Rosuvastatin, sold as Crestor and as generics, is a statin: a drug that blocks HMG-CoA reductase, the enzyme that controls the liver’s own cholesterol production. The FDA approved it in August 2003 (Drugs@FDA). It is one of the strongest statins by milligram, lowering LDL cholesterol (the “bad” cholesterol that builds up in artery walls) by about 45–63% across the labeled 5–40 mg dose range.

Its best-known trial, JUPITER, gave rosuvastatin 20 mg/day to 17,802 healthy adults without high LDL and cut major cardiovascular events by 44%. Rosuvastatin is discussed in anabolic steroid circles because androgens, especially oral ones, lower HDL and raise LDL. No trial has tested rosuvastatin specifically in people using anabolic steroids.

This page summarizes what the FDA label, the major clinical trials and published studies of steroid users report. It is for education only and is not medical advice.

Property	Detail
Drug class	HMG-CoA reductase inhibitor (statin)
Brand / approval	Crestor (AstraZeneca), NDA 021366, approved August 12, 2003; AB-rated generics
Route	Oral tablet, once daily, with or without food, any time of day
Strengths	5, 10, 20 and 40 mg
Labeled adult dose	5–40 mg once daily; start at 5 mg in Asian patients and in severe kidney impairment
Half-life (label)	About 19 h
Metabolism	Minimal (about 10% of a dose); mainly CYP2C9, not CYP3A4
Key transporters	OATP1B1 (liver uptake) and BCRP; the basis of most serious interactions
US status	Prescription only
WADA status	Not named on the WADA 2026 Prohibited List

What it is

Rosuvastatin is a statin licensed from Shionogi of Japan, and is supplied as rosuvastatin calcium (FDA label). The label describes it as hydrophilic (water-loving), with an octanol/water partition coefficient of 0.13 at pH 7.0. The tablet strengths refer to rosuvastatin itself: a 10 mg tablet contains 10.4 mg of the calcium salt.

It works in two steps:

it inhibits HMG-CoA reductase, the rate-limiting enzyme that turns HMG-CoA into mevalonate, an early building block of cholesterol;
the liver responds to its lower cholesterol supply by making more LDL receptors, which pull LDL particles out of the blood.

The label states that the maximum LDL drop is usually reached by 4 weeks and holds after that.

Pharmacokinetics

From the current Crestor label (FDA label):

Parameter	Value
Time to peak level	3–5 h after an oral dose
Absolute bioavailability	About 20%
Effect of food or dosing time	None on total exposure (AUC)
Plasma protein binding	88%, mostly albumin
Volume of distribution	About 134 L
Metabolism	About 10% of a dose; main metabolite N-desmethyl rosuvastatin (via CYP2C9)
Excretion	About 90% in feces
Elimination half-life	About 19 h

Because rosuvastatin barely uses CYP3A4, it avoids many of the interactions seen with statins that do (the label notes that ketoconazole, itraconazole and erythromycin change its exposure little). Its weak point is instead the liver uptake transporter OATP1B1 and the efflux transporter BCRP. Drugs that block these transporters can raise rosuvastatin levels several-fold (see Interactions below).

Kidney and liver impairment

Severe kidney impairment (creatinine clearance under 30 mL/min/1.73 m², not on dialysis): blood levels about 3 times higher. Mild to moderate impairment has no effect.
Hemodialysis: steady-state levels about 50% higher.
Liver disease: in Child-Pugh B disease, peak level doubled and AUC rose 21%.

Asian ancestry

The label reports an approximately 2-fold higher median exposure (AUC and peak level) in Asian subjects than in White controls, including in a US study. For this reason it recommends starting Asian patients at 5 mg and weighing risks and benefits if LDL is not controlled at doses up to 20 mg (FDA label).

A single-dose (40 mg) study in Singapore compared groups living in the same environment (Lee et al., Clin Pharmacol Ther 2005):

Group (n)	AUC ratio vs White subjects	Peak level ratio vs White subjects
Chinese (36)	2.31	2.36
Malay (35)	1.91	2.00
Asian-Indian (35)	1.63	1.68

Variants in SLCO1B1, the gene for OATP1B1, did not explain these differences. The label separately notes that the rare SLCO1B1 521 C/C genotype (generally under 5% of most groups) has been linked to higher rosuvastatin levels in very small groups of patients.

