipoprotein levels.
Definition (MSH) Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.
Concepts Pharmacologic Substance (T121) , Organic Chemical (T109)
MSH D019161
SnomedCT 372912004, 96302009
English HMG CoA Reductase Inhibitors, HMG-CoA Reductase Inhibitors, Inhibitors, HMG-CoA Reductase, Reductase Inhibitors, HMG-CoA, Hydroxymethylglutaryl CoA Reductase Inhibitors, Hydroxymethylglutaryl-CoA Inhibitors, Hydroxymethylglutaryl-Coenzyme A Inhibitors, Inhibitors, HMG CoA Reductase, Inhibitors, Hydroxymethylglutaryl CoA, Inhibitors, Hydroxymethylglutaryl Coenzyme A, Inhibitors, Hydroxymethylglutaryl-CoA, Inhibitors, Hydroxymethylglutaryl-CoA Reductase, Inhibitors, Hydroxymethylglutaryl-Coenzyme A, Reductase Inhibitors, Hydroxymethylglutaryl-CoA, Statin, 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, INHIB HMG COA REDUCTASE, INHIB HYDROXYMETHYLGLUTARYL COA, HMG COA REDUCTASE INHIB, HYDROXYMETHYLGLUTARYL COA REDUCTASE INHIB, HMG-CoA reductase inhibitors (medication), HMG-CoA reductase inhibitors, statin, Hydroxymethylglutaryl-coenzyme A reductase inhibitor, HMG-CoA reductase inhibitor (product), Hydroxymethylglutaryl-coenzyme A reductase inhibitor (product), 3-Hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor (substance), 3-Hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (substance), HMG-CoA Statins, Statins, HMG CoA, Statins, HMG-CoA, hydroxymethylglutaryl-coenzyme A reductase inhibitor, HMG COA reductase inhibitor, HMG-CoA reductase inhibitor, Statins, HMG-CoA reductase inhibitor, NOS, HMG-CoA reductase inhibitor (substance), HMG-CoA Reductase Inhibitor, Hydroxymethylglutaryl CoenzymeA Reductase Inhibitors, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) Reductase Inhibitors, Hydroxymethylglutaryl-CoA Reductase Inhibitors
Spanish inhibidor de la HMG - CoA reductasa, inhibidor de 3-hidroxi-3-metilglutaril coenzima A reductasa, inhibidor de 3-hidroxi-3-metilglutaril coenzima A reductasa (sustancia), inhibidor de la HMG - CoA reductasa (sustancia), inhibidor de hidroximetilglutaril coenzima A reductasa, inhibidor de hidroximetilglutaril coenzima A reductasa (producto), inhibidor de la HMG-CoA reductasa (producto), inhibidor de la HMG-CoA reductasa (sustancia), inhibidor de la HMG-CoA reductasa, estatina, inhibidor de la 3-hidroxi-3-metilglutaril coenzima A reductasa, Estatinas HMG-CoA, Inhibidores de Hidroximetilglutaril-CoA Reductasas, Inhibidores de HMG CoA Reductasa
French Inhibiteurs de l'hydroxyméthylglutaryl-CoA réductase, Inhibiteurs de l'hydroxyméthylglutaryl-Coenzyme A réductase, Inhibiteurs de l'HMG-CoA réductase, Statines
Swedish Hydroximetylglutaryl-CoA-reduktashämmare
Czech HMG-CoA-reduktasa - inhibitory, statiny, inhibitory 3HMG CoA-reduktázy, hydroxymethylglutaryl-CoA-reduktasa - inhibitory
Finnish Hydroksimetyyliglutaryyli-KoA-reduktaasin estäjät
Russian GIDROKSIMETILGLUTARIL-KOA-REDUKTAZY INGIBITORY, HMG-COA REDUKTAZY INGIBITORY, GMG-KOA REDUKTAZY INGIBITORY, STATINY GMG-KOA-REDUKTAZY, HMG-COA-РЕДУКТАЗЫ СТАТИНЫ, СТАТИНЫ ГМГ-КОA-РЕДУКТАЗЫ, HMG-COA-REDUKTAZY STATINY, HMG-COA РЕДУКТАЗЫ ИНГИБИТОРЫ, ГИДРОКСИМЕТИЛГЛУТАРИЛ-КОA-РЕДУКТАЗЫ ИНГИБИТОРЫ, ГМГ-КОA РЕДУКТАЗЫ ИНГИБИТОРЫ
Japanese ヒドロキシメチルグルタリルCoAレダクターゼ抑制剤, ヒドロキシメチルグルタリル-CoAレダクターゼ阻害剤, ヒドロキシメチルグルタリルCoAレダクターゼ阻害剤, HMG-CoA還元酵素阻害剤, HMG-CoAレダクターゼ抑制剤, HMG-CoAレダクターゼ阻害剤, HMG-CoAレダクターゼインヒビター, HMG-CoA還元酵素阻害薬
Polish Statyny, HMG-CoA, Inhibitory reduktazy hydroksymetyloglutarylo CoA, Inhibitory reduktazy HMG-CoA, Inhibitory reduktazy 3-hydroksy-3-metyloglutarylo-koenzymu A
German HMG-CoA-Reduktase-Inhibitoren, Hydroxymethylglutaryl-CoA-Reductase-Inhibitoren, Hydroxymethylglutaryl-CoA-Reduktase-Inhibitoren, Inhibitoren, HMG-CoA Reduktase, Inhibitoren, Hydroxymethylglutaryl-CoA, Inhibitoren, Hydroxymethylglutaryl-Coenzym A, Statine, HMG-CoA
Italian Inibitori della reduttasi del coenzima A idrossimetilglutarilico
Portuguese Estatinas de HMG-CoA, Inibidores de Hidroximetilglutaril-CoA Redutases, Inibidores de HMG-CoA Redutases
Sources
Derived from the NIH UMLS (Unified Medical Language System)


