crestor
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| Product dosage: 20mg | |||
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| Product dosage: 5mg | |||
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Synonyms | |||
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Crestor, known generically as rosuvastatin calcium, is a synthetic lipid-lowering agent belonging to the statin class of medications. Marketed globally by AstraZeneca, this HMG-CoA reductase inhibitor represents one of the most potent prescription medications available for managing dyslipidemia. Unlike many dietary supplements that make vague health claims, Crestor’s mechanism, efficacy, and safety profile have been rigorously evaluated through extensive clinical trials and real-world use spanning decades.
Crestor: Potent LDL-C Reduction for Cardiovascular Risk Management - Evidence-Based Review
1. Introduction: What is Crestor? Its Role in Modern Medicine
Crestor occupies a critical position in contemporary cardiology practice as a third-generation statin with demonstrated efficacy in both primary and secondary prevention of atherosclerotic cardiovascular disease (ASCVD). What is Crestor used for? Primarily, it’s indicated for managing hypercholesterolemia and mixed dyslipidemia when lifestyle modifications alone prove insufficient. The medication’s significance stems from its ability to achieve substantial LDL-C reductions—often exceeding 50% at higher doses—which translates directly into reduced cardiovascular morbidity and mortality.
Unlike earlier statins, Crestor’s molecular structure includes a polar methane-sulfonamide group that enhances hepatoselectivity while minimizing systemic exposure. This characteristic contributes to both its potency and generally favorable side effect profile, though like all statins, it requires appropriate patient selection and monitoring.
2. Key Components and Bioavailability Crestor
The active pharmaceutical ingredient in Crestor is rosuvastatin calcium in crystalline form. The standard tablet composition includes:
- Rosuvastatin calcium (equivalent to 5, 10, 20, or 40 mg rosuvastatin)
- Microcrystalline cellulose
- Lactose monohydrate
- Tribasic calcium phosphate
- Crospovidone
- Magnesium stearate
- Hyprolose
- Triacetin
- Titanium dioxide
- Yellow ferric oxide (10 mg and 20 mg tablets)
- Red ferric oxide (20 mg tablets)
Bioavailability of Crestor is approximately 20%, with peak plasma concentrations occurring 3-5 hours post-administration. Unlike some supplements that require special formulations for absorption, rosuvastatin doesn’t require additional compounds for bioavailability enhancement. The medication demonstrates minimal metabolism via cytochrome P450 2C9, reducing its potential for drug interactions compared to other statins metabolized through CYP3A4.
3. Mechanism of Action Crestor: Scientific Substantiation
Understanding how Crestor works requires examining the cholesterol synthesis pathway. Rosuvastatin competitively inhibits HMG-CoA reductase, the enzyme that catalyzes the conversion of HMG-CoA to mevalonate—the rate-limiting step in hepatic cholesterol synthesis. This inhibition creates a cascade of effects:
The liver responds to decreased intracellular cholesterol concentrations by upregulating LDL receptors on hepatocyte surfaces. These additional receptors clear circulating LDL particles more efficiently, resulting in substantial reductions in LDL-C levels—typically 45-63% depending on dose.
Beyond LDL reduction, Crestor demonstrates pleiotropic effects including:
- Moderate HDL-C increases (8-14%)
- Triglyceride reductions (10-35%)
- Anti-inflammatory properties (evidenced by hs-CRP reduction)
- Endothelial function improvement
- Plaque stabilization potential
The scientific research supporting these mechanisms spans thousands of publications, with particular emphasis on the JUPITER trial which demonstrated significant cardiovascular risk reduction in patients with elevated hs-CRP but normal LDL levels.
4. Indications for Use: What is Crestor Effective For?
Crestor for Primary Hypercholesterolemia
As first-line therapy for elevated LDL-C, Crestor demonstrates dose-dependent efficacy across diverse patient populations. The 5-40 mg dosing range allows tailored treatment based on baseline levels and target goals.
Crestor for Mixed Dyslipidemia
Patients with combined lipid abnormalities—elevated LDL-C, elevated triglycerides, and low HDL-C—often respond well to rosuvastatin’s comprehensive lipid-modifying effects.
