Rosuvastatin Calcium Tablets SMPC Taj Pharmaceuticals

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Rosuvastatin Calcium Tablets diet and other non-pharmacological treatments

(e.g. exercise, weight reduction) is inadequate.
10mg/20mg/40mg
Adults, adolescents and children aged 6 years or
1. Name of the medicinal older with homozygous familial
hypercholesterolaemia as an adjunct to diet and
product other lipid lowering treatments (e.g. LDL
Rosuvastatin Calcium Tablets 10mg Taj Pharma apheresis) or if such treatments are not
appropriate.
Rosuvastatin Calcium Tablets 20mg Taj Pharma
Rosuvastatin Calcium Tablets 40mg Taj Pharma Prevention of Cardiovascular Events
2. Qualitative and quantitative Prevention of major cardiovascular events in

patients who are estimated to have a high risk
composition for a first cardiovascular event (see section 5.1),
a) Each film coated tablet contains: as an adjunct to correction of other risk factors.
Rosuvastatin Calcium 4.2 Posology and method of administration
Equivalent to Rosuvastatin 10mg Before treatment initiation the patient should be
Excipients q.s. placed on a standard cholesterol-lowering diet
Colour: Titanium Dioxide USP that should continue during treatment. The dose
b) Each film coated tablet contains: should be individualised according to the goal of
Rosuvastatin Calcium therapy and patient response, using current
Equivalent to Rosuvastatin 20mg consensus guidelines.
Excipients q.s. Rosuvastatin Tablets may be given at any time
Colour: Titanium Dioxide USP of day, with or without food.
c) Each film coated tablet contains: Treatment of Hypercholesterolaemia
Rosuvastatin Calcium
Equivalent to Rosuvastatin 40mg The recommended start dose is 5 or 10 mg orally
Excipients q.s. once daily in both statin naïve or patients
Colour: Titanium Dioxide USP switched from another HMG CoA reductase
inhibitor. The choice of start dose should take
For the full list of excipients, see section 6.1. into account the individual patient's cholesterol
level and future cardiovascular risk as well as
3. Pharmaceutical form the potential risk for adverse reactions (see
Film-coated tablet. below). A dose adjustment to the next dose level
can be made after 4 weeks, if necessary (see
Biconvex, film-coated tablets. section 5.1). In light of the increased reporting
rate of adverse reactions with the 40 mg dose
4. Clinical particulars compared to lower doses (see section 4.8), a
final titration to the maximum dose of 40 mg
4.1 Therapeutic indications should only be considered in patients with
Treatment of hypercholesterolaemia severe hypercholesterolaemia at high
Adults, adolescents and children aged 6 years or cardiovascular risk (in particular those with
older with primary hypercholesterolaemia (type familial hypercholesterolaemia), who do not
IIa including heterozygous familial achieve their treatment goal on 20 mg, and in
hypercholesterolaemia) or mixed dyslipidaemia whom routine follow-up will be performed (see
(type IIb) as an adjunct to diet when response to section 4.4). Specialist supervision is
recommended when the 40 mg dose is initiated.
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Prevention of cardiovascular events paediatric treatment recommendations (see

section 4.4). Children and adolescents should be
In the cardiovascular events risk reduction study, placed on standard cholesterol-lowering diet
the dose used was 20 mg daily (see section 5.1).
before rosuvastatin treatment initiation; this diet
Pediatric population should be continued during rosuvastatin
treatment.
Pediatric use should only be carried out by
specialists. There is limited experience with doses other
than 20 mg in this population.
Children and adolescents 6 to 17 years of age
(Tanner Stage <II-V) The 40 mg tablet is not suitable for use in
paediatric patients.
Heterozygous familial hypercholesterolaemia
Children younger than 6 years
In children and adolescents with heterozygous
familial hypercholesterolaemia the usual start The safety and efficacy of use in children
dose is 5 mg daily. younger than 6 years has not been studied.
Therefore, Rosuvastatin is not recommended for
• In children 6 to 9 years of age with use in children younger than 6 years.
heterozygous familial hypercholesterolaemia,
the usual dose range is 5-10 mg orally once Use in the elderly
daily. Safety and efficacy of doses greater than
A start dose of 5 mg is recommended in patients
10 mg have not been studied in this population.
>70 years (see section 4.4). No other dose
• In children 10 to 17 years of age with adjustment is necessary in relation to age.
heterozygous familial hypercholesterolaemia, Dosage in patients with renal insufficiency
the usual dose range is 5-20 mg orally once
daily. Safety and efficacy of doses greater than No dose adjustment is necessary in patients with
20 mg have not been studied in this population. mild to moderate renal impairment. The
recommended start dose is 5 mg in patients with
Titration should be conducted according to the moderate renal impairment (creatinine clearance
individual response and tolerability in paediatric of <60 ml/min). The 40 mg dose is
patients, as recommended by the paediatric contraindicated in patients with moderate renal
treatment recommendations (see Section 4.4). impairment. The use of Rosuvastatin Tablets in
Children and adolescents should be placed on
patients with severe renal impairment is
standard cholesterol-lowering diet before
contraindicated for all doses (see section 4.3 and
rosuvastatin treatment initiation; this diet should section 5.2).
be continued during rosuvastatin treatment.
