Rosuvastatin

updated

Rosuvastatin is an FDA-approved statin (CRESTOR, initial U.S. approval 2003) with outcome trials in 17,802 (JUPITER) and 12,705 (HOPE-3) people without cardiovascular disease and a 26-trial meta-analysis of about 170,000 people for the statin class. The supplier sequence, ezetimibe first and rosuvastatin only if ezetimibe fails, has no study behind it: a PubMed search on 9 October 2026 returned 20 records on statins with anabolic steroid terms, none a trial or cohort of a statin in steroid users, and the ZETIA label sets the opposite order. The benefit evidence comes from trials of at least 2 years, not cycle-length use.

Statin (HMG-CoA reductase inhibitor)

  • The CRESTOR label lists initial U.S. approval in 2003; the earliest generic rosuvastatin calcium approvals among the records returned were ANDA 079170 and ANDA 079172 on 19 July 2016.
  • JUPITER randomized 17,802 apparently healthy adults with LDL cholesterol below 130 mg/dL and hsCRP of 2.0 mg/L or higher; stopped at a median 1.9 years, the primary composite was 0.77 versus 1.36 per 100 person-years (HR 0.56, 95% CI 0.46 to 0.69).
  • HOPE-3 randomized 12,705 intermediate-risk people without cardiovascular disease for a median 5.6 years: the composite occurred in 3.7% versus 4.8% (HR 0.76, 95% CI 0.64 to 0.91).
  • A 26-trial meta-analysis of about 170,000 people found each 1.0 mmol/L fall in LDL cholesterol lowered major vascular events (RR 0.78, 95% CI 0.76 to 0.80); included trials ran at least 2 years.
  • A PubMed search on 9 October 2026 for statins with anabolic steroid terms returned 20 records; none was a trial or cohort of a statin in steroid users.
  • In 100 men on an androgen cycle, LDL cholesterol rose 0.45 mmol/L (95% CI 0.29 to 0.61) and returned to baseline 3 months after the cycle; no lipid-lowering drug was tested.

What is rosuvastatin approved to do?

CRESTOR is labeled to reduce the risk of major cardiovascular events in adults at increased risk, to lower LDL-C in hypercholesterolemia, to slow progression of atherosclerosis, and for familial hypercholesterolemia and other lipid disorders. The label lists initial U.S. approval in 2003.

CRESTOR is labeled to reduce the risk of major adverse cardiovascular events (cardiovascular death, nonfatal MI, nonfatal stroke or arterial revascularization) in adults at increased risk. It is also labeled as an adjunct to diet and exercise to lower LDL-C in adults with hypercholesterolemia, to slow progression of atherosclerosis, and in heterozygous (8 and older) and homozygous (7 and older) familial hypercholesterolemia, and as an adjunct to diet for primary dysbetalipoproteinemia and hypertriglyceridemia. The label version used here took effect on 23 September 2026.

The label lists initial U.S. approval in 2003. The FDA application record for CRESTOR was not among the records retrieved, so its NDA number and exact approval date are not stated here. The earliest generic rosuvastatin calcium approvals among the records returned were ANDA 079170 and ANDA 079172, both on 19 July 2016. Approvals outside the United States are not covered here.

Rosuvastatin free acid is C22H28FN3O6S (481.5 g/mol, CAS 287714-41-4, PubChem CID 446157). Rosuvastatin calcium, the salt in CRESTOR, is C44H54CaF2N6O12S2 (1001.1 g/mol, CAS 147098-20-2, CID 5282455), and label strengths are stated as rosuvastatin.

CRESTOR label, version effective 23 September 2026: indications, LDL-C, PK, muscle, liver, kidney, glucose

FDA prescribing information

DailyMed, U.S. National Library of Medicine. CRESTOR (rosuvastatin) film-coated oral tablets, prescribing information, label version effective 23 September 2026. Set ID 325a5d0e-9a72-4015-9fcd-1655fb504cee.

The label approves CRESTOR to reduce the risk of major adverse cardiovascular events (cardiovascular death, nonfatal MI, nonfatal stroke or arterial revascularization) in adults at increased risk; as an adjunct to diet and exercise to lower LDL-C in adults with hypercholesterolemia, to slow progression of atherosclerosis, and in heterozygous (8 and older) and homozygous (7 and older) familial hypercholesterolemia; and as an adjunct to diet for primary dysbetalipoproteinemia and hypertriglyceridemia. Initial U.S. approval was in 2003. In a 6-week placebo-controlled study in hypercholesterolemia, LDL-C fell 45% to 63% across the four doses studied (17 to 18 patients per dose) versus 7% on placebo (13 patients). Absolute oral bioavailability is about 20%, about 10% of a dose is recovered as metabolite (mainly N-desmethyl rosuvastatin, formed by CYP2C9), 90% is excreted in feces, and elimination half-life is about 19 hours; median exposure is about 2-fold higher in Asian patients than in White controls. The label warns of myopathy and rhabdomyolysis, with risk factors including age 65 or older, uncontrolled hypothyroidism, renal impairment, certain interacting drugs and higher dosage; risk is greater at the highest labeled dose than at lower doses, and Asian patients may be at higher risk. It describes rare immune-mediated necrotizing myopathy; transaminase elevations above 3 times normal in 1.1% versus 0.5% on placebo, with rare postmarketing hepatic failure and a contraindication in acute liver failure or decompensated cirrhosis; dipstick proteinuria and microscopic hematuria, more frequent at the highest dose and generally transient; and increases in HbA1c and fasting glucose that can exceed the threshold for diagnosing diabetes.

Participants / model
Adults and children with the labeled indications; label PK participants; patients in CRESTOR trials and postmarketing reports
Treatment
CRESTOR film-coated oral tablets (rosuvastatin as rosuvastatin calcium)
Follow-up
Label version effective 23 September 2026
Study design
FDA prescribing information
Funding
not stated in the source

Label-level statements. The page does not reproduce label dosing. Asian-ancestry exposure and proteinuria stay at label level.

Read the original source
Drugs@FDA: earliest generic approvals in the records returned, 19 July 2016

Regulatory record

U.S. Food and Drug Administration. Drugs@FDA application records for generic rosuvastatin calcium, ANDA 079170 and ANDA 079172. Dates read from the openFDA Drugs@FDA records.

The CRESTOR label lists initial U.S. approval in 2003. The earliest generic rosuvastatin calcium approvals among the records returned were ANDA 079170 and ANDA 079172, both on 19 July 2016. The CRESTOR NDA record was not among the records returned, so its application number and exact approval date are not established here.

Participants / model
Not a clinical population
Treatment
Drug applications
Follow-up
Approvals in 2003 and 2016
Study design
FDA application records
Funding
not stated in the source

The CRESTOR NDA number and exact approval date are not established from these records. The generic dates are the earliest among the records returned.

Read the original source
PubChem: rosuvastatin and rosuvastatin calcium identity

Chemical identity record

National Library of Medicine. PubChem compound records CID 446157 (rosuvastatin) and CID 5282455 (rosuvastatin calcium).

Rosuvastatin free acid: C22H28FN3O6S, 481.5 g/mol, CAS 287714-41-4 (PubChem also lists 1354641-88-5 as a synonym). Rosuvastatin calcium, the salt in CRESTOR: CID 5282455, C44H54CaF2N6O12S2, 1001.1 g/mol, CAS 147098-20-2; the label gives (C22H27FN3O6S)2Ca and 1,001.14. Label strengths are stated as rosuvastatin.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule and salt
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

Identity record only; it says nothing about efficacy or safety.

Read the original source

What did the outcome trials find?

