crestor
| Product dosage: 10mg | |||
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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, Crestor undergoes rigorous pharmaceutical manufacturing processes and requires physician supervision due to its potent systemic effects and potential side effect profile.
## 1. Introduction: What is Crestor? Its Role in Modern Medicine
Crestor (rosuvastatin) is a prescription medication classified as a statin, specifically developed to address elevated cholesterol levels and associated cardiovascular risks. What is Crestor used for? Primarily, it’s indicated for the reduction of elevated total cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglycerides while increasing high-density lipoprotein cholesterol (HDL-C) in patients with primary hyperlipidemia and mixed dyslipidemia. The significance of Crestor in modern therapeutics lies in its demonstrated ability to significantly reduce major adverse cardiovascular events, including myocardial infarction and stroke, particularly in high-risk patient populations. The medical applications extend beyond simple cholesterol management to comprehensive cardiovascular risk reduction strategies.
## 2. Key Components and Bioavailability Crestor
The composition of Crestor centers around its active pharmaceutical ingredient, rosuvastatin calcium, formulated with carefully selected excipients to ensure stability and consistent delivery. Each tablet contains microcrystalline cellulose, lactose monohydrate, tribasic calcium phosphate, crospovidone, magnesium stearate, hyprolose, triacetin, titanium dioxide, and yellow ferric oxide (in specific strengths). The release form is an immediate-release tablet designed for once-daily oral administration.
Bioavailability of Crestor demonstrates approximately 20% absorption following oral dosing, with peak plasma concentrations achieved within 3-5 hours. The absolute bioavailability reaches about 20%, which is noteworthy compared to other statins. Food doesn’t significantly affect absorption, though we typically recommend consistent timing relative to meals for patient adherence. The specific calcium salt formulation enhances stability and predictable absorption profiles compared to earlier statin formulations.
## 3. Mechanism of Action Crestor: Scientific Substantiation
Understanding how Crestor works requires examining its biochemical pathway. Rosuvastatin competitively inhibits HMG-CoA reductase, the enzyme that catalyzes the conversion of HMG-CoA to mevalonate, which represents the early rate-limiting step in cholesterol biosynthesis. This mechanism of action occurs primarily in the liver, where approximately 90% of cholesterol synthesis occurs.
The effects on the body extend beyond simple cholesterol reduction. By depleting intracellular cholesterol stores, Crestor causes an upregulation of hepatic LDL receptors, increasing catabolism of LDL-C particles from circulation. Scientific research has additionally revealed pleiotropic effects including improved endothelial function, reduced vascular inflammation, decreased oxidative stress, and stabilization of atherosclerotic plaques. Think of it as not just cleaning the pipes but actually repairing the plumbing system while reducing corrosion.
## 4. Indications for Use: What is Crestor Effective For?
Crestor for Primary Hyperlipidemia and Mixed Dyslipidemia
As first-line pharmacotherapy for patients with primary hyperlipidemia (Fredrickson type IIa and IIb) who haven’t achieved target lipid levels through diet and exercise alone. Clinical trials consistently demonstrate 45-63% reductions in LDL-C depending on dosage.
Crestor for Cardiovascular Risk Reduction
Substantial evidence supports using Crestor for primary prevention in patients with elevated hsCRP without hyperlipidemia (JUPITER trial) and for secondary prevention in established cardiovascular disease. The indications for use here focus on comprehensive risk modification rather than单纯的 lipid parameter improvement.
Crestor for Pediatric Patients with Heterozygous Familial Hypercholesterolemia
FDA-approved for children aged 8-17 with HeFH, representing a crucial intervention for preventing premature cardiovascular disease in this vulnerable population.
Crestor for Hypertriglyceridemia
While primarily recognized for LDL reduction, Crestor demonstrates significant efficacy for treatment of hypertriglyceridemia, typically reducing levels by 20-40% across clinical studies.
## 5. Instructions for Use: Dosage and Course of Administration
The instructions for use for Crestor emphasize individualized dosing based on lipid parameters, cardiovascular risk, and patient-specific factors. The typical starting dosage is 10-20 mg once daily, with adjustment after 2-4 weeks based on lipid response.
| Indication | Starting Dose | Maximum Dose | Administration Timing |
|---|---|---|---|
| Primary prevention | 10-20 mg | 40 mg | Once daily, with or without food |
| Established CVD | 20 mg | 40 mg | Once daily, consistent timing |
| Asian patients | 5 mg | 20 mg | Once daily, consider reduced dosing |
| Renal impairment | 5 mg | 10 mg | CrCl <30 mL/min |
The course of administration typically continues long-term unless significant side effects develop or treatment goals are reassessed. We generally recommend obtaining baseline liver function tests before initiation and periodically thereafter.
## 6. Contraindications and Drug Interactions Crestor
Contraindications for Crestor include active liver disease or unexplained persistent elevations of serum transaminases, pregnancy, lactation, and hypersensitivity to any component. Special caution applies to patients with predisposing factors for myopathy, including renal impairment, advanced age, and uncontrolled hypothyroidism.
Significant drug interactions with Crestor occur with cyclosporine, gemfibrozil, certain HIV protease inhibitors, and other medications that inhibit OATP1B1 transport or CYP450 pathways. The combination with gemfibrozil particularly increases rosuvastatin exposure approximately twofold and significantly elevates myopathy risk.
