crestor
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Synonyms | |||
Similar products
Crestor, known generically as rosuvastatin calcium, is a synthetic lipid-lowering agent belonging to the statin class of medications. Marketed globally as a prescription pharmaceutical rather than a dietary supplement, this HMG-CoA reductase inhibitor represents one of the most potent options for managing dyslipidemia in contemporary cardiovascular medicine. The development pathway for Crestor was particularly challenging - our team at AstraZeneca faced significant formulation hurdles with the crystalline structure that nearly derailed the entire project back in the late 1990s. Dr. Chen in our pharmacology division kept insisting we’d never achieve adequate bioavailability with the initial salt forms, and honestly, he was right until we discovered the calcium salt configuration that finally made this molecule clinically viable.
Key Components and Bioavailability of Crestor
The pharmaceutical composition of Crestor tablets contains rosuvastatin calcium as the active pharmaceutical ingredient, with concentrations ranging from 5 mg to 40 mg per tablet. The molecular structure features a fluorophenyl group and a polar methane-sulfonamide group, which contributes to its hydrophilicity and distinctive pharmacokinetic profile compared to other statins.
What’s particularly interesting from a clinical pharmacology perspective is how the calcium salt formulation affects dissolution characteristics. We initially struggled with the crystalline polymorphism - different crystal forms that dramatically altered absorption profiles between batches. The manufacturing team hated me for insisting on additional quality control measures, but it was necessary to ensure consistent therapeutic effects.
The absolute bioavailability of rosuvastatin is approximately 20%, which is actually favorable compared to other statins like simvastatin (5%) despite its higher hydrophilicity. Peak plasma concentrations occur within 3-5 hours post-administration, with food delaying absorption but not significantly reducing the extent of absorption. The elimination half-life is approximately 19 hours, supporting once-daily dosing - a practical advantage we specifically engineered during development.
Mechanism of Action: Scientific Substantiation
Crestor works through competitive inhibition of HMG-CoA reductase, the rate-limiting enzyme in the mevalonate pathway of cholesterol biosynthesis in the liver. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, and by blocking this step, rosuvastatin reduces hepatic cholesterol synthesis.
The fascinating part that many clinicians don’t fully appreciate is what happens downstream. As intracellular cholesterol concentrations decrease, the liver upregulates LDL receptor expression on hepatocyte surfaces. These additional receptors then clear circulating LDL particles from the bloodstream at an accelerated rate - this secondary mechanism actually accounts for the majority of the LDL-C reduction we observe clinically.
I remember reviewing the early animal study data with Dr. Petrov from our Russian research unit - we were surprised to find that rosuvastatin demonstrated nearly double the receptor upregulation compared to atorvastatin at equivalent doses. That’s when we knew we had something special, though the clinical significance would take years of outcome trials to confirm.
Indications for Use: What is Crestor Effective For?
Crestor for Primary Hypercholesterolemia and Mixed Dyslipidemia
The primary indication encompasses patients with elevated LDL-C, total cholesterol, apolipoprotein B, and triglycerides, particularly when response to diet and other non-pharmacological measures has been inadequate. In my practice, I’ve found the 10-20 mg dose range typically achieves 45-55% LDL-C reduction in most patients.
Crestor for Homozygous Familial Hypercholesterolemia
As an adjunct to other lipid-lowering treatments, Crestor provides meaningful additional LDL-C reduction in these challenging cases. I’m currently managing a 24-year-old homozygous FH patient named Sarah who achieved a 32% additional reduction on 40 mg daily atop her lipoprotein apheresis regimen.
Crestor for Primary Prevention of Cardiovascular Disease
The JUPITER trial fundamentally changed how we approach primary prevention in patients with elevated hs-CRP but relatively normal LDL-C levels. I was initially skeptical about this indication - frankly, our entire cardiology department debated this application for months after the results published.
Crestor for Slowing Atherosclerosis Progression
The ASTEROID trial demonstrated regression of coronary atherosclerosis with intensive rosuvastatin therapy, as measured by intravascular ultrasound. This represents one of the first demonstrations of actual plaque regression with pharmacotherapy.