Approved medical use

The FDA label covers the following uses (FDA label):

reducing the risk of major cardiovascular events (cardiovascular death, nonfatal heart attack, nonfatal stroke or arterial revascularization) in adults at increased risk;
lowering LDL cholesterol, alongside diet and exercise, in adults with hypercholesterolemia;
slowing the progression of atherosclerosis in adults;
heterozygous familial hypercholesterolemia (HeFH) in adults and children 8 years and older;
homozygous familial hypercholesterolemia (HoFH) in adults and children 7 years and older;
primary dysbetalipoproteinemia and hypertriglyceridemia in adults, alongside diet.

Population	Labeled dose
Adults	5–40 mg once daily, based on indication, LDL and cardiovascular risk
Asian patients	Start at 5 mg once daily
Severe kidney impairment, not on dialysis	Start at 5 mg; do not exceed 10 mg once daily
Children with HeFH, 8 to under 10 years	5–10 mg once daily
Children with HeFH, 10 years and older	5–20 mg once daily
Children with HoFH, 7 years and older	20 mg once daily

The label advises checking LDL as early as 4 weeks after starting, and taking rosuvastatin at least 2 hours before an aluminum and magnesium hydroxide antacid.

What the research shows

LDL lowering by dose

In a 6-week placebo-controlled trial in adults with high cholesterol, the label reports these mean changes from baseline (FDA label):

Daily dose	n	LDL-C	Non-HDL-C	ApoB	Triglycerides	HDL-C
Placebo	13	−7%	−7%	−3%	−3%	+3%
5 mg	17	−45%	−44%	−38%	−35%	+13%
10 mg	17	−52%	−48%	−42%	−10%	+14%
20 mg	17	−55%	−51%	−46%	−23%	+8%
40 mg	18	−63%	−60%	−54%	−28%	+10%

The pattern is typical for statins: the first dose step gives most of the effect, and each doubling adds only a few percentage points. HDL rose modestly, by 8–14%, with no clear dose trend.

Compared with other statins

In a 6-week open-label trial of 2,240 adults (mean baseline LDL 189 mg/dL), the label reports these LDL reductions by dose:

Daily dose	Rosuvastatin	Atorvastatin	Simvastatin	Pravastatin
10 mg	−46%	−37%	−28%	−20%
20 mg	−52%	−43%	−35%	−24%
40 mg	−55%	−48%	−39%	−30%
80 mg	Not studied	−51%	−46%	Not studied

For the most commonly compared alternative, see atorvastatin (Lipitor). Rosuvastatin 10 mg lowered LDL significantly more than atorvastatin 10 mg, and 20 mg more than atorvastatin 20 and 40 mg (p under 0.002). In adults with HeFH, rosuvastatin 40 mg lowered LDL by 55%, against 52% for atorvastatin 80 mg.

JUPITER: primary prevention with normal LDL

JUPITER randomized 17,802 apparently healthy men (50 and older) and women (60 and older) to rosuvastatin 20 mg/day or placebo. To enter, they had to have LDL under 130 mg/dL and high-sensitivity C-reactive protein (hsCRP, a blood marker of inflammation) of 2 mg/L or more. The trial was stopped early for benefit after a median 1.9 years (Ridker et al., NEJM 2008):

Outcome	Rosuvastatin vs placebo
LDL cholesterol	−50%
hsCRP	−37%
Primary end point (heart attack, stroke, revascularization, unstable angina or CV death)	HR 0.56 (95% CI 0.46–0.69)
Heart attack	HR 0.46 (95% CI 0.30–0.70)
Stroke	HR 0.52 (95% CI 0.34–0.79)
Death from any cause	HR 0.80 (95% CI 0.67–0.97)

In absolute terms, the label counts 142 primary events on rosuvastatin against 252 on placebo, an absolute risk reduction of 1.2% over about 2 years. The label also notes a post-hoc limit: in participants (725 on rosuvastatin, 680 on placebo) whose only risk factors were age and high hsCRP, there was no significant benefit.

HOPE-3: intermediate-risk adults, lower dose

HOPE-3 randomized 12,705 people in 21 countries without cardiovascular disease, at intermediate risk, to rosuvastatin 10 mg/day or placebo for a median 5.6 years (Yusuf et al., NEJM 2016). LDL was 26.5% lower on rosuvastatin on average. Cardiovascular death, heart attack or stroke occurred in 3.7% vs 4.8% (HR 0.76, 95% CI 0.64–0.91). The benefit was consistent across race and ethnic groups.

