| Ημερομηνία | barcode | code | περιεχομενο | τιμή παραγωγός | χονδρική | λιανική |
|---|---|---|---|---|---|---|
| 05/2018 | 2803112001013 | 311200101 | ROSUVASTATIN/MYLAN F.C.TAB 5MG/TAB BTx14 (Polyamide/Al/LDPE DESICCANT-HDPE/Al/ blister) (Polyamide/Al/LDPE DESICCANT-HDPE/Al/ blister) | 2.13 | 2.23 | 03.07 |
| 05/2018 | 2803112001037 | 311200103 | ROSUVASTATIN/MYLAN F.C.TAB 5MG/TAB BTx28 (Polyamide/Al/LDPE DESICCANT-HDPE/Al/ blister) | 3.74 | 3.93 | 5.41 |
| 05/2018 | 2803112002010 | 311200201 | ROSUVASTATIN/MYLAN F.C.TAB 10MG/TAB BTx14 (Polyamide/Al/LDPE DESICCANT-HDPE/Al/ blister) (Polyamide/Al/LDPE DESICCANT-HDPE/Al/ blister) | 4.97 | 5.21 | 7.18 |
| 05/2018 | 2803112002034 | 311200203 | ROSUVASTATIN/MYLAN F.C.TAB 10MG/TAB BTx28 (Polyamide/Al/LDPE DESICCANT-HDPE/Al/ blister) | 8.73 | 9.16 | 12.62 |
| 05/2018 | 2803112003017 | 311200301 | ROSUVASTATIN/MYLAN F.C.TAB 20MG/TAB BTx14 (Polyamide/Al/LDPE DESICCANT-HDPE/Al/ blister) (Polyamide/Al/LDPE DESICCANT-HDPE/Al/ blister) | 6.99 | 7.33 | 10.10 |
| 05/2018 | 2803112003031 | 311200303 | ROSUVASTATIN/MYLAN F.C.TAB 20MG/TAB BTx28 (Polyamide/Al/LDPE DESICCANT-HDPE/Al/ blister) | 12.30 | 12.90 | 17.78 |
| 05/2018 | 2803112004014 | 311200401 | ROSUVASTATIN/MYLAN F.C.TAB 40MG/TAB BTx14 (Polyamide/Al/LDPE DESICCANT-HDPE/Al/ blister) (Polyamide/Al/LDPE DESICCANT-HDPE/Al/ blister) | 8.54 | 8.96 | 12.35 |
| 05/2018 | 2803112004038 | 311200403 | ROSUVASTATIN/MYLAN F.C.TAB 40MG/TAB BTx28 (Polyamide/Al/LDPE DESICCANT-HDPE/Al/ blister) (Polyamide/Al/LDPE DESICCANT-HDPE/Al/ blister) | 15.02 | 15.76 | 21.72 |
Used as an adjunct to dietary therapy to treat primary hypercholesterolemia (heterozygous familial and nonfamilial), mixed dyslipidemia and hypertriglyceridemia. Also indicated for homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering therapies or when other such therapies are not available.
Rosuvastatin is a competitive inhibitor of HMG-CoA reductase. HMG-CoA reductase catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis. Rosuvastatin acts primarily in the liver. Decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low density lipoprotein (LDL) receptors which increases hepatic uptake of LDL. Rosuvastatin also inhibits hepatic synthesis of very low density lipoprotein (VLDL). The overall effect is a decrease in plasma LDL and VLDL. In vitro and in vivo animal studies also demonstrate that rosuvastatin exerts vasculoprotective effects independent of its lipid-lowering properties. Rosuvastatin exerts an anti-inflammatory effect on rat mesenteric microvascular endothelium by attenuating leukocyte rolling, adherence and transmigration (PMID: 11375257). The drug also modulates nitric oxide synthase (NOS) expression and reduces ischemic-reperfusion injuries in rat hearts (PMID: 15914111). Rosuvastatin increases the bioavailability of nitric oxide (PMID: 11375257, 12031849, 15914111) by upregulating NOS (PMID: 12354446) and by increasing the stability of NOS through post-transcriptional polyadenylation (PMID: 17916773). It is unclear as to how rosuvastatin brings about these effects though they may be due to decreased concentrations of mevalonic acid.
Generally well-tolerated. Side effects may include myalgia, constipation, asthenia, abdominal pain, and nausea. Other possible side effects include myotoxicity (myopathy, myositis, rhabdomyolysis) and hepatotoxicity. To avoid toxicity in Asian patients, lower doses should be considered. Pharmacokinetic studies show an approximately two-fold increase in peak plasma concentration and AUC in Asian patients (Philippino, Chinese, Japanese, Korean, Vietnamese, or Asian-Indian descent) compared to Caucasians patients.
Bioavailability is approximately 20%
19 hours
Rosuvastatin is not extensively metabolized; approximately 10% of a radiolabeled dose is recovered as metabolite. Following oral administration, rosuvastatin and its metabolites are primarily excreted in the feces (90%).
* 134 L