Dosage in patients with hepatic impairment
Homozygous familial hypercholesterolaemia
There was no increase in systemic exposure to
In children 6 to 17 years of age with rosuvastatin in subjects with Child-Pugh scores
homozygous familial hypercholesterolaemia, the
of 7 or below. However, increased systemic
recommended maximum dose is/20 mg once exposure has been observed in subjects with
daily.
Child-Pugh scores of 8 and 9 (See Section 5.2).
A starting dose of 5 to 10 mg once daily In these patients an assessment of renal function
depending on age, weight and prior statin use is should be considered (see Section 4.4). There is
advised. Titration to the maximum dose of 20 no experience in subjects with Child-Pugh
mg once daily should be conducted according to scores above 9. Rosuvastatin Tablets is
the individual response and tolerability in contraindicated in patients with active liver
paediatric patients, as recommended by the disease (See Section 4.3).
Race - in patients with hypersensitivity to rosuvastatin

or to any of the excipients.
Increased systemic exposure has been seen in
Asian subjects (See Section 4.3, Section 4.4and - in patients with active liver disease including
5.2). The recommended start dose is 5 mg for unexplained, persistent elevations of serum
patients of Asian ancestry. The 40 mg dose is transaminases and any serum transaminase
contraindicated in these patients. elevation exceeding 3 times the upper limit of
normal (ULN).
Genetic polymorphisms
- in patients with severe renal impairment
Specific types of genetic polymorphisms are (creatinine clearance <30 ml/min).
known that can lead to increased rosuvastatin
exposure (see Section 5.2). For patients who are - in patients with myopathy.
known to have such specific types of
- in patients receiving concomitant ciclosporin.
polymorphisms, a lower daily dose of
Rosuvastatin Tablets is recommended. - during pregnancy and lactation and in women
of childbearing potential not using appropriate
Dosage in patients with pre-disposing factors
contraceptive measures.
to myopathy
The 40 mg dose is contraindicated in patients
The recommended start dose is 5 mg in patients
with pre-disposing factors for
with predisposing factors to myopathy (See
Section 4.4). myopathy/rhabdomyolysis. Such factors include:
The 40 mg dose is contraindicated in some of - moderate renal impairment (creatinine

clearance < 60 ml/min)
these patients (See Section 4.3).
- hypothyroidism
Concomitant therapy
- personal or family history of hereditary
Rosuvastatin is a substrate of various transporter
muscular disorders
proteins (e.g. OATP1B1 and BCRP). The risk of
myopathy (including rhabdomyolysis) is - previous history of muscular toxicity with
increased when Rosuvastatin Tablets is another HMG-CoA reductase inhibitor or fibrate
administered concomitantly with certain
medicinal products that may increase the plasma - alcohol abuse
concentration of rosuvastatin due to interactions - situations where an increase in plasma levels
with these transporter proteins (e.g. ciclosporine may occur
and certain protease inhibitors including
combinations of ritonavir with atazanavir, - asian patients
lopinavir, and/or tipranavir see sections 4.4 and - concomitant use of fibrates.
4.5). Whenever possible, alternative medications
should be considered, and, if necessary, consider (see section 4.4, 4.5 and 5.2)
temporarily discontinuing Rosuvastatin therapy.
4.4 Special warnings and precautions for use
In situations where co-administration of these
Renal Effects
medicinal products with Rosuvastatin Tablets is
unavoidable, the benefit and the risk of Proteinuria, detected by dipstick testing and
concurrent treatment and Rosuvastatin Tablets mostly tubular in origin, has been observed in
dosing adjustments should be carefully patients treated with higher doses of
considered (see section 4.5). Rosuvastatin, in particular 40 mg, where it was
transient or intermittent in most cases.
4.3 Contraindications
Proteinuria has not been shown to be predictive
Rosuvastatin Tablets is contraindicated:
of acute or progressive renal disease (see section
4.8). The reporting rate for serious renal events • alcohol abuse
in post-marketing use is higher at the 40 mg
dose. An assessment of renal function should be • age>70 years
considered during routine follow-up of patients • situations where an increase in plasma levels
treated with a dose of 40 mg. may occur (see sections 4.2, 4.5 and 5.2)
Skeletal Muscle Effects • concomitant use of fibrates.
Effects on skeletal muscle e.g. myalgia, In such patients the risk of treatment should be
myopathy and, rarely, rhabdomyolysis have considered in relation to possible benefit and
been reported in Rosuvastatin-treated patients clinical monitoring is recommended. If CK
with all doses and in particular with doses > 20 levels are significantly elevated at baseline
mg. Very rare cases of rhabdomyolysis have (>5xULN) treatment should not be started.
been reported with the use of ezetimibe in
combination with HMG-CoA reductase Whilst on Treatment
inhibitors. A pharmacodynamic interaction Patients should be asked to report inexplicable
cannot be excluded (see section 4.5) and caution muscle pain, weakness or cramps immediately,
should be exercised with their combined use. particularly if associated with malaise or fever.