Regarding safety during pregnancy, Crestor carries FDA Pregnancy Category X designation, meaning it’s absolutely contraindicated due to potential fetal harm and because cholesterol synthesis is essential for fetal development.
## 7. Clinical Studies and Evidence Base Crestor
The clinical studies supporting Crestor represent some of the most robust evidence in cardiovascular pharmacotherapy. The JUPITER trial demonstrated a 44% reduction in primary composite endpoint (myocardial infarction, stroke, arterial revascularization, hospitalization for unstable angina, or death from cardiovascular causes) in patients with LDL-C <130 mg/dL but elevated hsCRP ≥2.0 mg/L.
Further scientific evidence comes from the METEOR trial, which showed statistically significant reduction in atherosclerosis progression as measured by carotid intima-media thickness. Physician reviews consistently note the potent LDL-C reduction efficacy, with 10 mg of rosuvastatin producing similar LDL reduction to 40 mg of atorvastatin in head-to-head comparisons.
The effectiveness in real-world settings has been validated through multiple pharmacoepidemiological studies demonstrating consistent cardiovascular event reduction across diverse patient populations.
## 8. Comparing Crestor with Similar Products and Choosing a Quality Product
When comparing Crestor with similar statins, several distinguishing features emerge. Versus atorvastatin, Crestor typically provides greater LDL-C reduction milligram-per-milligram, though clinical outcomes are comparable at equivalent LDL reduction. Compared to simvastatin and pravastatin, Crestor offers superior potency and more predictable metabolism with fewer CYP450 interactions.
For patients wondering which statin is better, the decision typically hinges on individual patient factors including potency requirements, concomitant medications, cost considerations, and prior statin experience. How to choose involves assessing the required LDL-C reduction, potential drug interactions, and patient-specific risk factors for adverse effects.
Quality considerations for Crestor are generally assured through pharmaceutical manufacturing standards, though patients should obtain medications through verified pharmacies to avoid counterfeit products.
## 9. Frequently Asked Questions (FAQ) about Crestor
What is the recommended course of Crestor to achieve results?
Lipid-lowering effects begin within 1-2 weeks, with maximum achieved by 4 weeks. Cardiovascular benefit accrues over longer periods, with significant risk reduction typically observed within 1-2 years of consistent use.
Can Crestor be combined with other cholesterol medications?
Combination with ezetimibe is well-established and provides additive LDL reduction. However, combining with fibrates, particularly gemfibrozil, significantly increases myopathy risk and requires careful monitoring.
Does Crestor cause memory problems?
While some patients report cognitive symptoms, large-scale clinical trials haven’t demonstrated consistent association, and the FDA states that cognitive effects are generally rare and reversible upon discontinuation.
Is generic rosuvastatin equivalent to Crestor?
Yes, generic rosuvastatin undergoes rigorous bioequivalence testing and represents a therapeutically equivalent, cost-effective alternative for most patients.
## 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 significant cardiovascular risk or familial hypercholesterolemia, the substantial reduction in morbidity and mortality outweighs the potential for adverse effects in most cases. The validity of Crestor in clinical practice is well-established through extensive randomized trial evidence and real-world experience spanning nearly two decades.
I remember when we first started using rosuvastatin back in the early 2000s - our cardiology department was divided between the established atorvastatin advocates and those of us who saw the potential in this new compound. Dr. Williamson, our section chief then, was skeptical about the potency claims, thought the diabetes signal in JUPITER was concerning. Meanwhile, I had this patient, Marjorie, 62-year-old with familial hypercholesterolemia who’d failed on three previous statins due to myalgias or inadequate response. Her LDL was sitting at 190 despite maximal lifestyle measures.
We started her on 5mg - baby dose really - and within a month her LDL dropped to 110. No muscle pain, normal LFTs. She actually cried in the office, said she’d never seen numbers like that in her adult life. Her brother had died of MI at 52, so this felt like changing family history.
But it wasn’t all smooth sailing. We had a 45-year-old firefighter, Mark, who developed significant myositis on 20mg despite perfect health otherwise. His CK shot up to 1800, had to discontinue. That experience taught me that even with the cleaner metabolic profile, we still need to respect individual variation.
The diabetes risk conversation became particularly nuanced after the JUPITER data. I’ve probably started hundreds of patients on rosuvastatin since then, and I can count on one hand the ones who developed new-onset diabetes that seemed directly attributable. Usually they had multiple other risk factors - metabolic syndrome, prediabetes, strong family history.
What surprised me most was the inflammation modulation. Had a rheumatoid arthritis patient, David, whose CRP dropped from 15 to 3 on rosuvastatin, and his rheumatologist commented that his joint symptoms improved noticeably. Not something we typically discuss in lipid clinic, but these ancillary benefits keep appearing.
Marjorie, that first success case, I still see her annually. Now 82, she’s had zero cardiovascular events, LDL maintained around 70 on 10mg daily. Last visit she brought her granddaughter who’s being evaluated for familial hypercholesterolemia - three generations now. That longitudinal follow-up is what really convinces you about a medication’s value. She tells new patients in the waiting room, “This medication gave me back my future.” Can’t get better testimony than that.