Rosuvastatin Calcium Tablets

Category:Finished Dosage > Cardiovascular Preparations
Product Name:Rosuvastatin Calcium Tablets
Price(USD):0.00
Company:Jiangsu Simcere Pharmaceutical Co., Ltd.

Basic Info
  • Factory Location: Nanjing Xianshengdongyuan Pharmaceutical Co. Ltd.

    Main Sales Markets: North America,Central/South America,Western Europe,Eastern Europe,Australasia,Asia,Middle East,Africa

  • Monthly Production Capacity: 10, 000, 000

    Packaging Information: Box Carton

  • Sample Provided: no

    Payment Terms: L/C, T/T, D/P, Western Union, Paypal, Money Gram

    Rosuvastatin Calcium Tablets

     

    Generic name: Rosuvastatin Calcium Tablets
    Brand name: Softan
    Composition:
    The main ingredient of this product is Rosuvastatin Calcium.
    Chemical name: calcium (3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(N-methylmethan-3- ylsulfonamido)
    pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoate
    Chemical structure:

     

    Rosuvastatin Calcium Tablets
     

     

    Molecular formula: (C22H27FN3O6S)2 Ca
    Molecular weight: 1001.14
    Description:
    This product is film-coated tablets, remove the coating was white or almost white.
    Indications:
    This product is suitable for primary hypercholesterolemia (type IIa) or mixed dyslipidemia (type IIb) that is not
    adequately controlled by dyslipidemia due to dietary control and other non-medical treatments (eg exercise
    therapy, weight loss).This product is also suitable for patients with homozygotic familial hypercholesterolemia
    as adjuvant therapy for dietary control and other lipid-lowering measures such as LDL removal, or if 
    treatments are not appropriate.
    Strength:(1) 5 mg (based on C22H27FN3O6S); (2) 5 mg (based on C22H27FN3O6S);
    Dosage and Administration:
    Before treatment initiation the patient should be placed on a standard cholesterol-lowering diet that should
    continue during treatment. The dose should be individualised according to the goal of therapy and patient
    response, and considering patient's individual cholesterol levels, expected cardiovascular risk, and potential
    risk of adverse reactions.Oral. This product commonly used initial dose of 5 mg, once daily. The initial dose
    should be selected taking into account patient's individual cholesterol level, expected cardiovascular risk, and
    the potential risk of adverse reactions. For those who need to lower LDL-C more strongly, consider 10 mg
    once daily as the starting dose, which will control the level of blood lipids in most patients. If necessary, dose
    levels up can be adjusted after 4 weeks of treatment. The daily maximum dose of this product is 20 mg.
    This product can be administered at any time of the day, can be taken when eating or on an empty stomach.
    Dosage in patients with renal insufficiency:
    No need to adjust dose in patients with mild and moderate renal impairment. Patients with severe impairment
    disable all doses of this product.
    Dosage in patients with hepatic impairment:
    There was no increase in systemic exposure to rosuvastatin in subjects with Child-Pugh scores of 7 or below.
    However, increased systemic exposure has been observed in subjects with Child-Pugh scores of 8 and 9.
    In these patients an assessment of renal function should be considered. There is no experience in subjects
    with Child-Pugh scores above 9. Rosuvastatin Calcium Tablets are contraindicated in patients with active liver
    disease.
    Race:
    Asian subjects have been observed with increased systemic exposure.This factor should be considered when
    deciding the dosage of a patient of Asian descent.
    Contraindications:
    Rosuvastatin Calcium Tablets are contraindicated:
    - in patients with hypersensitivity to the active substance or any of the excipients of this product.
    - in patients with active liver disease including unexplained, persistent elevations of serum transaminases and
    any serum transaminase elevation exceeding 3 x the upper limit of normal (ULN).
    - in patients with severe renal impairment (creatinine clearance <30 mL/min).
    - in patients with myopathy.
    - in patients receiving concomitant ciclosporin.
    - during pregnancy and lactation and in women of childbearing potential not using appropriate contraceptive
    measures.
    Precautions:
    Renal Effects
    Proteinuria, detected by dipstick testing and mostly tubular in origin, has been observed in patients treated
    with higher doses of rosuvastatin, in particular 40 mg, where it was transient or intermittent in most cases.
    Skeletal Muscle Effects
    Effects on skeletal muscle e.g. myalgia, myopathy and, , rhabdomyolysis have been reported in rosuvastatin-