As with other HMG-CoA reductase inhibitors, CK levels should be measured in these patients.
the reporting rate for rhabdomyolysis associated Therapy should be discontinued if CK levels are
with Rosuvastatin in post-marketing use is markedly elevated (>5xULN) or if muscular
higher at the 40 mg dose. symptoms are severe and cause daily discomfort
(even if CK levels are ≤ 5x ULN). If symptoms
Creatine Kinase Measurement resolve and CK levels return to normal, then
Creatine Kinase (CK) should not be measured consideration should be given to re-introducing
following strenuous exercise or in the presence Rosuvastatin Tablets or an alternative HMG-
of a plausible alternative cause of CK increase CoA reductase inhibitor at the lowest dose with
which may confound interpretation of the result. close monitoring. Routine monitoring of CK
levels in asymptomatic patients is not warranted.
If CK levels are significantly elevated at
There have been very rare reports of an immune-
baseline (>5xULN) a confirmatory test should
be carried out within 5 – 7 days. If the repeat test mediated necrotising myopathy (IMNM) during
confirms a baseline CK >5xULN, treatment or after treatment with statins, including
should not be started. rosuvastatin. IMNM is clinically characterised
by proximal muscle weakness and elevated
Before Treatment serum creatine kinase, which persist despite
discontinuation of statin treatment.
Rosuvastatin Tablets, as with other HMG-CoA
reductase inhibitors, should be prescribed with In clinical trials there was no evidence of
caution in patients with pre-disposing factors for increased skeletal muscle effects in the small
myopathy/rhabdomyolysis. Such factors include: number of patients dosed with Rosuvastatin and
concomitant therapy. However, an increase in
• renal impairment
the incidence of myositis and myopathy has
• hypothyroidism been seen in patients receiving other HMG-CoA
reductase inhibitors together with fibric acid
• personal or family history of hereditary derivatives including gemfibrozil, ciclosporin,
muscular disorders nicotinic acid, azoles antifungal, protease
• previous history of muscular toxicity with inhibitors and macrolide antibiotics. Gemfibrozil
another HMG-CoA reductase inhibitor or fibrate increases the risk of myopathy when given
concomitantly with some HMG-CoA reductase
inhibitors. Therefore, the combination of It is recommended that liver function tests be

Rosuvastatin Tablets and gemfibrozil is not carried out prior to, and 3 months following, the
recommended. The benefit of further alterations initiation of treatment. Rosuvastatin Tablets
in lipid levels by the combined use of should be discontinued or the dose reduced if the
Rosuvastatin Tablets with fibrates or niacin level of serum transaminases is greater than 3
should be carefully weighed against the potential times the upper limit of normal. The reporting
risks of such combinations. The 40 mg dose is rate for serious hepatic events (consisting mainly
contraindicated with concomitant use of a fibrate of increased hepatic transaminases) in post-
(see section 4.5 and section 4.8). marketing use is higher at the 40 mg dose.
Rosuvastatin Tablets must not be co- In patients with secondary
administered with systemic formulations of hypercholesterolaemia caused by
fusidic acid or within 7 days of stopping fusidic hypothyroidism or nephrotic syndrome, the
acid treatment. In patients where the use of underlying disease should be treated prior to
systemic fusidic acid is considered essential, initiating therapy with Rosuvastatin Tablets.
statin treatment should be discontinued
Race
throughout the duration of fusidic acid
treatment. There have been reports of Pharmacokinetic studies show an increase in
rhabdomyolysis (including some fatalities) in exposure in Asian subjects compared with
patients receiving fusidic acid and statins in Caucasians (see section 4.2, 4.3and 4.5).
combination (see section 4.5). Patients should be
advised to seek medical advice immediately if Protease inhibitors
they experience any symptoms of muscle Increased systemic exposure to rosuvastatin has
weakness, pain or tenderness. Statin therapy been observed in subjects receiving rosuvastatin
may be re-introduced seven days after the last concomitantly with various protease inhibitors in
dose of fusidic acid. In exceptional combination with ritonavir. Consideration
circumstances, where prolonged systemic fusidic should be given both to the benefit of lipid
acid is needed, e.g. for the treatment of severe lowering by use of Rosuvastatin Tablets in HIV
infections, the need for co-administration of patients receiving protease inhibitors and the
Rosuvastatin Tablets and fusidic acid should potential for increased rosuvastatin plasma
only be considered on a case by case basis and concentrations when initiating and up titrating
under close medical supervision. Rosuvastatin doses in patients treated with
Rosuvastatin Tablets should not be used in any protease inhibitors. The concomitant use with
patient with an acute, serious condition certain protease inhibitors is not recommended
suggestive of myopathy or predisposing to the unless the dose of Rosuvastatin Tablets is
development of renal failure secondary to adjusted (see section 4.2 and 4.5).
rhabdomyolysis (e.g. sepsis, hypotension, major Lactose intolerance
surgery, trauma, severe metabolic, endocrine
and electrolyte disorders; or uncontrolled This product contains lactose. Patients with rare
seizures). hereditary problems of galactose intolerance, the
Lapp lactase deficiency or glucose-
Liver Effects galactosemalabsorption should not take this
As with other HMG-CoA reductase inhibitors, medicine.