In two large placebo-controlled trials in people without cardiovascular disease, rosuvastatin lowered LDL cholesterol and cardiovascular events. A meta-analysis of 26 statin trials found fewer major vascular events for each 1.0 mmol/L fall in LDL cholesterol.

In a 6-week placebo-controlled study in hypercholesterolemia reported in the CRESTOR label, LDL-C fell 45% to 63% across the four doses studied (17 to 18 patients per dose) versus 7% on placebo (13 patients).

JUPITER randomized 17,802 apparently healthy men and women with LDL cholesterol below 130 mg/dL and high-sensitivity CRP of 2.0 mg/L or higher to rosuvastatin or placebo (NCT00239681). Stopped at a median 1.9 years, it found LDL cholesterol 50% lower and CRP 37% lower. The primary composite (MI, stroke, arterial revascularization, hospitalization for unstable angina, or cardiovascular death) was 0.77 versus 1.36 per 100 person-years (HR 0.56, 95% CI 0.46 to 0.69), and death from any cause was 1.00 versus 1.25 per 100 person-years (HR 0.80, 95% CI 0.67 to 0.97).

HOPE-3 randomized 12,705 intermediate-risk people without cardiovascular disease in 21 countries to rosuvastatin or placebo for a median 5.6 years (NCT00468923). LDL cholesterol averaged 26.5% lower, and cardiovascular death, nonfatal MI or nonfatal stroke occurred in 3.7% versus 4.8% (HR 0.76, 95% CI 0.64 to 0.91).

A Cholesterol Treatment Trialists' individual-participant meta-analysis of 26 randomized trials (about 170,000 participants) found that each 1.0 mmol/L reduction in LDL cholesterol lowered major vascular events by just over a fifth (RR 0.78, 95% CI 0.76 to 0.80) and all-cause mortality by 10% (RR 0.90, 95% CI 0.87 to 0.93), with no effect on cancer incidence.

CRESTOR label, version effective 23 September 2026: indications, LDL-C, PK, muscle, liver, kidney, glucose

FDA prescribing information

DailyMed, U.S. National Library of Medicine. CRESTOR (rosuvastatin) film-coated oral tablets, prescribing information, label version effective 23 September 2026. Set ID 325a5d0e-9a72-4015-9fcd-1655fb504cee.

The label approves CRESTOR to reduce the risk of major adverse cardiovascular events (cardiovascular death, nonfatal MI, nonfatal stroke or arterial revascularization) in adults at increased risk; as an adjunct to diet and exercise to lower LDL-C in adults with hypercholesterolemia, to slow progression of atherosclerosis, and in heterozygous (8 and older) and homozygous (7 and older) familial hypercholesterolemia; and as an adjunct to diet for primary dysbetalipoproteinemia and hypertriglyceridemia. Initial U.S. approval was in 2003. In a 6-week placebo-controlled study in hypercholesterolemia, LDL-C fell 45% to 63% across the four doses studied (17 to 18 patients per dose) versus 7% on placebo (13 patients). Absolute oral bioavailability is about 20%, about 10% of a dose is recovered as metabolite (mainly N-desmethyl rosuvastatin, formed by CYP2C9), 90% is excreted in feces, and elimination half-life is about 19 hours; median exposure is about 2-fold higher in Asian patients than in White controls. The label warns of myopathy and rhabdomyolysis, with risk factors including age 65 or older, uncontrolled hypothyroidism, renal impairment, certain interacting drugs and higher dosage; risk is greater at the highest labeled dose than at lower doses, and Asian patients may be at higher risk. It describes rare immune-mediated necrotizing myopathy; transaminase elevations above 3 times normal in 1.1% versus 0.5% on placebo, with rare postmarketing hepatic failure and a contraindication in acute liver failure or decompensated cirrhosis; dipstick proteinuria and microscopic hematuria, more frequent at the highest dose and generally transient; and increases in HbA1c and fasting glucose that can exceed the threshold for diagnosing diabetes.

Participants / model
Adults and children with the labeled indications; label PK participants; patients in CRESTOR trials and postmarketing reports
Treatment
CRESTOR film-coated oral tablets (rosuvastatin as rosuvastatin calcium)
Follow-up
Label version effective 23 September 2026
Study design
FDA prescribing information
Funding
not stated in the source

Label-level statements. The page does not reproduce label dosing. Asian-ancestry exposure and proteinuria stay at label level.

Read the original source
JUPITER: 17,802 healthy adults, HR 0.56, stopped at 1.9 years

Randomized controlled trial

Ridker PM et al. N Engl J Med. 2008;359(21):2195-207. PMID 18997196.

Stopped at a median 1.9 years, it found LDL cholesterol 50% lower and CRP 37% lower, and the primary composite (MI, stroke, arterial revascularization, hospitalization for unstable angina, or cardiovascular death) at 0.77 versus 1.36 per 100 person-years (HR 0.56, 95% CI 0.46 to 0.69). Death from any cause was 1.00 versus 1.25 per 100 person-years (HR 0.80, 95% CI 0.67 to 0.97). Myopathy and cancer did not increase significantly; physician-reported diabetes was more common on rosuvastatin.

Participants / model
17,802 apparently healthy men and women with LDL cholesterol below 130 mg/dL and high-sensitivity CRP of 2.0 mg/L or higher
Treatment
Oral rosuvastatin 20 mg daily or placebo
Follow-up
Stopped at a median 1.9 years
Study design
Randomized placebo-controlled trial
Funding
not stated in the source

Apparently healthy adults with raised hsCRP; the result does not address anabolic steroid users.

Read the original source
HOPE-3: 12,705 intermediate-risk adults, median 5.6 years, HR 0.76

Randomized controlled trial

Yusuf S et al. N Engl J Med. 2016;374(21):2021-31. PMID 27040132.

LDL cholesterol averaged 26.5% lower, and cardiovascular death, nonfatal MI or nonfatal stroke occurred in 3.7% versus 4.8% (HR 0.76, 95% CI 0.64 to 0.91). There was no excess of diabetes or cancer, but more cataract surgery (3.8% versus 3.1%) and muscle symptoms (5.8% versus 4.7%).

Participants / model
12,705 intermediate-risk people without cardiovascular disease in 21 countries
Treatment
Oral rosuvastatin 10 mg daily or placebo
Follow-up
Median 5.6 years
Study design
Randomized placebo-controlled trial
Funding
not stated in the source

Intermediate-risk adults followed for years; the result does not address anabolic steroid users or short use.

Read the original source
CTT meta-analysis: 26 trials, about 170,000 people, RR 0.78 per 1.0 mmol/L

Systematic review and meta-analysis

Baigent C et al. Lancet. 2010;376(9753):1670-81. PMID 21067804.

Each 1.0 mmol/L reduction in LDL cholesterol lowered major vascular events by just over a fifth (RR 0.78, 95% CI 0.76 to 0.80) and all-cause mortality by 10% (RR 0.90, 95% CI 0.87 to 0.93), with no effect on cancer incidence. Included trials had to run at least 2 years, with median follow-up of 4.8 to 5.1 years.

Participants / model
About 170,000 participants in 26 statin trials of at least 1,000 people and 2 years
Treatment
Statin versus control and more versus less intensive statin regimens
Follow-up
Included trials ran at least 2 years; median follow-up 4.8 to 5.1 years
Study design
Systematic review and individual-participant meta-analysis
Funding
not stated in the source

The benefit evidence comes from years of treatment, not cycle-length use.

Read the original source

Does rosuvastatin belong after ezetimibe when steroids raise LDL?

No trial tested any lipid-lowering drug in steroid users, and the ezetimibe-first order has no study behind it. A PubMed search on 9 October 2026 returned 20 records on statins with anabolic steroid terms, none a trial or cohort of a statin in steroid users. The ZETIA label sets the opposite order.