    treated patients with all doses and in particular with doses > 20 mg.
    Creatine Kinase Measurement
    Creatine Kinase (CK) should not be measured following strenuous exercise or in the presence of a plausible
    alternative cause of CK increase which may confound interpretation of the result. If CK levels are significantly
    elevated at baseline (>5xULN) a confirmatory test should be carried out within 5-7 days. If the repeat test
    confirms a baseline CK >5xULN, treatment should not be started.
    Before Treatment
    Rosuvastatin, as with other HMG-CoA reductase inhibitors, should be prescribed with caution in patients with
    pre-disposing factors for myopathy/rhabdomyolysis.
    Such factors include:
    • renal impairment
    • hypothyroidism
    • personal or family history of hereditary muscular disorders
    • previous history of muscular toxicity with another HMG-CoA reductase inhibitor or fibrate
    • alcohol abuse
    • age >70 years
    • situations where an increase in plasma levels may occur
    • concomitant use of fibrates.
    In such patients the risk of treatment should be considered in relation to possible benefit clinical monitoring is
    recommended. If CK levels are significantly elevated at baseline (>5xULN) treatment should not be started.
    Whilst on Treatment
    Patients should be asked to report inexplicable muscle pain, weakness or cramps immediately, particularly if
    associated with malaise or fever. CK levels should be measured in patients. Therapy should be discontinued
    if CK levels are markedly elevated (>5xULN) or if muscular symptoms are severe and cause daily discomfort
    (even if CK levels are ≤ 5x ULN). If symptoms resolve and CK levels return to normal, then consideration
    should be given to re-introducing rosuvastatin or an alternative HMG-CoA reductase inhibitor at the lowest
    dose with close monitoring.
    Routine monitoring of CK levels in asymptomatic patients is not warranted.
    In clinical trials there was no evidence of increased skeletal muscle effects in the small number of patients
    dosed with rosuvastatin and concomitant therapy. However, an increase in the incidence of myositis and
    myopathy has been seen in patients receiving other HMG-CoA reductase inhibitors together with fibric acid
    derivatives including gemfibrozil, ciclosporin, nicotinic acid, azole antifungals, protease inhibitors macrolide
    antibiotics. Gemfibrozil increases the risk of myopathy when given concomitantly with some HMG-CoA
    reductase inhibitors. Therefore, the combination of rosuvastatin and gemfibrozil is not recommended. The
    benefit of further alterations in lipid levels by the combined use of rosuvastatin with fibrates or niacin should
    be carefully weighed against the potential risks of such combinations.
    Rosuvastatin should not be used in any patient with an acute, serious condition suggestive of myopathy or
    predisposing to the development of renal failure secondary to rhabdomyolysis (e.g. sepsis, hypotension,
    major surgery, trauma, severe metabolic, endocrine and electrolyte disorders; or uncontrolled seizures).
    Liver Effects
    As with other HMG-CoA reductase inhibitors, rosuvastatin should be used with caution in patients who
    consume excessive quantities of alcohol and/or have a history of liver disease.It is recommended that liver
    function tests be carried out prior to, and 3 months following, the initiation of treatment. Rosuvastatin should
    be discontinued or the dose reduced if the level of serum transaminases is greater than 3 times the upper
    limit of normal.In patients with secondary hypercholesterolaemia caused by hypothyroidism or nephrotic
    syndrome, the underlying disease should be treated prior to initiating therapy with rosuvastatin.
    Race
    Pharmacokinetic studies show an increase in exposure in Asian subjects compared with Caucasians.
    Protease inhibitors
    The concomitant use with protease inhibitors is not recommended.
    Effects on ability to drive and use machines
    Studies to determine the effect of rosuvastatin on the ability to drive and use machines have not been
    conducted. However, based on its pharmacodynamic properties, rosuvastatin is unlikely to affect this ability.
    When driving vehicles or operating machines, it should be taken into account that dizziness may occur during
    treatment.
    Pharmacology and toxicology:
    Pharmacology
    Rosuvastatin is a selective and competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that
    converts 3-hydroxy-3-methylglutaryl coenzyme A to mevalonate, a precursor for cholesterol. The primary
    site of action of rosuvastatin is the liver, the target organ for cholesterol lowering. Rosuvastatin increases the