Rosuvastatin Tablets should be used with Azocolouring agents: This product also contains
caution in patients who consume excessive azocolouring agents, allura red AC (E129),
quantities of alcohol and/or have a history of tartrazine (E102) and sunset yellow FCF (E110)
liver disease. which may cause allergic reactions.
Interstitial lung disease 4.5 Interaction with other medicinal products

and other forms of interaction
Exceptional cases of interstitial lung disease Effect of co-administered medicinal products on
have been reported with some statins, especially rosuvastatin
with long term therapy (see section 4.8).
Presenting features can include dyspnoea, non- Transporter protein inhibitors: Rosuvastatin
productive cough and deterioration in general is a substrate for certain transporter proteins
health (fatigue, weight loss and fever). If it is including the hepatic uptake transporter
suspected a patient has developed interstitial OATP1B1 and efflux transporter BCRP.
lung disease, statin therapy should be Concomitant administration of Rosuvastatin
discontinued. Tablets with medicinal products that are
inhibitors of these transporter proteins may
Diabetes Mellitus
result in increased rosuvastatin plasma
Some evidence suggests that statins as a class concentrations and an increased risk of
raise blood glucose and in some patients, at high myopathy (see section 4.2, 4.4 and 4.5 Table 1).
risk of future diabetes, may produce a level of Ciclosporin: During concomitant treatment with
hyperglycemia where formal diabetes care is Rosuvastatin Tablets and ciclosporin,
appropriate. This risk, however, is outweighed rosuvastatin AUC values were on average 7
by the reduction in vascular risk with statins and times higher than those observed in healthy
therefore should not be a reason for stopping
volunteers (see Table 1). Rosuvastatin Tablets is
statin treatment. Patients at risk (fasting glucose contraindicated in patients receiving
5.6 to 6.9 mmol/l, BMI >30 kg/m2, raised concomitant cyclosporine (see section 4.3).
triglycerides, hypertension) should be monitored
both clinically and biochemically according to Concomitant administration did not affect
national guidelines. plasma concentrations of ciclosporin.
In the JUPITER study, the reported overall Protease inhibitors: Although the exact
frequency of diabetes mellitus was 2.8% in mechanism of interaction is unknown,
rosuvastatin and 2.3% in placebo, mostly in concomitant protease inhibitor use may strongly
patients with fasting glucose 5.6 to 6.9 mmol/l. increase rosuvastatin exposure (see Table 1). For
instance, in a pharmacokinetic study, co-
Pediatric population
administration of 10 mg rosuvastatin and a
The evaluation of linear growth (height), weight, combination product of two protease inhibitors
BMI (body mass index), and secondary (300 mg atazanavir / 100 mg ritonavir) in
characteristics of sexual maturation by Tanner healthy volunteers was associated with an
staging in pediatric patients 6 to 17 years of age approximately three-fold and seven-fold
taking rosuvastatin is limited to a two-year increase in rosuvastatin AUC and C max
period. After two years of study treatment, no respectively. The concomitant use of
effect on growth, weight, BMI or sexual Rosuvastatin Tablets and some protease
maturation was detected (see section 5.1). inhibitor combinations may be considered after
careful consideration of Rosuvastatin Tablets
In a clinical trial of children and adolescents dose adjustments based on the expected increase
receiving rosuvastatin for 52 weeks, CK in rosuvastatin exposure(see sections 4.2, 4.4,
elevations >10xULN and muscle symptoms and 4.5 Table 1).
following exercise or increased physical activity
were observed more frequently compared to Gemfibrozil and other lipid-lowering
observations in clinical trials in adults (see products: Concomitant use of Rosuvastatin and
section 4.8). gemfibrozil resulted in a 2- fold increase in
rosuvastatin C max and AUC (see section 4.4).
Based on data from specific interaction studies inhibitor of CYP2C9 and CYP3A4) or
no pharmacokinetic relevant interaction with ketoconazole (an inhibitor of CYP2A6 and
fenofibrate is expected, however a CYP3A4).
pharmacodynamic interaction may occur.
Gemfibrozil, fenofibrate, and other fibrates and Interactions requiring rosuvastatin dose
lipid lowering doses (> or equal to 1g/day) of adjustments (see also Table 1): When it is
niacin (nicotinic acid) increase the risk of necessary to co-administer Rosuvastatin Tablets
myopathy when given concomitantly with with other medicinal products known to increase
HMG-CoA reductase inhibitors, probably exposure to rosuvastatin, doses of Rosuvastatin
because they can produce myopathy when given Tablets should be adjusted. Start with a 5 mg
once daily dose of Rosuvastatin Tablets if the
alone. The 40 mg dose is contraindicated with
expected increase in exposure (AUC) is
concomitant use of a fibrate (see section 4.3 and
4.4). These patients should also start with the 5 approximately 2-fold or higher. The maximum
mg dose. daily dose of Rosuvastatin Tablets should be
adjusted so that the expected rosuvastatin
Ezetimibe: Concomitant use of 10 mg exposure would not likely exceed that of a 40
Rosuvastatin and 10 mg ezetimibe resulted in a mg daily dose of Rosuvastatin Tablets taken
1.2 fold increase in AUC of rosuvastatin in without interacting medicinal products, for
hypercholesterolaemia subjects (Table 1). A example a 20 mg dose of Rosuvastatin Tablets
pharmacodynamic interaction, in terms of with gemfibrozil (1.9-fold increase), and a 10
adverse effects, between Rosuvastatin Tablets mg dose of Rosuvastatin Tablets with
and ezetimibe cannot be ruled out (see section combination ritonavir/atazanavir (3. 1- fold
4.4). increase).