Sellers describe rosuvastatin as the option for steroid-induced LDL elevation, ideally only when ezetimibe alone has not resolved it. A PubMed search on 9 October 2026 for statins, rosuvastatin, atorvastatin, simvastatin or HMG-CoA reductase inhibitors with anabolic steroid, bodybuilding, nandrolone, stanozolol, oxandrolone, oxymetholone or methyltestosterone terms returned 20 records. None was a trial or cohort of a statin in steroid users. They covered reviews, case reports, studies of steroid use in other groups, analytical chemistry and a 1997 Dutch case report in which simvastatin plus gemfibrozil did not raise low HDL in a man later found to be using anabolic steroids.

The ZETIA label indicates ezetimibe for primary hyperlipidemia in combination with a statin, or alone when additional LDL-C-lowering therapy is not possible. The supplier's order reverses that. In separate label trials, ezetimibe alone lowered LDL-C 18% and rosuvastatin lowered it 45% to 63% across the doses studied. These come from different trials, not a head-to-head comparison.

The size of the steroid-related LDL change was measured in one prospective cohort of 100 men performing a self-directed androgen cycle. LDL cholesterol rose 0.45 mmol/L (95% CI 0.29 to 0.61) and ApoB rose 18.2 mg/dL during use, and both returned to baseline 3 months after the cycle. Follow-up was 1 year, and no lipid-lowering drug was tested.

In a qualitative interview study of men using steroids for 8 weeks or more (thematic saturation at 12 interviews), participants described avoiding oral steroids, self-directed lab testing that included cholesterol, and taking medicines without a prescription, statins and angiotensin receptor blockers among them. This documents a use pattern. It measured no outcome, and the authors call for research on each intervention.

PubMed search, 9 October 2026: 20 records, none a trial or cohort of a statin in steroid users

PubMed search record

PubMed search run on 9 October 2026: (statin*[tiab] OR rosuvastatin[tiab] OR atorvastatin[tiab] OR simvastatin[tiab] OR HMG-CoA reductase inhibitor*[tiab]) AND (anabolic steroid*[tiab] OR anabolic-androgenic[tiab] OR anabolic androgenic[tiab] OR bodybuild*[tiab] OR nandrolone[tiab] OR stanozolol[tiab] OR oxandrolone[tiab] OR oxymetholone[tiab] OR methyltestosterone[tiab]). 20 records returned.

The search returned 20 records. None was a trial or cohort of a statin in anabolic steroid users. They covered tendinopathy and drug-induced cholestasis reviews, cachexia, inclusion body myositis, expectorant, androgen deficiency and renal-failure reviews, case reports (myocardial infarction in a young steroid user, clenbuterol-related MI, antibiotic-associated tendonitis), studies of steroid use in arrested substance users and Olympic athletes, analytical chemistry, a drug-induced liver injury ranking, lipid and HIV reviews, the interview study above, and a 1997 Dutch case report in which simvastatin plus gemfibrozil did not raise low HDL in a man later found to be using anabolic steroids. The ezetimibe-first sequence has no study behind it in these records.

Participants / model
Records returned, not a population
Treatment
Not applicable
Follow-up
Search run on 9 October 2026
Study design
Literature search
Funding
not stated in the source

A search result shows what PubMed returned on that date. It is not proof that no unindexed study exists.

Read the original source
ZETIA label, version effective 25 November 2025: ezetimibe positioned with a statin

FDA prescribing information

DailyMed, U.S. National Library of Medicine. ZETIA (ezetimibe) oral tablets, prescribing information, label version effective 25 November 2025. Set ID 174e45e0-45bb-48b7-9e60-8f6cfc1d22bb.

The label indicates ezetimibe for primary hyperlipidemia in combination with a statin, or alone when additional LDL-C-lowering therapy is not possible. The supplier's order, ezetimibe first and rosuvastatin only if ezetimibe fails, reverses the order in the ezetimibe label. In separate label trials, ezetimibe alone lowered LDL-C 18% and rosuvastatin lowered it 45% to 63% across the doses studied.

Participants / model
Adults with primary hyperlipidemia
Treatment
Oral ezetimibe; oral rosuvastatin (separate label trials)
Follow-up
Label version effective 25 November 2025
Study design
FDA prescribing information
Funding
not stated in the source

The two LDL-C figures come from separate label trials, not a head-to-head comparison.

Read the original source
CRESTOR label, version effective 23 September 2026: indications, LDL-C, PK, muscle, liver, kidney, glucose

FDA prescribing information

DailyMed, U.S. National Library of Medicine. CRESTOR (rosuvastatin) film-coated oral tablets, prescribing information, label version effective 23 September 2026. Set ID 325a5d0e-9a72-4015-9fcd-1655fb504cee.

The label approves CRESTOR to reduce the risk of major adverse cardiovascular events (cardiovascular death, nonfatal MI, nonfatal stroke or arterial revascularization) in adults at increased risk; as an adjunct to diet and exercise to lower LDL-C in adults with hypercholesterolemia, to slow progression of atherosclerosis, and in heterozygous (8 and older) and homozygous (7 and older) familial hypercholesterolemia; and as an adjunct to diet for primary dysbetalipoproteinemia and hypertriglyceridemia. Initial U.S. approval was in 2003. In a 6-week placebo-controlled study in hypercholesterolemia, LDL-C fell 45% to 63% across the four doses studied (17 to 18 patients per dose) versus 7% on placebo (13 patients). Absolute oral bioavailability is about 20%, about 10% of a dose is recovered as metabolite (mainly N-desmethyl rosuvastatin, formed by CYP2C9), 90% is excreted in feces, and elimination half-life is about 19 hours; median exposure is about 2-fold higher in Asian patients than in White controls. The label warns of myopathy and rhabdomyolysis, with risk factors including age 65 or older, uncontrolled hypothyroidism, renal impairment, certain interacting drugs and higher dosage; risk is greater at the highest labeled dose than at lower doses, and Asian patients may be at higher risk. It describes rare immune-mediated necrotizing myopathy; transaminase elevations above 3 times normal in 1.1% versus 0.5% on placebo, with rare postmarketing hepatic failure and a contraindication in acute liver failure or decompensated cirrhosis; dipstick proteinuria and microscopic hematuria, more frequent at the highest dose and generally transient; and increases in HbA1c and fasting glucose that can exceed the threshold for diagnosing diabetes.

Participants / model
Adults and children with the labeled indications; label PK participants; patients in CRESTOR trials and postmarketing reports
Treatment
CRESTOR film-coated oral tablets (rosuvastatin as rosuvastatin calcium)
Follow-up
Label version effective 23 September 2026
Study design
FDA prescribing information
Funding
not stated in the source

Label-level statements. The page does not reproduce label dosing. Asian-ancestry exposure and proteinuria stay at label level.

Read the original source
Androgen cycle cohort: LDL cholesterol up 0.45 mmol/L, back to baseline 3 months after

Human study

Smit DL et al. Andrologia. 2022;54(4):e14372. PMID 35014715.

LDL cholesterol rose 0.45 mmol/L (95% CI 0.29 to 0.61) and ApoB 18.2 mg/dL during use, and both returned to baseline 3 months after the cycle. Follow-up was 1 year.

Participants / model
100 men performing a self-directed androgen cycle
Treatment
Self-administered androgens (observational); no lipid-lowering drug was tested
Follow-up
Follow-up of 1 year
Study design
Prospective cohort study
Funding
not stated in the source

The size of the steroid-related LDL change the supplier claim targets, measured in the one prospective cohort reviewed.