    number of hepatic LDL receptors on the cell-surface, enhancing uptake and catabolism of LDL and it inhibits
    the hepatic synthesis of VLDL, thereby reducing the total number of VLDL and LDL particles.
    In patients with homozygous and heterozygous familial hypercholesterolemia, non-familial hypercholesterole
    mia, mixed dyslipidemia, rosuvastatin can reduce total cholesterol, LDL-C, ApoB, non-HDL-C levels.
    Rosuvastatin also lowers TG and increases HDL-C levels. Rosuvastatin can reduce total cholesterol, LDL-C,
    VLDL-C, ApoB, non-HDL-C, TG levels and increase HDL-C levels hypertriglyceridemic patients. The impact
    of rosuvastatin on the morbidity and mortality of cardiovascular disease has not been established.
    Toxicology
    Central nervous system toxicity
    Several dog trials of similar drugs found CNS vascular injury, showing perivascular hemorrhage, edema,
    perivascular mononuclear cell infiltration. A drug similar in structure to this class of drugs appears to have a
    dose-dependent optic nerve degeneration (retinal-kinetochore Wallerian degeneration) at doses of dog
    plasma drug concentrations higher than the 30-fold average concentration of the human plasma.
    1 female dog orally administered rosuvastatin 90 mg/kg/day (calculated by AUC, systemic expose equivalent
    to 100 times the human 40 mg/day exposure), euthanasia was applied to this dog at the 24th day because it's
    dying, we can see choroid plexus edema, hemorrhage and partial necrosis. Administration of rosuvastatin
    6 mg/kg/day (calculated by AUC, systemic exposure equivalent to 20 times the human 40 mg/day exposure)
    for 52 weeks, corneal turbidity can be seen. Dog oral administration of rosuvastatin 30 mg/kg/day (calculated
    according to AUC, systemic exposure equivalent to 60 times the human 40 mg/day exposure) for 12
    consecutive weeks, visible cataract. Dog oral administration of rosuvastatin 90 mg/kg/day (calculated by AUC
    , systemic exposure equivalent to 100 times the human 40 mg/day exposure) for 4 weeks, showing retinal
    dysplasia and retinal detachment. Dog at dose ≤30 mg/kg/day (calculated by AUC, systemic exposure
    equivalent to 60 times the human 40 mg/day exposure), continuous administration of 1 year, no effect on the
    retina.
    Genetic toxicity
    In the Ames test, mouse lymphoma test, CHL cell chromosome aberration test, and mouse micronucleus test,
    the results of rosuvastatin were all negative.
    Reproductive toxicity
    In the rat fertility test, male rats were orally administered 5, 15 and 50 mg/kg/day from 9 weeks before mating
    to mating, and female rats were orally administered 5, 15 and 50 mg/kg/day from 2 weeks before mating to 7
    days of gestation. At the highest dose (calculated by AUC, systemic exposure equivalent to 10 times the
    human 40 mg/day exposure), no adverse effects on fertility. Dogs were orally administered rosuvastatin 30
    mg/kg/day for 1 month, the giant sperm cells (Spermatidic giant cell) were found in the testes. The monkey
    orally administered rosuvastatin 30 mg/kg/day for 6 months, showing giant sperm cells, vas deferens
    epithelial vacuoles. The above dose of dog and monkey estimated by body surface area equivalent to
    20 times and 10 times the human 40 mg/day exposure, respectively. Similar drugs can also see a similar
    phenomenon.
    Female rats oral administration of 5,15,50 mg/kg/day from pre-mating to 7 days after mating, high-dose group
    (calculated by AUC, body exposure equivalent to 10 times the human 40 mg/day exposure) shows fetal body
    weight reduce and ossification delay.
    The rats were orally administered with 2, 10, 50 mg/kg/day from the 7th day of pregnancy to the 21st day of
    lactation (ablactation) and the high dose group (calculated by body surface area, body exposure equivalent to
    12 times the human 40 mg/day exposure or more) shows survival rates of cub is reduced. Rabbits orally were
    administered 0.3,1,3 mg/kg/day from the 6th day of pregnancy to the 18th day of lactation (ablactation), and
    the high dose group ((calculated by body surface area, body exposure equivalent to the human 40 mg/day
    exposure) shows reduced fetal survival rates of cub and maternal animals death. When  dose of rosuvastatin
    was ≤25 mg/kg/day in rats ≤3 mg/kg/day in rabbits. No teratogenicity was observed (equivalent to a human
    exposure of 40 mg/day, calculated by AUC and body surface area, respectively).
    Carcinogenicity
    In a 104-week carcinogenicity test in rats, the oral dose was 2, 20, 60, 80 mg/kg/day. 80 mg/kg/day dose
    group (calculated according to AUC, systemic exposure equivalent to 20 times the human 40 mg/day
    exposure) of female animals showed a significant increase in the incidence of uterine polyps, no increase in