Antacid: The simultaneous dosing of Table 1 Effect of co-administered medicinal
Rosuvastatin with an antacid suspension products on rosuvastatin exposure (AUC; in
containing aluminum and magnesium hydroxide order of decreasing magnitude) from
resulted in a decrease in rosuvastatin plasma published clinical trials
concentration of approximately 50%. This effect
Interacting Change in
was mitigated when the antacid was dosed 2 Rosuvastatin
drug dose rosuvastatin
hours after Rosuvastatin. The clinical relevance dose regimen
regimen AUC *
of this interaction has not been studied.
Ciclosporin 75
Erythromycin: Concomitant use of mg BID to 200 10 mg OD, 10
Rosuvastatin and erythromycin resulted in a 7.1- fold ↑
mg BID, 6 days
20% decrease in AUC and a 30% decrease in C months
max of rosuvastatin. This interaction may be
Atazanavir 300
caused by the increase in gut motility caused by
mg/ritonavir 10 mg Single
erythromycin. 3.1- fold ↑
100 mg OD, 8 Dose
Cytochrome P450 enzymes: Results from in days
vitro and in vivo studies show that rosuvastatin Simeprevir 150 10 mg, single
is neither an inhibitor nor an inducer of 2.8 fold ↑
mg OD, 7 days dose
cytochrome P450 isoenzymes. In addition,
Lopinavir 400
rosuvastatin is a poor substrate for these
mg/ ritonavir 20 mg OD, 7
isoenzymes. Therefore, drug interactions 2.1- fold ↑
100 mg BID, days
resulting from cytochrome P450-mediated
17 days
metabolism are not expected. No clinically
relevant interactions have been observed Clopidogrel 20 mg, single
2-fold ↑
between rosuvastatin and either fluconazole (an 300 mg dose
loading, Erythromycin
80mg, single
followed by 75 500 mg QID, 7 20% ↓
dose
mg at 24 hours days
Gemifibrozil Baicalin 50mg 20 mg, single
80 mg, single 47% ↓
600 mg BID, 7 1.9- fold ↑ TID, 14 days dose
dose
days Regorafenib
5 mg single
Eltrombopag 160 mg, OD, 3.8-fold ↑
10 mg, single dose
75 mg OD, 5 1.6- fold ↑ 14 days
dose
days Velpatasvir 10 mg, single
2.7-fold ↑
Darunavir 600 100 mg OD dose
mg/ 10 mg OD, 7 Ombitasvir 25
1.5- fold ↑
ritonavir100 days mg/paritaprevir
mg BID, 7 days 150
Tipranavir 500 mg/Ritonavir 5 mg, single
2.6-fold ↑
mg/ ritonavir 10 mg, single 100 mg OD/ dose
1.4- fold ↑
200 mg BID, dose dasabuvir 400
11 days mg BID, 14
Dronedarone days
Not Available 1.4- fold ↑
400 mg BID Grazoprevir
Itraconazole 200
10 mg, single 10 mg, single
200 mg OD, 5 **
1.4- fold ↑ mg/elbasvir 2.3-fold ↑
dose dose
days 50mg OD, 11
days
Ezetimibe 10
10 mg OD, 14 Glecaprevir
mg OD, 14 **
1.2- fold ↑
days 400
days 5 mg OD, 7
mg/pibrentasvir 2.2-fold ↑
Fosamprenavir days
120 mg OD, 7
700 mg/ 10 mg, single
↔ days
ritonavir 100 dose *
mg BID 8 days Data given as x-fold change represent a simple
ratio between co-administration and rosuvastatin
Aleglitazar 0.3
40 mg, 7 days ↔ alone. Data given as % change represent %
mg, 7 days difference relative to rosuvastatin alone.
Silymarin 140 10 mg, single
↔ Increase is indicated as “↑”, no change as “↔”,
mg TID, 5 days dose and decrease as “↓”.
**
Fenofibrate 67 Several Interaction studies have been
10 mg, 7 days ↔ performed at different Rosuvastatindosages, the
mg TID, 7 days
table shows the most significant ratio.