Crestor for Primary Prevention of Cardiovascular Events
The JUPITER trial established Crestor’s role in primary prevention, showing 44% relative risk reduction in major cardiovascular events among patients with LDL <130 mg/dL but elevated hs-CRP (>2.0 mg/L).
Crestor for Secondary Prevention in Established ASCVD
For patients with known cardiovascular disease, Crestor reduces the risk of recurrent events, including myocardial infarction, stroke, and revascularization procedures.
Crestor for Pediatric Patients with Heterozygous Familial Hypercholesterolemia
Approved for children 8 years and older with HeFH, Crestor provides early intervention to prevent premature cardiovascular complications.
5. Instructions for Use: Dosage and Course of Administration
Crestor dosing should be individualized based on treatment indication, baseline LDL-C, goal LDL-C, and patient-specific factors. The usual starting dose is 10-20 mg once daily, with adjustment after 2-4 weeks based on response.
| Indication | Starting Dose | Maximum Dose | Administration |
|---|---|---|---|
| Primary prevention | 10-20 mg daily | 40 mg daily | With or without food, same time each day |
| Secondary prevention | 20 mg daily | 40 mg daily | Evening administration may provide slight additional benefit |
| Severe hypercholesterolemia | 20 mg daily | 40 mg daily | Consider split dosing for 40 mg if not tolerated |
| Asian patients | 5 mg daily | 20 mg daily | Increased systemic exposure in Asian populations |
Patients should undergo liver function tests before initiation and periodically thereafter. The course of administration is typically long-term, as discontinuation leads to return to baseline lipid levels within 2-4 weeks.
6. Contraindications and Drug Interactions Crestor
Absolute Contraindications:
- Active liver disease or unexplained persistent elevations in hepatic transaminases
- Pregnancy and breastfeeding (Category X)
- Concomitant use with cyclosporine
Relative Contraindications:
- History of statin intolerance
- Asian ancestry (requires lower starting dose)
- Severe renal impairment (CrCl <30 mL/min)
- Concomitant use with gemfibrozil
Significant Drug Interactions:
- Gemfibrozil: Increases rosuvastatin exposure approximately twofold
- Antacids: Administration simultaneously decreases absorption; separate by 2 hours
- Warfarin: May potentiate anticoagulant effect; monitor INR closely
- Protease inhibitors: Some may increase rosuvastatin concentrations
Regarding safety during pregnancy, Crestor is absolutely contraindicated as cholesterol synthesis is crucial for fetal development. Women of childbearing potential should use effective contraception while taking rosuvastatin.
7. Clinical Studies and Evidence Base Crestor
The evidence base for Crestor spans numerous landmark trials:
JUPITER Trial (2008): 17,802 patients with LDL <130 mg/dL and hs-CRP >2.0 mg/L randomized to rosuvastatin 20 mg or placebo. The trial was stopped early due to dramatic benefit—44% reduction in primary endpoint (myocardial infarction, stroke, arterial revascularization, hospitalization for unstable angina, or death from cardiovascular causes).
ASTEROID Trial (2006): Demonstrated regression of coronary atherosclerosis with IVUS following 24 months of rosuvastatin 40 mg daily.
METEOR Trial (2007): Showed halted progression of carotid intima-media thickness in patients with subclinical atherosclerosis and mild to moderate hypercholesterolemia.
CORONA and GISSI-HF Trials: Explored statin therapy in heart failure populations, with mixed results that helped refine appropriate patient selection.
The scientific evidence consistently supports Crestor’s effectiveness in appropriate patient populations, with real-world studies confirming the randomized trial findings.
8. Comparing Crestor with Similar Products and Choosing a Quality Product
When comparing Crestor with similar statins, several distinctions emerge:
Versus Atorvastatin: Crestor typically provides greater LDL-C reduction milligram-per-milligram, though clinical outcomes are comparable at equivalent LDL reduction.
Versus Simvastatin: Crestor demonstrates more predictable metabolism with fewer drug interactions and generally better tolerability.