Read the original source
Interview study: men using steroids described taking statins and ARBs without a prescription

Human study

Kutscher E et al. Harm Reduct J. 2024;21(1):196. PMID 39523302.

Participants described avoiding oral steroids, self-directed lab testing that included cholesterol, and taking medicines without a prescription, statins and angiotensin receptor blockers among them. The authors call for research on each intervention.

Participants / model
Men using anabolic steroids for 8 weeks or more in New York City and online; thematic saturation at 12 interviews
Treatment
Not applicable (self-reported practices)
Follow-up
Interviews, not a treatment period
Study design
Qualitative interview study
Funding
not stated in the source

Documents a use pattern; it measured no outcome.

Read the original source

Does the statin outcome data cover short, cycle-length use?

No. The Cholesterol Treatment Trialists' meta-analysis included only trials of at least 2 years, with median follow-up of 4.8 to 5.1 years. No data on short, cycle-length statin use were found.

The meta-analysis of 26 statin trials required each trial to run at least 2 years, with median follow-up of 4.8 to 5.1 years. JUPITER was stopped at a median 1.9 years and HOPE-3 followed people for a median 5.6 years.

The benefit seen in those trials comes from years of treatment in the populations they enrolled, such as apparently healthy adults with raised hsCRP in JUPITER and intermediate-risk adults in HOPE-3. None of the records reviewed tested a statin over a short, cycle-length course, and none tested one in steroid users.

CTT meta-analysis: 26 trials, about 170,000 people, RR 0.78 per 1.0 mmol/L

Systematic review and meta-analysis

Baigent C et al. Lancet. 2010;376(9753):1670-81. PMID 21067804.

Each 1.0 mmol/L reduction in LDL cholesterol lowered major vascular events by just over a fifth (RR 0.78, 95% CI 0.76 to 0.80) and all-cause mortality by 10% (RR 0.90, 95% CI 0.87 to 0.93), with no effect on cancer incidence. Included trials had to run at least 2 years, with median follow-up of 4.8 to 5.1 years.

Participants / model
About 170,000 participants in 26 statin trials of at least 1,000 people and 2 years
Treatment
Statin versus control and more versus less intensive statin regimens
Follow-up
Included trials ran at least 2 years; median follow-up 4.8 to 5.1 years
Study design
Systematic review and individual-participant meta-analysis
Funding
not stated in the source

The benefit evidence comes from years of treatment, not cycle-length use.

Read the original source
JUPITER: 17,802 healthy adults, HR 0.56, stopped at 1.9 years

Randomized controlled trial

Ridker PM et al. N Engl J Med. 2008;359(21):2195-207. PMID 18997196.

Stopped at a median 1.9 years, it found LDL cholesterol 50% lower and CRP 37% lower, and the primary composite (MI, stroke, arterial revascularization, hospitalization for unstable angina, or cardiovascular death) at 0.77 versus 1.36 per 100 person-years (HR 0.56, 95% CI 0.46 to 0.69). Death from any cause was 1.00 versus 1.25 per 100 person-years (HR 0.80, 95% CI 0.67 to 0.97). Myopathy and cancer did not increase significantly; physician-reported diabetes was more common on rosuvastatin.

Participants / model
17,802 apparently healthy men and women with LDL cholesterol below 130 mg/dL and high-sensitivity CRP of 2.0 mg/L or higher
Treatment
Oral rosuvastatin 20 mg daily or placebo
Follow-up
Stopped at a median 1.9 years
Study design
Randomized placebo-controlled trial
Funding
not stated in the source

Apparently healthy adults with raised hsCRP; the result does not address anabolic steroid users.

Read the original source
HOPE-3: 12,705 intermediate-risk adults, median 5.6 years, HR 0.76

Randomized controlled trial

Yusuf S et al. N Engl J Med. 2016;374(21):2021-31. PMID 27040132.

LDL cholesterol averaged 26.5% lower, and cardiovascular death, nonfatal MI or nonfatal stroke occurred in 3.7% versus 4.8% (HR 0.76, 95% CI 0.64 to 0.91). There was no excess of diabetes or cancer, but more cataract surgery (3.8% versus 3.1%) and muscle symptoms (5.8% versus 4.7%).

Participants / model
12,705 intermediate-risk people without cardiovascular disease in 21 countries
Treatment
Oral rosuvastatin 10 mg daily or placebo
Follow-up
Median 5.6 years
Study design
Randomized placebo-controlled trial
Funding
not stated in the source

Intermediate-risk adults followed for years; the result does not address anabolic steroid users or short use.

Read the original source

How does rosuvastatin work, and what does the body do with it?

Rosuvastatin is a statin (HMG-CoA reductase inhibitor) that lowers LDL-C. Absolute oral bioavailability is about 20%, and the elimination half-life is about 19 hours.

The sources reviewed describe rosuvastatin as a statin (HMG-CoA reductase inhibitor) and report its effect on LDL-C. In a 6-week label study, LDL-C fell 45% to 63% across the four doses studied versus 7% on placebo.

Absolute oral bioavailability is about 20%. About 10% of a dose is recovered as metabolite, mainly N-desmethyl rosuvastatin formed by CYP2C9, and 90% is excreted in feces. Elimination half-life is about 19 hours. Median exposure is about 2-fold higher in Asian patients than in White controls.

CRESTOR label, version effective 23 September 2026: indications, LDL-C, PK, muscle, liver, kidney, glucose

FDA prescribing information

DailyMed, U.S. National Library of Medicine. CRESTOR (rosuvastatin) film-coated oral tablets, prescribing information, label version effective 23 September 2026. Set ID 325a5d0e-9a72-4015-9fcd-1655fb504cee.

The label approves CRESTOR to reduce the risk of major adverse cardiovascular events (cardiovascular death, nonfatal MI, nonfatal stroke or arterial revascularization) in adults at increased risk; as an adjunct to diet and exercise to lower LDL-C in adults with hypercholesterolemia, to slow progression of atherosclerosis, and in heterozygous (8 and older) and homozygous (7 and older) familial hypercholesterolemia; and as an adjunct to diet for primary dysbetalipoproteinemia and hypertriglyceridemia. Initial U.S. approval was in 2003. In a 6-week placebo-controlled study in hypercholesterolemia, LDL-C fell 45% to 63% across the four doses studied (17 to 18 patients per dose) versus 7% on placebo (13 patients). Absolute oral bioavailability is about 20%, about 10% of a dose is recovered as metabolite (mainly N-desmethyl rosuvastatin, formed by CYP2C9), 90% is excreted in feces, and elimination half-life is about 19 hours; median exposure is about 2-fold higher in Asian patients than in White controls. The label warns of myopathy and rhabdomyolysis, with risk factors including age 65 or older, uncontrolled hypothyroidism, renal impairment, certain interacting drugs and higher dosage; risk is greater at the highest labeled dose than at lower doses, and Asian patients may be at higher risk. It describes rare immune-mediated necrotizing myopathy; transaminase elevations above 3 times normal in 1.1% versus 0.5% on placebo, with rare postmarketing hepatic failure and a contraindication in acute liver failure or decompensated cirrhosis; dipstick proteinuria and microscopic hematuria, more frequent at the highest dose and generally transient; and increases in HbA1c and fasting glucose that can exceed the threshold for diagnosing diabetes.

Participants / model
Adults and children with the labeled indications; label PK participants; patients in CRESTOR trials and postmarketing reports
Treatment
CRESTOR film-coated oral tablets (rosuvastatin as rosuvastatin calcium)
Follow-up
Label version effective 23 September 2026
Study design
FDA prescribing information
Funding
not stated in the source

Label-level statements. The page does not reproduce label dosing. Asian-ancestry exposure and proteinuria stay at label level.