Lipitor (C0593906)

Concepts Pharmacologic Substance (T121) , Organic Chemical (T109)
MSH C065179
English Lipitor, lipitor
Sources
Derived from the NIH UMLS (Unified Medical Language System)


Zocor (C0678181)

Concepts Pharmacologic Substance (T121) , Organic Chemical (T109)
MSH D019821
German Zocor
English zocor, Zocor
Sources
Derived from the NIH UMLS (Unified Medical Language System)


rosuvastatin (C0965129)

Definition (NCI) A statin with antilipidemic and potential antineoplastic activities. Rosuvastatin selectively and competitively binds to and inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a precursor of cholesterol. This leads to a decrease in hepatic cholesterol levels and increase in uptake of LDL cholesterol. In addition, rosuvastatin, like other statins, exhibits pro-apoptotic, growth inhibitory, and pro-differentiation activities in a variety of tumor cell types; these antineoplastic activities may be due, in part, to inhibition of the isoprenylation of Ras and Rho GTPases and related signaling cascades.
Concepts Pharmacologic Substance (T121) , Organic Chemical (T109)
MSH C422923
SnomedCT 700067006, 406436002
LNC LP171638-2
English rosuvastatin [Chemical/Ingredient], rosuvastatin, Rosuvastatin (substance), ROSUVASTATIN, 6-Heptenoic acid, 7-(4-(4-fluorophenyl)-6-(1-methylethyl)-2-(ethyl(methylsulfonyl)amino)-5-pyrimidinyl)-3,5-dihydroxy-, (3R,5S,6E), Rosuvastatin, Rosuvastatin (product)
Spanish rosuvastatina (producto), rosuvastatina
Sources
Derived from the NIH UMLS (Unified Medical Language System)


Rosuvastatin calcium (C1101751)

Definition (NCI) The calcium salt form of rosuvastatin, a statin with antilipidemic activity. Rosuvastatin selectively and competitively binds to and inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a precursor of cholesterol. This leads to a decrease in hepatic cholesterol levels and increase in uptake of LDL cholesterol.
Definition (NCI_NCI-GLOSS) A drug used to lower the amount of cholesterol and other harmful substances, such as triglycerides, in the blood. It is also being studied in the prevention and treatment of some types of cancer and other conditions. Crestor blocks an enzyme that helps make cholesterol in the body and it helps break down cholesterol. It also may cause cancer cells to die and may inhibit the growth of blood vessels that cancer cells need to grow. It is a type of HMG-CoA reductase inhibitor and a type of statin.
Concepts Biologically Active Substance (T123) , Organic Chemical (T109) , Pharmacologic Substance (T121)
MSH C422923
SnomedCT 406435003
English HMG-CoA reductase inhibitors rosuvastatin calcium, rosuvastatin calcium (medication), ROSUVASTATIN CALCIUM, Rosuvastatin calcium (substance), Rosuvastatin calcium, rosuvastatin calcium, Rosuvastatin Calcium
Spanish rosuvastatina cálcica (sustancia), rosuvastatina cálcica
Sources
Derived from the NIH UMLS (Unified Medical Language System)


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