METEOR: slowing artery wall thickening

METEOR randomized 984 low-risk adults with elevated LDL and early carotid thickening to rosuvastatin 40 mg or placebo for 2 years (FDA label). Carotid intima-media thickness (the thickness of the artery wall on ultrasound) grew by 0.0131 mm/year on placebo and did not change significantly on rosuvastatin (−0.0014 mm/year). This trial is the basis of the label’s “slow the progression of atherosclerosis” indication.

Androgen use reliably shifts blood lipids in an unfavorable direction. The studies that measured this report:

Study	Design	Main lipid findings
Hartgens et al., Br J Sports Med 2004	19 strength athletes self-administering several AAS for 8 or 14 weeks, vs 16 non-users	HDL fell from 1.08 to 0.43 mmol/L (≈42 to 17 mg/dL); ApoB rose from 0.96 to 1.32 g/L; Lp(a) fell. Not back to baseline 6 weeks after stopping
Same paper, randomized arm	16 bodybuilders, nandrolone decanoate 200 mg/week vs placebo, 8 weeks	No change in total cholesterol, HDL, ApoA1 or ApoB; Lp(a) fell
Smit et al., Andrologia 2022 (HAARLEM)	Prospective cohort, 100 men doing a self-chosen androgen cycle	LDL +0.45 mmol/L (≈ +17 mg/dL); ApoB +18.2 mg/dL; HDL −0.40 mmol/L (≈ −15 mg/dL); values back to baseline 3 months after the cycle
Bhasin et al., Am J Physiol 2001	61 young men, testosterone enanthate 25–600 mg/week for 20 weeks	HDL change was negatively correlated with testosterone levels (higher dose, lower HDL)

A 2026 narrative review from the HAARLEM group adds context (Bond et al., Clin Cardiol 2026):

oral androgens are consistently linked to strong HDL suppression and LDL increases, while injectable testosterone and nandrolone at studied doses generally leave LDL unchanged;
the HDL drop is generally attributed to higher hepatic lipase activity, though the mechanism is not fully clear;
the authors argue that androgen use should count as a cardiovascular risk-enhancing factor in young men.

The review names statins as first-line drug treatment when treatment is indicated. It mentions low-dose hydrophilic statins such as rosuvastatin because of a “purported” lower rate of muscle complaints. That is expert opinion.

What has not been studied. We found no randomized or controlled study of rosuvastatin, or any statin, in people using anabolic steroids. It is not known how well rosuvastatin offsets steroid-induced lipid changes, or whether doing so changes cardiovascular outcomes in this group. Rosuvastatin mainly lowers LDL and ApoB. In the label’s dose trial it raised HDL by only 8–14%, while the Bond review reports an HDL fall of about 33% during cycles in the HAARLEM cohort.

For steroid-specific details, see Anavar (oxandrolone), Winstrol (stanozolol) and testosterone cypionate.

Side effects and risks

Common side effects

In placebo-controlled trials of up to 12 weeks, the label lists headache, nausea, myalgia (muscle pain), asthenia (weakness) and constipation as the reactions seen in 2% or more of patients (FDA label). In JUPITER, the rates over about 2 years were:

Reaction	Placebo (n=8,901)	Rosuvastatin 20 mg (n=8,901)
Myalgia	6.6%	7.6%
Arthralgia (joint pain)	3.2%	3.8%
Constipation	3.0%	3.3%
Diabetes mellitus	2.3%	2.8%
Nausea	2.3%	2.4%

Muscle: myopathy and rhabdomyolysis

The label warns of myopathy (muscle pain, tenderness or weakness with raised creatine kinase, CK) and, rarely, rhabdomyolysis, a breakdown of muscle that can cause kidney failure (FDA label). Risk factors named on the label:

age 65 or older;
uncontrolled hypothyroidism;
kidney impairment;
certain other drugs, including other lipid-lowering drugs;
higher dose: risk is greater at 40 mg than at lower doses;
Asian ancestry.

The label says to stop rosuvastatin if CK is markedly raised or myopathy is suspected, and to pause it during acute conditions that raise the risk of kidney failure from muscle breakdown, such as sepsis, major surgery or trauma. It also describes rare immune-mediated necrotizing myopathy, an autoimmune muscle disease that persists after the statin is stopped.