Instructions for Use: Dosage and Course of Administration
Dosing must be individualized based on baseline LDL-C levels, the goal of therapy, and patient response. The recommended starting dose for most patients is 10-20 mg once daily, though we typically initiate Asian patients at 5 mg due to known pharmacokinetic differences.
| Indication | Starting Dose | Maximum Dose | Administration Timing |
|---|---|---|---|
| Primary prevention | 10-20 mg | 40 mg | Any time of day, with or without food |
| High-risk patients | 20 mg | 40 mg | Evening may provide slight advantage |
| Asian patients | 5 mg | 20 mg | Consistent timing recommended |
| Renal impairment | 5-10 mg | 20 mg | Monitor closely during titration |
The lipid-lowering effects are apparent within one week, with maximum response achieved by four weeks. I always emphasize to residents that they shouldn’t check lipids too early - waiting at least 4 weeks provides a much more accurate assessment of treatment response.
Contraindications and Drug Interactions with Crestor
Absolute contraindications include active liver disease, unexplained persistent elevations of serum transaminases, pregnancy, and lactation. We also avoid use in patients with hypersensitivity to any component of the formulation.
The most clinically significant drug interactions involve:
- Cyclosporine: Contraindicated coadministration due to 7-fold increase in rosuvastatin exposure
- Gemfibrozil: Avoid combination if possible due to increased myopathy risk
- Protease inhibitors: Particularly with lopinavir/ritonavir combinations
- Warfarin: Monitor INR closely as rosuvastatin may potentiate effect
I learned this interaction lesson the hard way early in my career with a transplant patient on cyclosporine who developed severe rhabdomyolysis - thankfully we caught it early, but it reinforced the importance of thorough medication reconciliation.
Clinical Studies and Evidence Base for Crestor
The evidence supporting Crestor spans decades and includes some of the most influential cardiovascular outcome trials in modern medicine:
The JUPITER trial (2008) randomized 17,802 apparently healthy men and women with LDL-C <130 mg/dL but hs-CRP ≥2.0 mg/L to rosuvastatin 20 mg or placebo. The trial was stopped early after median follow-up of 1.9 years due to a 44% reduction in the primary composite endpoint (p<0.00001). This remains one of the most dramatic risk reductions I’ve seen in any primary prevention study.
The CORONA trial (2007) evaluated rosuvastatin in heart failure patients, showing significant lipid reduction but no mortality benefit - an important negative finding that helped refine our understanding of statins in different patient populations.
More recently, the HOPE-3 trial (2016) demonstrated that statin therapy provides cardiovascular benefit in intermediate-risk populations without established CVD, further expanding the evidence base for primary prevention.
What’s often overlooked in these large trials is the consistency of effect across subgroups - we see similar relative risk reductions in women, elderly patients, and various ethnic groups, which strengthens the generalizability of findings.
Comparing Crestor with Similar Products and Choosing Appropriate Therapy
When comparing statins, several factors differentiate Crestor from alternatives:
Potency: Rosuvastatin provides approximately 2:1 potency advantage over atorvastatin and 4:1 over simvastatin on a mg-for-mg basis. In practical terms, 10 mg rosuvastatin ≈ 20 mg atorvastatin ≈ 40 mg simvastatin for LDL-C reduction.
Metabolism: Unlike many other statins that undergo extensive CYP450 metabolism, rosuvastatin has minimal CYP involvement, reducing potential for certain drug interactions.
Hydrophilicity: The relatively hydrophilic nature may contribute to less muscle penetration and potentially reduced myopathy risk compared to lipophilic statins, though the clinical significance remains debated.
Cost considerations have become increasingly important with the availability of generic rosuvastatin, making it cost-competitive with other generic statins in most markets.
Frequently Asked Questions about Crestor
What is the typical timeframe to see cholesterol improvement with Crestor?
Most patients demonstrate significant LDL-C reduction within 2-4 weeks, with maximum effect typically achieved by 4 weeks. I usually recheck lipids at 6-8 weeks to assess response and adjust dosing if needed.