Rifampin 450 20 mg, single
↔ OD = once daily; BID = twice daily; TID = three
mg OD, 7 days dose
times daily; QID = four times daily
Ketoconazole Effect of rosuvastatin on co-administered
80mg, single
200 mg BID, 7 ↔ medicinal products
dose
days
Fluconazole Vitamin K antagonists: As with other HMG-
80 mg, single CoA reductase inhibitors, the initiation of
200 mg OD, 11 ↔
dose treatment or dosage up titration of Rosuvastatin
days
Tablets in patients treated concomitantly with
vitamin K antagonists (e.g. warfarin or another Pregnancy

coumarin anticoagulant) may result in an
increase in International Normalised Ratio Rosuvastatin Tablets are contraindicated in
pregnancy and lactation.
(INR). Discontinuation or down-titration of
Rosuvastatin Tablets may result in a decrease in Women of child bearing potential should use
INR. In such situations, appropriate monitoring appropriate contraceptive measures.
of INR is desirable.
Since cholesterol and other products of
Oral contraceptive/hormone replacement cholesterol biosynthesis are essential for the
therapy (HRT): Concomitant use of development of the foetus, the potential risk
Rosuvastatin Tablets and an oral contraceptive from inhibition of HMG-CoA reductase
resulted in an increase in ethinyl estradiol and outweighs the advantage of treatment during
norgestrel AUC of 26% and 34%, respectively. pregnancy. Animal studies provide limited
These increased plasma levels should be evidence of reproductive toxicity (see section
considered when selecting oral contraceptive 5.3). If a patient becomes pregnant during use of
doses. There are no pharmacokinetic data this product, treatment should be discontinued
available in subjects taking concomitant immediately.
Rosuvastatin Tablets and HRT and therefore a
similar effect cannot be excluded. However, the Breast-feeding
combination has been extensively used in Rosuvastatin is excreted in the milk of rats.
women in clinical trials and was well tolerated. There are no data with respect to excretion in
Other medicinal products: milk in humans (see section 4.3).
Digoxin: Based on data from specific interaction Fertility

studies no clinically relevant interaction with Rosuvastatin is not known to affect fertility in
digoxin is expected. animals. Rosuvastatin effects in humans are
Fusidic Acid: Interaction studies with unknown.
rosuvastatin and fusidic acid have not been 4.7 Effects on ability to drive and use
conducted. The risk of myopathy including machines
rhabdomyolysis may be increased by the Studies to determine the effect of Rosuvastatin
concomitant administration of systemic fusidic Tablets on the ability to drive and use machines
acid with statins. The mechanism of this have not been conducted. However, based on its
interaction (whether it is pharmacodynamic or pharmacodynamic properties, Rosuvastatin
pharmacokinetic, or both) is yet unknown. There Tablets is unlikely to affect this ability. When
have been reports of rhabdomyolysis (including driving vehicles or operating machines, it should
some fatalities) in patients receiving this be taken into account that dizziness may occur
combination. during treatment.
If treatment with systemic fusidic acid is 4.8 Undesirable effects
necessary, Rosuvastatin treatment should be The adverse reactions seen with Rosuvastatin
discontinued throughout the duration of the Tablets are generally mild and transient. In
fusidic acid treatment. Also see section 4.4. controlled clinical trials, less than 4% of
Pediatric population: Interaction studies have Rosuvastatin-treated patients were withdrawn
only been performed in adults. The extent of due to adverse reactions.
interactions in the pediatric population is not Tabulated list of adverse reactions
known.
Based on data from clinical studies and
4.6 Fertility, pregnancy and lactation extensive post-marketing experience, the
following table presents the adverse reaction ding

profile for rosuvastatin. Adverse reactions listed insom
below are classified according to frequency and nia
system organ class (SOC). and
The frequencies of adverse reactions are ranked night
according to the following convention: Common mares
(≥1/100 to <1/10); Uncommon (≥1/1,000 to )
<1/100); Rare (≥1/10,000 to <1/1000); Very rare Respir Coug
(<1/10,000); Not known (cannot be estimated atory, h
from the available data). thoraci Dyspn
c and oea
Table 2. Adverse reactions based on data from medias
clinical studies and post-marketing experience tinal
System Com Unco Rare Very Not disorde
Organ mon mmo Rare Know rs
Class n n Gastro Consti Pancreati Diarrh
Blood Thrombo - pation tis oea
and cytopenia intestin Nause
lympha al a
tic disorde Abdo
system rs minal
disorde pain
r Hepato Increased Jaundic
Immun Hypersen biliary hepatic e
e sitivity disorde transamin Hepatiti
system reactions rs ases s
disorde including Skin Pruriti Steve
rs angioede and s ns-
ma subcut Rash Johns
Endocr Diabet aneous Urtica on
ine es tissue ria syndr
disorde Mellit disorde ome
rs us 1 rs
Psychi Depre Muscul Myalg Myopath Arthral Tendo
atric ssion o- ia y gia n
disorde skeletal (includin disord
rs and g ers,
connec myositis) somet
Nervou Heada Polyneu Periph tive Rhabdom imes
s che ropathy eral tissue yolysis compl
system Dizzin Memor neuro disorde icated
disorde ess y loss pathy rs by
rs Sleep ruptur
distur e
bance Immu
s ne-
(inclu
media experience to date has not identified a causal

ted association between proteinuria and acute or
necrot progressive renal disease.
izing Haematuria has been observed in patients treated
myop with Rosuvastatin and clinical trial data show
athy that the occurrence is low.