How often statins really cause muscle symptoms was tested in an individual-patient meta-analysis of 19 placebo-controlled trials with 123,940 participants (CTT Collaboration, Lancet 2022):

muscle pain or weakness was reported by 27.1% on statins vs 26.6% on placebo (RR 1.03, 95% CI 1.01–1.06);
the small excess was mostly in year 1, and the authors estimated that over 90% of muscle complaints on statins were not caused by the statin;
high-intensity regimens (including rosuvastatin 20–40 mg) had a slightly higher rate ratio, 1.08 (95% CI 1.04–1.13).

In HOPE-3, muscle symptoms occurred in 5.8% on rosuvastatin 10 mg vs 4.7% on placebo (Yusuf et al., NEJM 2016).

Kidney: proteinuria and hematuria

The label reports dipstick-positive proteinuria (protein in the urine) and microscopic hematuria (blood in the urine) in the trial program (FDA label). They were more frequent at 40 mg than at lower doses or with other statins, and were generally transient and not linked to worsening kidney function. The clinical significance is unknown; the label suggests considering a lower dose if unexplained proteinuria or hematuria persists.

Blood sugar and diabetes

The label warns that statins, including rosuvastatin, can raise HbA1c and fasting glucose, in some cases past the threshold for diabetes (FDA label). In JUPITER, mean HbA1c rose by 0.1% more on rosuvastatin than placebo.

Analysis	Finding
Sattar et al., Lancet 2010: 13 statin trials, 91,140 people	9% higher risk of new diabetes (OR 1.09, 95% CI 1.02–1.17); about 1 extra case per 255 people treated for 4 years
Ridker et al., Lancet 2012: JUPITER, 1 or more diabetes risk factors (n=11,508)	Diabetes HR 1.28 (95% CI 1.07–1.54); 134 vascular events or deaths avoided for every 54 new diabetes cases
Same analysis, no diabetes risk factors (n=6,095)	No increase in diabetes (HR 0.99, 95% CI 0.45–2.21)

In JUPITER, rosuvastatin brought forward the diagnosis of diabetes by an average of 5.4 weeks. The diabetes risk factors were metabolic syndrome, impaired fasting glucose, BMI of 30 or higher, or HbA1c over 6%.

Liver

In pooled placebo-controlled trials, transaminases (liver enzymes) rose above 3 times the upper limit of normal in 1.1% on rosuvastatin vs 0.5% on placebo (FDA label). Most rises were early, transient and without symptoms. Rare fatal and non-fatal liver failure has been reported after approval. The label recommends considering liver tests before starting and as clinically indicated. Heavy alcohol use or a history of liver disease may raise the risk. Oral 17α-alkylated steroids are separately linked to liver injury (see the Anavar page); we found no study of how they combine with rosuvastatin.

Other reported effects

Reports collected after approval include thrombocytopenia (low platelets), peripheral neuropathy, interstitial lung disease, depression, sleep disorders, gynecomastia (male breast enlargement), and rare reversible memory problems reported with all statins (FDA label). Their frequency cannot be estimated from these voluntary reports.

Who should not take it

The label contraindicates rosuvastatin in:

acute liver failure or decompensated cirrhosis;
hypersensitivity to rosuvastatin or the tablet ingredients.

It also advises stopping rosuvastatin when pregnancy is recognized (it may cause fetal harm based on its mechanism), and says breastfeeding is not recommended during treatment.

Interactions

Most serious interactions raise rosuvastatin levels by blocking OATP1B1 or BCRP. The label sets these dose limits (FDA label):

Other drug	Rise in rosuvastatin exposure (AUC)	Label instruction
Sofosbuvir/velpatasvir/voxilaprevir; ledipasvir/sofosbuvir	7.39-fold (first combination)	Avoid
Gemfibrozil	About 1.9-fold	Avoid; if unavoidable, start at 5 mg, max 10 mg
Tafamidis	1.97-fold	Avoid; if unavoidable, start at 5 mg, max 20 mg
Cyclosporine	7.1-fold	Max 5 mg
Darolutamide	5.2-fold	Max 5 mg
Belumosudil	4.62-fold	Max 5 mg
Vadadustat	2.47-fold	Max 5 mg
Atazanavir/ritonavir, lopinavir/ritonavir and several hepatitis C antivirals	2.1–3.1-fold for the HIV combinations	Start at 5 mg, max 10 mg
Capmatinib, enasidenib, momelotinib, regorafenib, teriflunomide	About 2.1–3.8-fold	Max 10 mg
Ticagrelor, febuxostat, fostamatinib	About 1.9–2.3-fold	Max 20 mg