Read the original source

What risks does the label report?

The CRESTOR label warns of myopathy and rhabdomyolysis, rare immune-mediated necrotizing myopathy, liver enzyme elevations with rare hepatic failure, proteinuria and hematuria, and increases in HbA1c and fasting glucose. It is contraindicated in acute liver failure or decompensated cirrhosis.

The CRESTOR label warns of myopathy and rhabdomyolysis. Risk factors include age 65 or older, uncontrolled hypothyroidism, renal impairment, certain interacting drugs and higher dosage; risk is greater at the highest labeled dose than at lower doses, and Asian patients may be at higher risk. The label also describes rare immune-mediated necrotizing myopathy.

Transaminase elevations above 3 times normal occurred in 1.1% versus 0.5% on placebo in pooled trials, with rare postmarketing hepatic failure. CRESTOR is contraindicated in acute liver failure or decompensated cirrhosis. NIH's LiverTox record, dated 21 March 2025, describes mild, asymptomatic, self-limited aminotransferase elevations during therapy and rare clinically apparent acute liver injury.

The label also reports dipstick proteinuria and microscopic hematuria, more frequent at the highest dose and generally transient, and increases in HbA1c and fasting glucose that can exceed the threshold for diagnosing diabetes.

In JUPITER, myopathy and cancer did not increase significantly, but physician-reported diabetes was more common on rosuvastatin. In HOPE-3, there was no excess of diabetes or cancer, but more cataract surgery (3.8% versus 3.1%) and muscle symptoms (5.8% versus 4.7%). These come from the trial populations described above. No safety data in steroid users were found.

CRESTOR label, version effective 23 September 2026: indications, LDL-C, PK, muscle, liver, kidney, glucose

FDA prescribing information

DailyMed, U.S. National Library of Medicine. CRESTOR (rosuvastatin) film-coated oral tablets, prescribing information, label version effective 23 September 2026. Set ID 325a5d0e-9a72-4015-9fcd-1655fb504cee.

The label approves CRESTOR to reduce the risk of major adverse cardiovascular events (cardiovascular death, nonfatal MI, nonfatal stroke or arterial revascularization) in adults at increased risk; as an adjunct to diet and exercise to lower LDL-C in adults with hypercholesterolemia, to slow progression of atherosclerosis, and in heterozygous (8 and older) and homozygous (7 and older) familial hypercholesterolemia; and as an adjunct to diet for primary dysbetalipoproteinemia and hypertriglyceridemia. Initial U.S. approval was in 2003. In a 6-week placebo-controlled study in hypercholesterolemia, LDL-C fell 45% to 63% across the four doses studied (17 to 18 patients per dose) versus 7% on placebo (13 patients). Absolute oral bioavailability is about 20%, about 10% of a dose is recovered as metabolite (mainly N-desmethyl rosuvastatin, formed by CYP2C9), 90% is excreted in feces, and elimination half-life is about 19 hours; median exposure is about 2-fold higher in Asian patients than in White controls. The label warns of myopathy and rhabdomyolysis, with risk factors including age 65 or older, uncontrolled hypothyroidism, renal impairment, certain interacting drugs and higher dosage; risk is greater at the highest labeled dose than at lower doses, and Asian patients may be at higher risk. It describes rare immune-mediated necrotizing myopathy; transaminase elevations above 3 times normal in 1.1% versus 0.5% on placebo, with rare postmarketing hepatic failure and a contraindication in acute liver failure or decompensated cirrhosis; dipstick proteinuria and microscopic hematuria, more frequent at the highest dose and generally transient; and increases in HbA1c and fasting glucose that can exceed the threshold for diagnosing diabetes.

Participants / model
Adults and children with the labeled indications; label PK participants; patients in CRESTOR trials and postmarketing reports
Treatment
CRESTOR film-coated oral tablets (rosuvastatin as rosuvastatin calcium)
Follow-up
Label version effective 23 September 2026
Study design
FDA prescribing information
Funding
not stated in the source

Label-level statements. The page does not reproduce label dosing. Asian-ancestry exposure and proteinuria stay at label level.

Read the original source
NIH LiverTox, rosuvastatin record dated 21 March 2025: mild enzyme rises, rare liver injury

Regulatory record

Rosuvastatin. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. 2012. PMID 31643932.

The record describes mild, asymptomatic, self-limited serum aminotransferase elevations during therapy and rare clinically apparent acute liver injury.

Participants / model
People treated with rosuvastatin (reference summary)
Treatment
Oral rosuvastatin
Follow-up
Record dated 21 March 2025
Study design
NIH drug-induced liver injury reference (LiverTox)
Funding
not stated in the source

Reference summary; it describes rates and case patterns, not a trial.

Read the original source
JUPITER: 17,802 healthy adults, HR 0.56, stopped at 1.9 years

Randomized controlled trial

Ridker PM et al. N Engl J Med. 2008;359(21):2195-207. PMID 18997196.

Stopped at a median 1.9 years, it found LDL cholesterol 50% lower and CRP 37% lower, and the primary composite (MI, stroke, arterial revascularization, hospitalization for unstable angina, or cardiovascular death) at 0.77 versus 1.36 per 100 person-years (HR 0.56, 95% CI 0.46 to 0.69). Death from any cause was 1.00 versus 1.25 per 100 person-years (HR 0.80, 95% CI 0.67 to 0.97). Myopathy and cancer did not increase significantly; physician-reported diabetes was more common on rosuvastatin.

Participants / model
17,802 apparently healthy men and women with LDL cholesterol below 130 mg/dL and high-sensitivity CRP of 2.0 mg/L or higher
Treatment
Oral rosuvastatin 20 mg daily or placebo
Follow-up
Stopped at a median 1.9 years
Study design
Randomized placebo-controlled trial
Funding
not stated in the source

Apparently healthy adults with raised hsCRP; the result does not address anabolic steroid users.

Read the original source
HOPE-3: 12,705 intermediate-risk adults, median 5.6 years, HR 0.76

Randomized controlled trial

Yusuf S et al. N Engl J Med. 2016;374(21):2021-31. PMID 27040132.

LDL cholesterol averaged 26.5% lower, and cardiovascular death, nonfatal MI or nonfatal stroke occurred in 3.7% versus 4.8% (HR 0.76, 95% CI 0.64 to 0.91). There was no excess of diabetes or cancer, but more cataract surgery (3.8% versus 3.1%) and muscle symptoms (5.8% versus 4.7%).

Participants / model
12,705 intermediate-risk people without cardiovascular disease in 21 countries
Treatment
Oral rosuvastatin 10 mg daily or placebo
Follow-up
Median 5.6 years
Study design
Randomized placebo-controlled trial
Funding
not stated in the source

Intermediate-risk adults followed for years; the result does not address anabolic steroid users or short use.

Read the original source

How much of statin muscle pain is caused by the statin?

In pooled double-blind trials, muscle pain or weakness was reported by 27.1% on statin versus 26.6% on placebo (RR 1.03). In year 1 about 1 in 15 such reports on a statin was due to the statin, and after year 1 there was no significant excess. These are class-level figures, not specific to rosuvastatin.

A Cholesterol Treatment Trialists' individual-participant meta-analysis of 19 double-blind statin-versus-placebo trials (123,940 participants) and 4 more-versus-less-intensive trials (30,724) found muscle pain or weakness in 27.1% on statin versus 26.6% on placebo (RR 1.03, 95% CI 1.01 to 1.06).