Renal Haemat
and uria Skeletal muscle effects: Effects on skeletal
urinary muscle e.g. myalgia, myopathy (including
disorde myositis) and, rarely, rhabdomyolysis with and
rs without acute renal failure have been reported in
Rosuvastatin-treated patients with all doses and
Reprod Gynaec in particular with doses > 20 mg.
uctive omastia
system A dose-related increase in CK levels has been
and observed in patients taking rosuvastatin; the
breast majority of cases were mild, asymptomatic and
disorde transient. If CK levels are elevated (>5xULN),
rs treatment should be discontinued (see section
Genera Asthe Oede 4.4).
l nia ma Liver effects: As with other HMG-CoA
disorde reductase inhibitors, a dose-related increase in
rs & transaminases has been observed in a small
admini number of patients taking rosuvastatin; the
stratio majority of cases were mild, asymptomatic and
n site transient.
conditi
ons The following adverse events have been
1 reported with some statins:
Frequency will depend on the presence or
absence of risk factors (fasting blood glucose ≥ - Sexual dysfunction.
5.6 mmol/L, BMI >30 kg/m2, raised
triglycerides, history of hypertension). - - Exceptional cases of interstitial lung disease,
especially with long term therapy (see section
As with other HMG-CoA reductase inhibitors, 4.4).
the incidence of adverse drug reactions tends to
be dose dependent. The reporting rates for rhabdomyolysis, serious
renal events and serious hepatic events
Renal Effects: Proteinuria, detected by dipstick (consisting mainly of increased hepatic
testing and mostly tubular in origin, has been transaminases) are higher at the 40 mg dose.
observed in patients treated with Rosuvastatin.
Shifts in urine protein from none or trace to ++ Pediatric population: Creatine kinase
or more were seen in <1% of patients at some elevations >10xULN and muscle symptoms
time during treatment with 10 and 20 mg, and in following exercise or increased physical activity
approximately 3% of patients treated with 40 were observed more frequently in a 52-week
mg. A minor increase in shift from none or trace clinical trial of children and adolescents
to + was observed with the 20 mg dose. In most compared to adults (see section 4.4). In other
cases, proteinuria decreases or disappears respects, the safety profile of Rosuvastatin was
spontaneously on continued therapy. Review of similar in children and adolescents compared to
data from clinical trials and post-marketing adults.
Reporting of suspected adverse reactions Dose N LD Tota HD T Non Apo Apo

Reporting suspected adverse reactions after L-C l-C L-C G HD B A-I
authorisation of the medicinal product is L-C
important. It allows continued monitoring of the Place 1 -7 -5 3 -3 -7 -3 0
benefit/risk balance of the medicinal product. bo 3
4.9 Overdose 5 1 -45 -33 13 - -44 -38 4
There is no specific treatment in the event of 7 35
overdose. In the event of overdose, the patient 10 1 -52 -36 14 - -48 -42 4
should be treated symptomatically and 7 10
supportive measures instituted as required. Liver 20 1 -55 -40 8 - -51 -46 5
function and CK levels should be monitored. 7 23
Haemodialysis is unlikely to be of benefit.
40 1 -63 -46 10 - -60 -54 0
5. Pharmacological properties 8 28
A therapeutic effect is obtained within 1 week
5.1 Pharmacodynamic properties following treatment initiation and 90% of
Pharmacotherapeutic Group: HMG-CoA maximum response is achieved in 2 weeks. The
reductase inhibitors maximum response is usually achieved by 4
weeks and is maintained after that.
Mechanism of Action
Clinical Efficacy and safety
Rosuvastatin is a selective and competitive
inhibitor of HMG-CoA reductase, the rate- Rosuvastatin Tablets is effective in adults with
limiting enzyme that converts 3- hydroxy-3- hypercholesterolaemia, with and without
methylglutaryl coenzyme A to mevalonate, a hypertriglyceridaemia, regardless of race, sex, or
precursor for cholesterol. The primary site of age and in special populations such as diabetics,
action of rosuvastatin is the liver, the target or patients with familial hypercholesterolaemia.
organ for cholesterol lowering.
From pooled phase III data, Rosuvastatin has
Rosuvastatin increases the number of hepatic been shown to be effective at treating the
LDL receptors on the cell-surface, enhancing majority of patients with type IIa and
uptake and catabolism of LDL and it inhibits the IIbhypercholesterolaemia (mean baseline LDL-
hepatic synthesis of VLDL, thereby reducing the C about 4.8 mmol/l) to recognised European
total number of VLDL and LDL particles. Atherosclerosis Society (EAS; 1998) guideline
targets; about 80% of patients treated with 10
Pharmacodynamic effects
mg reached the EAS targets for LDL-C levels
Rosuvastatin reduces elevated LDL-cholesterol, (<3 mmol/l).