    the low doses.In a 107-week carcinogenicity test in mice, the dose was orally administered at 10, 60, 200 mg
    /kg/day. 200 mg/kg/day dose group (calculated according to AUC, systemic exposure equivalent to 20 times
    the human 40 mg/day exposure) of animals showed increased incidence of hepatocellular adenoma/cancer,
    no increase in the low doses.
    Pharmacokinetics:
    The pharmacokinetics of rosuvastatin in caucasian people showed that:
    Absorption: Maximum rosuvastatin plasma concentrations are achieved approximately 5 hours after oral
    administration. The absolute bioavailability is approximately 20%.
    Distribution: Rosuvastatin is taken up extensively by the liver which is the primary site of cholesterol synthesis
    and LDL-C clearance. The volume of distribution of rosuvastatin is approximately 134 L. Approximately 90%
    of rosuvastatin is bound to plasma proteins, mainly to albumin.
    Biotransformation: Rosuvastatin undergoes limited metabolism (approximately 10%). In vitro metabolism
    studies using human hepatocytes indicate that rosuvastatin is a poor substrate for cytochrome P450-based
    metabolism. CYP2C9 was the principal isoenzyme involved, with 2C19, 3A4 and 2D6 involved to a lesser
    extent. The main metabolites identified are the N-desmethyl and lactone metabolites. The N-desmethyl
    metabolite is approximately 50% less active than rosuvastatin whereas  lactone form is considered clinically
    inactive.
    Rosuvastatin accounts for greater than 90% of the circulating HMG-CoA reductase inhibitor activity.
    Elimination: Approximately 90% of the rosuvastatin dose is excreted unchanged in the faeces (consisting of
    absorbed and non-absorbed active substance) and the remaining part is excreted in urine. Approximately 5%
    is excreted unchanged in urine.
    The plasma elimination half-life is approximately 19 hours. The elimination half-life does not increase at higher
    doses. The geometric mean plasma clearance is approximately 50 litres/hour (coefficient of variation 21.7%).
    As with other HMG-CoA reductase inhibitors, the hepatic uptake of rosuvastatin involves the membrane
    transporter OATP-C. This transporter is important in the hepatic elimination of rosuvastatin.
    Linearity: Systemic exposure of rosuvastatin increases in proportion to dose. There are no changes in
    pharmacokinetic parameters following multiple daily doses.
    Only about 10% of rosuvastatin is metabolized at the oral dose, mainly N-bit demethylation.
    Special populations:
    Age and sex: Age or sex did not have a clinically significant effect on rosuvastatin pharmacokinetics.
    Renal impairment: In a study in subjects with varying degrees of renal impairment, mild to moderate renal
    disease had no influence on plasma concentration of rosuvastatin or the N-desmethyl metabolite. Subjects
    with severe impairment (CrCl <30 mL/min) had a 3-fold increase in plasma concentration and a 9increase in
    the N-desmethyl metabolite concentration compared healthy volunteers. Steady-state plasma concentrations
    of rosuvastatin in subjects undergoing haemodialysis were approximately 50% greater compared to healthy
    volunteers.
    Hepatic impairment: In a study with subjects with varying degrees of hepatic impairment there was no
    evidence of increased exposure to rosuvastatin in subjects with Child-Pugh scores of 7 or below. However,
    two subjects with Child-Pugh scores of 8 and 9 showed an increase in systemic exposure of at least 2-fold
    compared to subjects with lower Child-Pugh scores. There is no experience in subjects with Child-Pugh
    scores above 9.
    Race: Pharmacokinetic studies show an approximate 2-fold elevation in median AUC and Cmax in Asian
    subjects (Japanese, Chinese, Filipino, Vietnamese and Koreans) compared with Caucasians. A population
    pharmacokinetic analysis revealed no clinically relevant differences in pharmacokinetics between Caucasian
    and Black groups.
    Studies have shown that: Chinese single-dose administration of healthy volunteers, tmax median range of
    2.5-5 hours, followed by an exponential decline. The half-life (t1/2) is about 11 to 12 hours. The third day of
    multiple administrations. Blood concentration reached steady state. After repeated administration, drug
    accumulation is small, and has nothing to do with the dose.
    Storage:Protect from light, and seal up.
    Packs: Package material: Blister packaging;5 mg: 7 tablets/blister, 10 tablets/blister, 12 tablets/blister;
    10 mg: 7 tablets/blister, 10 tablets/blister, 12 tablets/blister, 7 tablets/blister × 2 blisters/box, 7 tablets/blister
    × 4 blisters/box.
    Shelf-life:24 months
     

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