In year 1 the relative increase was 7% (11 extra reports per 1,000 person-years), so only about 1 in 15 such reports on statin was due to the statin. After year 1 there was no significant excess. More intensive regimens, including rosuvastatin 20 to 40 mg, had a higher rate ratio than less intensive ones (1.08 versus 1.03). Median creatine kinase rose by about 0.02 times the upper limit of normal.

These are class-level figures from long-term trials, not rosuvastatin-specific, and they do not address steroid users.

CTT muscle meta-analysis: 27.1% on statin versus 26.6% on placebo

Systematic review and meta-analysis

Lancet. 2022;400(10355):832-845. PMID 36049498.

Muscle pain or weakness was reported by 27.1% on statin versus 26.6% on placebo (RR 1.03, 95% CI 1.01 to 1.06). In year 1 the relative increase was 7% (11 extra reports per 1,000 person-years), so only about 1 in 15 such reports on statin was due to the statin; after year 1 there was no significant excess. More intensive regimens, including rosuvastatin 20 to 40 mg, had a higher rate ratio than less intensive ones (1.08 versus 1.03). Median creatine kinase rose by about 0.02 times the upper limit of normal.

Participants / model
123,940 participants in 19 double-blind statin-versus-placebo trials and 30,724 in 4 more-versus-less-intensive trials
Treatment
Statins, including rosuvastatin 20 to 40 mg daily
Follow-up
Large long-term double-blind trials
Study design
Systematic review and individual-participant meta-analysis
Funding
not stated in the source

Class-level figures from the Cholesterol Treatment Trialists, not specific to rosuvastatin.

Read the original source

Why does rosuvastatin sit in S tier?

Outcome trials in 17,802 and 12,705 people without cardiovascular disease, a class meta-analysis of about 170,000 people, initial U.S. approval in 2003 and more than two decades of use support the S for the approved uses. The grade does not cover the supplier's ezetimibe-first sequence.

The S applies to the labeled uses. The supplier claim is a separate verdict: the ezetimibe-first sequence is unsupported. The ezetimibe label sets the opposite order, rosuvastatin lowered LDL-C more in separate label trials, the statin outcome evidence comes from trials of at least 2 years rather than cycle-length use, and no trial tested any lipid-lowering drug in steroid users.

The steroid-related LDL rise in the one prospective cohort reviewed was 0.45 mmol/L and reversed within 3 months of stopping the cycle.

CRESTOR label, version effective 23 September 2026: indications, LDL-C, PK, muscle, liver, kidney, glucose

FDA prescribing information

DailyMed, U.S. National Library of Medicine. CRESTOR (rosuvastatin) film-coated oral tablets, prescribing information, label version effective 23 September 2026. Set ID 325a5d0e-9a72-4015-9fcd-1655fb504cee.

The label approves CRESTOR to reduce the risk of major adverse cardiovascular events (cardiovascular death, nonfatal MI, nonfatal stroke or arterial revascularization) in adults at increased risk; as an adjunct to diet and exercise to lower LDL-C in adults with hypercholesterolemia, to slow progression of atherosclerosis, and in heterozygous (8 and older) and homozygous (7 and older) familial hypercholesterolemia; and as an adjunct to diet for primary dysbetalipoproteinemia and hypertriglyceridemia. Initial U.S. approval was in 2003. In a 6-week placebo-controlled study in hypercholesterolemia, LDL-C fell 45% to 63% across the four doses studied (17 to 18 patients per dose) versus 7% on placebo (13 patients). Absolute oral bioavailability is about 20%, about 10% of a dose is recovered as metabolite (mainly N-desmethyl rosuvastatin, formed by CYP2C9), 90% is excreted in feces, and elimination half-life is about 19 hours; median exposure is about 2-fold higher in Asian patients than in White controls. The label warns of myopathy and rhabdomyolysis, with risk factors including age 65 or older, uncontrolled hypothyroidism, renal impairment, certain interacting drugs and higher dosage; risk is greater at the highest labeled dose than at lower doses, and Asian patients may be at higher risk. It describes rare immune-mediated necrotizing myopathy; transaminase elevations above 3 times normal in 1.1% versus 0.5% on placebo, with rare postmarketing hepatic failure and a contraindication in acute liver failure or decompensated cirrhosis; dipstick proteinuria and microscopic hematuria, more frequent at the highest dose and generally transient; and increases in HbA1c and fasting glucose that can exceed the threshold for diagnosing diabetes.

Participants / model
Adults and children with the labeled indications; label PK participants; patients in CRESTOR trials and postmarketing reports
Treatment
CRESTOR film-coated oral tablets (rosuvastatin as rosuvastatin calcium)
Follow-up
Label version effective 23 September 2026
Study design
FDA prescribing information
Funding
not stated in the source

Label-level statements. The page does not reproduce label dosing. Asian-ancestry exposure and proteinuria stay at label level.

Read the original source
JUPITER: 17,802 healthy adults, HR 0.56, stopped at 1.9 years

Randomized controlled trial

Ridker PM et al. N Engl J Med. 2008;359(21):2195-207. PMID 18997196.

Stopped at a median 1.9 years, it found LDL cholesterol 50% lower and CRP 37% lower, and the primary composite (MI, stroke, arterial revascularization, hospitalization for unstable angina, or cardiovascular death) at 0.77 versus 1.36 per 100 person-years (HR 0.56, 95% CI 0.46 to 0.69). Death from any cause was 1.00 versus 1.25 per 100 person-years (HR 0.80, 95% CI 0.67 to 0.97). Myopathy and cancer did not increase significantly; physician-reported diabetes was more common on rosuvastatin.

Participants / model
17,802 apparently healthy men and women with LDL cholesterol below 130 mg/dL and high-sensitivity CRP of 2.0 mg/L or higher
Treatment
Oral rosuvastatin 20 mg daily or placebo
Follow-up
Stopped at a median 1.9 years
Study design
Randomized placebo-controlled trial
Funding
not stated in the source

Apparently healthy adults with raised hsCRP; the result does not address anabolic steroid users.

Read the original source
HOPE-3: 12,705 intermediate-risk adults, median 5.6 years, HR 0.76

Randomized controlled trial

Yusuf S et al. N Engl J Med. 2016;374(21):2021-31. PMID 27040132.

LDL cholesterol averaged 26.5% lower, and cardiovascular death, nonfatal MI or nonfatal stroke occurred in 3.7% versus 4.8% (HR 0.76, 95% CI 0.64 to 0.91). There was no excess of diabetes or cancer, but more cataract surgery (3.8% versus 3.1%) and muscle symptoms (5.8% versus 4.7%).

Participants / model
12,705 intermediate-risk people without cardiovascular disease in 21 countries
Treatment
Oral rosuvastatin 10 mg daily or placebo
Follow-up
Median 5.6 years
Study design
Randomized placebo-controlled trial
Funding
not stated in the source

Intermediate-risk adults followed for years; the result does not address anabolic steroid users or short use.

Read the original source
CTT meta-analysis: 26 trials, about 170,000 people, RR 0.78 per 1.0 mmol/L

Systematic review and meta-analysis

Baigent C et al. Lancet. 2010;376(9753):1670-81. PMID 21067804.

Each 1.0 mmol/L reduction in LDL cholesterol lowered major vascular events by just over a fifth (RR 0.78, 95% CI 0.76 to 0.80) and all-cause mortality by 10% (RR 0.90, 95% CI 0.87 to 0.93), with no effect on cancer incidence. Included trials had to run at least 2 years, with median follow-up of 4.8 to 5.1 years.

Participants / model
About 170,000 participants in 26 statin trials of at least 1,000 people and 2 years
Treatment
Statin versus control and more versus less intensive statin regimens
Follow-up
Included trials ran at least 2 years; median follow-up 4.8 to 5.1 years
Study design
Systematic review and individual-participant meta-analysis
Funding
not stated in the source

The benefit evidence comes from years of treatment, not cycle-length use.