Versus Pravastatin: Crestor provides substantially greater potency, making it preferable when aggressive LDL lowering is required.
For patients wondering which statin is better, the answer depends on individual factors including required LDL reduction, concomitant medications, comorbidities, and cost considerations. How to choose involves shared decision-making between patient and clinician.
All prescription Crestor products undergo rigorous quality control, unlike some dietary supplements that may have variability in composition and purity.
9. Frequently Asked Questions (FAQ) about Crestor
What is the recommended course of Crestor to achieve results?
Lipid lowering begins within 1 week, with maximal effect at 2-4 weeks. Cardiovascular risk reduction requires long-term therapy, typically lifelong unless contraindications develop.
Can Crestor be combined with other cholesterol medications?
Yes, often combined with ezetimibe for additional LDL reduction, or with fenofibrate in mixed dyslipidemia with high triglycerides, though gemfibrozil should be avoided.
Does Crestor cause weight gain?
No, statins don’t typically cause weight gain, though some patients may reduce physical activity if cholesterol improvement creates false security about lifestyle.
How long do Crestor side effects take to appear?
Muscle symptoms typically appear within weeks to months, while rare serious side effects like rhabdomyolysis can occur at any time during treatment.
Can Crestor be taken intermittently to reduce side effects?
No, consistent daily dosing is necessary for maintained lipid lowering and cardiovascular protection.
10. Conclusion: Validity of Crestor Use in Clinical Practice
The risk-benefit profile of Crestor strongly supports its use in appropriate patient populations. For individuals with elevated cardiovascular risk—whether from established disease or multiple risk factors—rosuvastatin provides proven reduction in major adverse cardiovascular events. The validity of Crestor use in clinical practice is well-established through extensive evidence spanning basic science, clinical trials, and real-world experience.
I remember when we first started using rosuvastatin back in 2003—some of the senior cardiologists were skeptical about whether we really needed another statin. We’d been using atorvastatin pretty successfully, and the idea of switching to something new made the pharmacy committee nervous about costs. But then the early data started coming in from the ASTEROID trial, showing actual plaque regression, which was something we hadn’t really seen before.
There was this one patient, Margaret, 62-year-old schoolteacher with strong family history—her brother had his first MI at 48. She’d been on simvastatin 40 for years but still had LDL hanging around 130. We switched her to rosuvastatin 20, and within 6 weeks her LDL dropped to 68. More importantly, her carotid ultrasound showed stabilized plaque after 18 months. She’s now 78, still on the same dose, still teaching part-time, and hasn’t had a single cardiovascular event.
We did have some early struggles with the higher doses—the 40mg particularly. Had a construction worker, early 50s, who developed significant myalgia at that dose. We backed down to 20mg and added ezetimibe, got his LDL to 55 without the muscle symptoms. That experience taught me that sometimes the maximum tolerated dose isn’t the maximum approved dose.
The diabetes risk discussion was another learning curve. When the JUPITER data came out about increased diabetes incidence, we had several internal debates about whether we were trading cardiovascular protection for metabolic problems. Over time, we realized the absolute risk was small and the CV benefit substantial, but it did change how we monitor patients—now we check fasting glucose more regularly in prediabetic patients starting statins.
What surprised me most was the inflammation modulation. Had a rheumatoid arthritis patient whose rheumatologist commented that her inflammatory markers improved after starting rosuvastatin for cholesterol. Not something we typically think about, but the pleiotropic effects are real.
Follow-up on our long-term rosuvastatin patients has been revealing—the adherence is better than with some other statins, possibly because the efficacy is more noticeable on lipid panels. One of my patients, retired engineer who tracks everything, showed me his spreadsheet comparing his lipid responses to different statins over 15 years—rosuvastatin gave him the most consistent results with least variability.
The real testament came from Henry, early 70s with multivessel disease who’d refused statins for years because of “bad experience” with another medication. Finally agreed to try rosuvastatin 5mg, worked up to 10mg. At his last visit, he told me, “Doc, I wish I hadn’t been so stubborn earlier. I feel better than I have in years, and my numbers are the best they’ve ever been.” Those are the cases that remind you why evidence-based medicine matters.