Other interactions on the label:

Fenofibrate, colchicine and niacin (1 g/day or more): no large level change, but added muscle risk; the label asks prescribers to weigh benefit against risk and monitor for myopathy.
Aluminum and magnesium hydroxide antacids: halved rosuvastatin exposure when taken together; taking rosuvastatin 2 hours earlier reduced the drop to about 20%.
Warfarin: rosuvastatin significantly raised the INR (a clotting measure); the label calls for INR checks when starting, changing or stopping it.
Ezetimibe: no meaningful change in rosuvastatin exposure (AUC ratio 1.2).
Oral contraceptives: ethinyl estradiol and norgestrel exposure rose by about 30%.

The label does not list testosterone or other anabolic steroids among its interactions.

Key takeaways

A potent, mostly unmetabolized statin. Rosuvastatin lowers LDL by about 45% at 5 mg and 63% at 40 mg, with a 19-hour half-life and little CYP3A4 involvement.
Strong outcome evidence. JUPITER (20 mg) cut major cardiovascular events by 44% in people with normal LDL and high hsCRP; HOPE-3 (10 mg) lowered them in intermediate-risk adults (HR 0.76).
Asian ancestry doubles exposure. The label starts Asian patients at 5 mg and asks prescribers to weigh risks above 20 mg.
Known costs. Muscle risk rises at 40 mg and with interacting drugs; proteinuria is more common at 40 mg; diabetes risk rises slightly, mainly in people who already have diabetes risk factors.
Steroid users: no direct trials. Androgen cycles raise LDL and ApoB and sharply lower HDL. Rosuvastatin targets the LDL side, but it has not been studied in steroid users.

Sources

AstraZeneca. Crestor (rosuvastatin) tablets, prescribing information, revised 09/2026. DailyMed.
Food and Drug Administration. Drugs@FDA: Crestor, NDA 021366. FDA.
Lee E, Ryan S, Birmingham B, et al. Rosuvastatin pharmacokinetics and pharmacogenetics in white and Asian subjects residing in the same environment. Clin Pharmacol Ther. 2005;78(4):330–341. PubMed.
Ridker PM, Danielson E, Fonseca FA, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008;359(21):2195–2207. PubMed.
Ridker PM, Pradhan A, MacFadyen JG, Libby P, Glynn RJ. Cardiovascular benefits and diabetes risks of statin therapy in primary prevention: an analysis from the JUPITER trial. Lancet. 2012;380(9841):565–571. PubMed.
Yusuf S, Bosch J, Dagenais G, et al. Cholesterol lowering in intermediate-risk persons without cardiovascular disease. N Engl J Med. 2016;374(21):2021–2031. PubMed.
Cholesterol Treatment Trialists’ Collaboration. Effect of statin therapy on muscle symptoms: an individual participant data meta-analysis of large-scale, randomised, double-blind trials. Lancet. 2022;400(10355):832–845. PubMed.
Sattar N, Preiss D, Murray HM, et al. Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. Lancet. 2010;375(9716):735–742. PubMed.
Hartgens F, Rietjens G, Keizer HA, Kuipers H, Wolffenbuttel BH. Effects of androgenic-anabolic steroids on apolipoproteins and lipoprotein (a). Br J Sports Med. 2004;38(3):253–259. PubMed.
Smit DL, Grefhorst A, Buijs MM, et al. Prospective study on blood pressure, lipid metabolism and erythrocytosis during and after androgen abuse. Andrologia. 2022;54(4):e14372. PubMed.
Bhasin S, Woodhouse L, Casaburi R, et al. Testosterone dose-response relationships in healthy young men. Am J Physiol Endocrinol Metab. 2001;281(6):E1172–E1181. PubMed.
Bond P, Smit DL, Verdegaal T, de Ronde W. Preventing atherosclerotic cardiovascular disease in young male androgen abusers. Clin Cardiol. 2026;49(2):e70257. PubMed; PMC.
World Anti-Doping Agency. The 2026 Prohibited List. WADA 2026 Prohibited List.

Rosuvastatin (Crestor)