Read the original source
ZETIA label, version effective 25 November 2025: ezetimibe positioned with a statin

FDA prescribing information

DailyMed, U.S. National Library of Medicine. ZETIA (ezetimibe) oral tablets, prescribing information, label version effective 25 November 2025. Set ID 174e45e0-45bb-48b7-9e60-8f6cfc1d22bb.

The label indicates ezetimibe for primary hyperlipidemia in combination with a statin, or alone when additional LDL-C-lowering therapy is not possible. The supplier's order, ezetimibe first and rosuvastatin only if ezetimibe fails, reverses the order in the ezetimibe label. In separate label trials, ezetimibe alone lowered LDL-C 18% and rosuvastatin lowered it 45% to 63% across the doses studied.

Participants / model
Adults with primary hyperlipidemia
Treatment
Oral ezetimibe; oral rosuvastatin (separate label trials)
Follow-up
Label version effective 25 November 2025
Study design
FDA prescribing information
Funding
not stated in the source

The two LDL-C figures come from separate label trials, not a head-to-head comparison.

Read the original source
Androgen cycle cohort: LDL cholesterol up 0.45 mmol/L, back to baseline 3 months after

Human study

Smit DL et al. Andrologia. 2022;54(4):e14372. PMID 35014715.

LDL cholesterol rose 0.45 mmol/L (95% CI 0.29 to 0.61) and ApoB 18.2 mg/dL during use, and both returned to baseline 3 months after the cycle. Follow-up was 1 year.

Participants / model
100 men performing a self-directed androgen cycle
Treatment
Self-administered androgens (observational); no lipid-lowering drug was tested
Follow-up
Follow-up of 1 year
Study design
Prospective cohort study
Funding
not stated in the source

The size of the steroid-related LDL change the supplier claim targets, measured in the one prospective cohort reviewed.

Read the original source
PubMed search, 9 October 2026: 20 records, none a trial or cohort of a statin in steroid users

PubMed search record

PubMed search run on 9 October 2026: (statin*[tiab] OR rosuvastatin[tiab] OR atorvastatin[tiab] OR simvastatin[tiab] OR HMG-CoA reductase inhibitor*[tiab]) AND (anabolic steroid*[tiab] OR anabolic-androgenic[tiab] OR anabolic androgenic[tiab] OR bodybuild*[tiab] OR nandrolone[tiab] OR stanozolol[tiab] OR oxandrolone[tiab] OR oxymetholone[tiab] OR methyltestosterone[tiab]). 20 records returned.

The search returned 20 records. None was a trial or cohort of a statin in anabolic steroid users. They covered tendinopathy and drug-induced cholestasis reviews, cachexia, inclusion body myositis, expectorant, androgen deficiency and renal-failure reviews, case reports (myocardial infarction in a young steroid user, clenbuterol-related MI, antibiotic-associated tendonitis), studies of steroid use in arrested substance users and Olympic athletes, analytical chemistry, a drug-induced liver injury ranking, lipid and HIV reviews, the interview study above, and a 1997 Dutch case report in which simvastatin plus gemfibrozil did not raise low HDL in a man later found to be using anabolic steroids. The ezetimibe-first sequence has no study behind it in these records.

Participants / model
Records returned, not a population
Treatment
Not applicable
Follow-up
Search run on 9 October 2026
Study design
Literature search
Funding
not stated in the source

A search result shows what PubMed returned on that date. It is not proof that no unindexed study exists.

Read the original source

Studies and sources

CRESTOR label, version effective 23 September 2026: indications, LDL-C, PK, muscle, liver, kidney, glucose

FDA prescribing information

DailyMed, U.S. National Library of Medicine. CRESTOR (rosuvastatin) film-coated oral tablets, prescribing information, label version effective 23 September 2026. Set ID 325a5d0e-9a72-4015-9fcd-1655fb504cee.

The label approves CRESTOR to reduce the risk of major adverse cardiovascular events (cardiovascular death, nonfatal MI, nonfatal stroke or arterial revascularization) in adults at increased risk; as an adjunct to diet and exercise to lower LDL-C in adults with hypercholesterolemia, to slow progression of atherosclerosis, and in heterozygous (8 and older) and homozygous (7 and older) familial hypercholesterolemia; and as an adjunct to diet for primary dysbetalipoproteinemia and hypertriglyceridemia. Initial U.S. approval was in 2003. In a 6-week placebo-controlled study in hypercholesterolemia, LDL-C fell 45% to 63% across the four doses studied (17 to 18 patients per dose) versus 7% on placebo (13 patients). Absolute oral bioavailability is about 20%, about 10% of a dose is recovered as metabolite (mainly N-desmethyl rosuvastatin, formed by CYP2C9), 90% is excreted in feces, and elimination half-life is about 19 hours; median exposure is about 2-fold higher in Asian patients than in White controls. The label warns of myopathy and rhabdomyolysis, with risk factors including age 65 or older, uncontrolled hypothyroidism, renal impairment, certain interacting drugs and higher dosage; risk is greater at the highest labeled dose than at lower doses, and Asian patients may be at higher risk. It describes rare immune-mediated necrotizing myopathy; transaminase elevations above 3 times normal in 1.1% versus 0.5% on placebo, with rare postmarketing hepatic failure and a contraindication in acute liver failure or decompensated cirrhosis; dipstick proteinuria and microscopic hematuria, more frequent at the highest dose and generally transient; and increases in HbA1c and fasting glucose that can exceed the threshold for diagnosing diabetes.

Participants / model
Adults and children with the labeled indications; label PK participants; patients in CRESTOR trials and postmarketing reports
Treatment
CRESTOR film-coated oral tablets (rosuvastatin as rosuvastatin calcium)
Follow-up
Label version effective 23 September 2026
Study design
FDA prescribing information
Funding
not stated in the source

Label-level statements. The page does not reproduce label dosing. Asian-ancestry exposure and proteinuria stay at label level.

Read the original source
Drugs@FDA: earliest generic approvals in the records returned, 19 July 2016

Regulatory record

U.S. Food and Drug Administration. Drugs@FDA application records for generic rosuvastatin calcium, ANDA 079170 and ANDA 079172. Dates read from the openFDA Drugs@FDA records.

The CRESTOR label lists initial U.S. approval in 2003. The earliest generic rosuvastatin calcium approvals among the records returned were ANDA 079170 and ANDA 079172, both on 19 July 2016. The CRESTOR NDA record was not among the records returned, so its application number and exact approval date are not established here.

Participants / model
Not a clinical population
Treatment
Drug applications
Follow-up
Approvals in 2003 and 2016
Study design
FDA application records
Funding
not stated in the source

The CRESTOR NDA number and exact approval date are not established from these records. The generic dates are the earliest among the records returned.

Read the original source
JUPITER: 17,802 healthy adults, HR 0.56, stopped at 1.9 years

Randomized controlled trial

Ridker PM et al. N Engl J Med. 2008;359(21):2195-207. PMID 18997196.

Stopped at a median 1.9 years, it found LDL cholesterol 50% lower and CRP 37% lower, and the primary composite (MI, stroke, arterial revascularization, hospitalization for unstable angina, or cardiovascular death) at 0.77 versus 1.36 per 100 person-years (HR 0.56, 95% CI 0.46 to 0.69). Death from any cause was 1.00 versus 1.25 per 100 person-years (HR 0.80, 95% CI 0.67 to 0.97). Myopathy and cancer did not increase significantly; physician-reported diabetes was more common on rosuvastatin.