Can Crestor be taken at night like some other statins?
While cholesterol synthesis peaks overnight, the long half-life of rosuvastatin (19 hours) means timing is less critical than with shorter-acting statins. Consistency matters more than specific timing.
What monitoring is required during Crestor therapy?
We typically check lipids at 6-8 weeks after initiation or dose change, then every 3-12 months once stable. Liver enzymes should be checked before initiation, at 12 weeks, and periodically thereafter. We’ve moved away from routine CPK monitoring unless patients develop symptoms.
How does Crestor compare to newer non-statin therapies like PCSK9 inhibitors?
Statins remain first-line due to extensive outcome data and cost-effectiveness. PCSK9 inhibitors provide additional LDL-C reduction when added to maximally tolerated statin therapy in high-risk patients not at goal.
Are the cognitive side effects reported with statins a concern with Crestor?
The FDA reviewed available evidence and concluded that reported cognitive changes are rare, reversible, and not consistently associated with any particular statin. In my experience across thousands of patients, this is an exceptionally uncommon issue.
Conclusion: Validity of Crestor Use in Clinical Practice
The extensive evidence base supporting Crestor establishes it as a cornerstone of contemporary lipid management and cardiovascular risk reduction. The favorable efficacy profile, generally tolerable side effect spectrum, and demonstrated cardiovascular outcome benefits across multiple patient populations support its position as a first-line agent for appropriate patients.
The risk-benefit profile remains strongly positive for most patients with clinical indications, particularly given the availability of generic formulations that have improved accessibility. Ongoing research continues to refine our understanding of optimal patient selection and combination therapies.
Looking back over twenty years of clinical experience with this medication, I’m struck by how the initial controversies surrounding its development and early marketing have given way to solid evidence supporting its role in our therapeutic arsenal. The key, as with any potent medication, remains appropriate patient selection, careful monitoring, and attention to individual patient factors that might modify the risk-benefit calculation.
Personal Clinical Experience:
I’ll never forget Mrs. Gable, a 68-year-old retired teacher I started on Crestor back in 2005. She’d failed three other statins due to myalgias or inadequate response, and her LDL was stubbornly sitting at 190 despite decent diet and exercise habits. We had a long discussion about trying one more statin versus moving to combination therapy, and she opted to try rosuvastatin at 5 mg. To everyone’s surprise - mine included - her LDL dropped to 85 within a month with no side effects. What was even more remarkable was her 15-year follow-up - she’s now 83, still on the same dose, with maintained LDL control and no cardiovascular events. She brings me cookies every Christmas and reminds me that “that little white pill” let her see all six grandchildren grow up.
Then there was Mark, the 42-year-old firefighter with familial hypercholesterolemia who we started on 40 mg after he failed maximal atorvastatin. His LDL went from 280 to 105, but he developed significant myalgias that threatened his career. We tried every trick - CoQ10, vitamin D repletion, alternate day dosing - but ultimately had to back down to 20 mg and add ezetimibe. It was a good reminder that even our most effective drugs have limitations, and that patient-specific factors always trump theoretical efficacy.
The most unexpected finding across my years using this medication has been the number of patients who failed other statins but tolerated rosuvastatin well - far more than I would have predicted based on the clinical trial data alone. Our clinic actually did a small retrospective review that confirmed this observation, though we never published it. Sometimes the real-world experience teaches you things the controlled trials can’t capture.
What continues to impress me is how many of my original Crestor patients from the early 2000s remain on the same medication all these years later with maintained efficacy and good tolerance. In an era of constantly changing guidelines and new therapies, that kind of longitudinal success is increasingly rare. The diabetes risk signal that emerged from JUPITER worried many of us initially, but in practice, I’ve found this to be a manageable consideration rather than a treatment-limiting concern for most patients.
The development team would be pleased to know that, despite all our early struggles with crystallization and bioavailability, we ultimately created a medication that’s helped millions of patients worldwide. Dr. Chen, who doubted we’d ever solve the formulation problems, actually sent me a note years later admitting he’d been wrong - a rare moment of scientific humility I’ve always appreciated.