Participants / model
17,802 apparently healthy men and women with LDL cholesterol below 130 mg/dL and high-sensitivity CRP of 2.0 mg/L or higher
Treatment
Oral rosuvastatin 20 mg daily or placebo
Follow-up
Stopped at a median 1.9 years
Study design
Randomized placebo-controlled trial
Funding
not stated in the source

Apparently healthy adults with raised hsCRP; the result does not address anabolic steroid users.

Read the original source
HOPE-3: 12,705 intermediate-risk adults, median 5.6 years, HR 0.76

Randomized controlled trial

Yusuf S et al. N Engl J Med. 2016;374(21):2021-31. PMID 27040132.

LDL cholesterol averaged 26.5% lower, and cardiovascular death, nonfatal MI or nonfatal stroke occurred in 3.7% versus 4.8% (HR 0.76, 95% CI 0.64 to 0.91). There was no excess of diabetes or cancer, but more cataract surgery (3.8% versus 3.1%) and muscle symptoms (5.8% versus 4.7%).

Participants / model
12,705 intermediate-risk people without cardiovascular disease in 21 countries
Treatment
Oral rosuvastatin 10 mg daily or placebo
Follow-up
Median 5.6 years
Study design
Randomized placebo-controlled trial
Funding
not stated in the source

Intermediate-risk adults followed for years; the result does not address anabolic steroid users or short use.

Read the original source
CTT meta-analysis: 26 trials, about 170,000 people, RR 0.78 per 1.0 mmol/L

Systematic review and meta-analysis

Baigent C et al. Lancet. 2010;376(9753):1670-81. PMID 21067804.

Each 1.0 mmol/L reduction in LDL cholesterol lowered major vascular events by just over a fifth (RR 0.78, 95% CI 0.76 to 0.80) and all-cause mortality by 10% (RR 0.90, 95% CI 0.87 to 0.93), with no effect on cancer incidence. Included trials had to run at least 2 years, with median follow-up of 4.8 to 5.1 years.

Participants / model
About 170,000 participants in 26 statin trials of at least 1,000 people and 2 years
Treatment
Statin versus control and more versus less intensive statin regimens
Follow-up
Included trials ran at least 2 years; median follow-up 4.8 to 5.1 years
Study design
Systematic review and individual-participant meta-analysis
Funding
not stated in the source

The benefit evidence comes from years of treatment, not cycle-length use.

Read the original source
CTT muscle meta-analysis: 27.1% on statin versus 26.6% on placebo

Systematic review and meta-analysis

Lancet. 2022;400(10355):832-845. PMID 36049498.

Muscle pain or weakness was reported by 27.1% on statin versus 26.6% on placebo (RR 1.03, 95% CI 1.01 to 1.06). In year 1 the relative increase was 7% (11 extra reports per 1,000 person-years), so only about 1 in 15 such reports on statin was due to the statin; after year 1 there was no significant excess. More intensive regimens, including rosuvastatin 20 to 40 mg, had a higher rate ratio than less intensive ones (1.08 versus 1.03). Median creatine kinase rose by about 0.02 times the upper limit of normal.

Participants / model
123,940 participants in 19 double-blind statin-versus-placebo trials and 30,724 in 4 more-versus-less-intensive trials
Treatment
Statins, including rosuvastatin 20 to 40 mg daily
Follow-up
Large long-term double-blind trials
Study design
Systematic review and individual-participant meta-analysis
Funding
not stated in the source

Class-level figures from the Cholesterol Treatment Trialists, not specific to rosuvastatin.

Read the original source
NIH LiverTox, rosuvastatin record dated 21 March 2025: mild enzyme rises, rare liver injury

Regulatory record

Rosuvastatin. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. 2012. PMID 31643932.

The record describes mild, asymptomatic, self-limited serum aminotransferase elevations during therapy and rare clinically apparent acute liver injury.

Participants / model
People treated with rosuvastatin (reference summary)
Treatment
Oral rosuvastatin
Follow-up
Record dated 21 March 2025
Study design
NIH drug-induced liver injury reference (LiverTox)
Funding
not stated in the source

Reference summary; it describes rates and case patterns, not a trial.

Read the original source
ZETIA label, version effective 25 November 2025: ezetimibe positioned with a statin

FDA prescribing information

DailyMed, U.S. National Library of Medicine. ZETIA (ezetimibe) oral tablets, prescribing information, label version effective 25 November 2025. Set ID 174e45e0-45bb-48b7-9e60-8f6cfc1d22bb.

The label indicates ezetimibe for primary hyperlipidemia in combination with a statin, or alone when additional LDL-C-lowering therapy is not possible. The supplier's order, ezetimibe first and rosuvastatin only if ezetimibe fails, reverses the order in the ezetimibe label. In separate label trials, ezetimibe alone lowered LDL-C 18% and rosuvastatin lowered it 45% to 63% across the doses studied.

Participants / model
Adults with primary hyperlipidemia
Treatment
Oral ezetimibe; oral rosuvastatin (separate label trials)
Follow-up
Label version effective 25 November 2025
Study design
FDA prescribing information
Funding
not stated in the source

The two LDL-C figures come from separate label trials, not a head-to-head comparison.

Read the original source
Androgen cycle cohort: LDL cholesterol up 0.45 mmol/L, back to baseline 3 months after

Human study

Smit DL et al. Andrologia. 2022;54(4):e14372. PMID 35014715.

LDL cholesterol rose 0.45 mmol/L (95% CI 0.29 to 0.61) and ApoB 18.2 mg/dL during use, and both returned to baseline 3 months after the cycle. Follow-up was 1 year.

Participants / model
100 men performing a self-directed androgen cycle
Treatment
Self-administered androgens (observational); no lipid-lowering drug was tested
Follow-up
Follow-up of 1 year
Study design
Prospective cohort study
Funding
not stated in the source

The size of the steroid-related LDL change the supplier claim targets, measured in the one prospective cohort reviewed.

Read the original source
Interview study: men using steroids described taking statins and ARBs without a prescription

Human study

Kutscher E et al. Harm Reduct J. 2024;21(1):196. PMID 39523302.

Participants described avoiding oral steroids, self-directed lab testing that included cholesterol, and taking medicines without a prescription, statins and angiotensin receptor blockers among them. The authors call for research on each intervention.

Participants / model
Men using anabolic steroids for 8 weeks or more in New York City and online; thematic saturation at 12 interviews
Treatment
Not applicable (self-reported practices)
Follow-up
Interviews, not a treatment period
Study design
Qualitative interview study
Funding
not stated in the source

Documents a use pattern; it measured no outcome.

Read the original source
PubChem: rosuvastatin and rosuvastatin calcium identity

Chemical identity record

National Library of Medicine. PubChem compound records CID 446157 (rosuvastatin) and CID 5282455 (rosuvastatin calcium).

Rosuvastatin free acid: C22H28FN3O6S, 481.5 g/mol, CAS 287714-41-4 (PubChem also lists 1354641-88-5 as a synonym). Rosuvastatin calcium, the salt in CRESTOR: CID 5282455, C44H54CaF2N6O12S2, 1001.1 g/mol, CAS 147098-20-2; the label gives (C22H27FN3O6S)2Ca and 1,001.14. Label strengths are stated as rosuvastatin.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule and salt
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

Identity record only; it says nothing about efficacy or safety.

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Why is Rosuvastatin in S tier?

S fits an approved statin with outcome trials in 17,802 and 12,705 people without cardiovascular disease, class-level meta-analysis data from about 170,000 people, and more than two decades of use. The grade covers the approved uses. It does not extend to the supplier's ezetimibe-first sequence for steroid-related LDL, which no trial tested.