total cholesterol and triglycerides and increases
In a large study, 435 patients with heterozygous
HDL-cholesterol. It also lowers ApoB, non
familial hypercholesterolaemia were given
HDL-C, VLDL-C, VLDL-TG and increases
Rosuvastatin from 20 mg to 80 mg in a force-
ApoA-I (see Table 3). Rosuvastatin also lowers
titration design. All doses showed a beneficial
the LDL-C/ HDL-C, total C/HDL-C and non
effect on lipid parameters and treatment to target
HDL-C/HDL-C and the ApoB/ApoA-I ratios.
goals. Following titration to a daily dose of 40
Table 3 Dose response in patients with mg (12 weeks of treatment), LDL-C was
primary hypercholesterolaemia (type IIa and reduced by 53%. 33% of patients reached EAS
IIb) (adjusted mean percent change from guidelines for LDL-C levels (<3 mmol/l).
baseline)
In a force-titration, open label trial, 42 patients
(including 8 paediatric patients) with
homozygous familial hypercholesterolaemia Study participants were randomly assigned to

were evaluated for their response to placebo (n=8901) or rosuvastatin 20 mg once
Rosuvastatin 20 - 40 mg. In the overall daily (n=8901) and were followed for a mean
population, the mean LDL-C reduction was duration of 2 years.
22%.
LDL-cholesterol concentration was reduced by
In clinical studies with a limited number of 45% (p<0.001) in the rosuvastatin group
patients, Rosuvastatin has been shown to have compared to the placebo group.
additive efficacy in lowering triglycerides when
used in combination with fenofibrate and in In a post-hoc analysis of a high-risk subgroup of
increasing HDL-C levels when used in subjects with a baseline Framingham risk score
combination with niacin (see section 4.4). >20% (1558 subjects) there was a significant
reduction in the combined end-point of
In a multi-centre, double-blind, placebo- cardiovascular death, stroke and myocardial
controlled clinical study (METEOR), 984 infarction (p=0.028) on rosuvastatin treatment
patients between 45 and 70 years of age and at versus placebo. The absolute risk reduction in
low risk for coronary heart disease (defined as the event rate per 1000 patient-years was 8.8.
Framingham risk <10% over 10 years), with a Total mortality was unchanged in this high risk
mean LDL-C of 4.0 mmol/l (154.5 mg/dL), but group (p=0.193). In a post-hoc analysis of a
with subclinical atherosclerosis (detected by high-risk subgroup of subjects (9302 subjects
Carotid Intima Media Thickness) were total) with a baseline SCORE risk ≥5%
randomised to 40 mg rosuvastatin once daily or (extrapolated to include subjects above 65 yrs)
placebo for 2 years. Rosuvastatin significantly there was a significant reduction in the
slowed the rate of progression of the maximum combined end-point of cardiovascular death,
CIMT for the 12 carotid artery sites compared to stroke and myocardial infarction (p=0.0003) on
placebo by -0.0145 mm/year [95% confidence rosuvastatin treatment versus placebo. The
interval -0.0196, -0.0093; p<0.0001]. The absolute risk reduction in the event rate was 5.1
change from baseline was -0.0014 mm/year (- per 1000 patient-years. Total mortality was
0.12%/year (non-significant)) for rosuvastatin unchanged in this high risk group (p=0.076).
compared to a progression of +0.0131 mm/year
In the JUPITER trial there were 6.6% of
(1.12%/year (p<0.0001)) for placebo. No direct
correlation between CIMT decrease and rosuvastatin and 6.2% of placebo subjects who
reduction of the risk of cardiovascular events has discontinued use of study medication due to an
yet been demonstrated. The population studied adverse event. The most common adverse events
in METEOR is low risk for coronary heart that led to treatment discontinuation were:
disease and does not represent the target myalgia (0.3% rosuvastatin, 0.2% placebo),
population of Rosuvastatin 40 mg. The 40 mg abdominal pain (0.03% rosuvastatin, 0.02%
dose should only be prescribed in patients with placebo) and rash (0.02% rosuvastatin, 0.03%
severe hypercholesterolaemia at high placebo). The most common adverse events at a
cardiovascular risk (see section 4.2). rate greater than or equal to placebo were
urinary tract infection (8.7% rosuvastatin, 8.6%
In the Justification for the Use of Statins in placebo), nasopharyngitis (7.6% rosuvastatin,
Primary Prevention: An Intervention Trial 7.2% placebo), back pain (7.6% rosuvastatin,
Evaluating Rosuvastatin (JUPITER) study, the 6.9% placebo) and myalgia (7.6% rosuvastatin,
effect of rosuvastatin on the occurrence of major 6.6% placebo).
atherosclerotic cardiovascular disease events
was assessed in 17,802 men (≥50 years) and Paediatric population
women (≥60 years). In a double-blind, randomized, multi-centre,
placebo-controlled, 12-week study (n=176, 97
male and 79 female) followed by a 40-week Rosuvastatin 5 mg, 10 mg, and 20 mg also
(n=173, 96 male and 77 female), open-label, achieved statistically significant mean changes
rosuvastatin dose-titration phase, patients 10-17 from baseline for the following secondary lipid
years of age (Tanner stage II-V, females at least and lipoprotein variables: HDL-C, TC, non-
1 year post-menarche) with heterozygous HDL-C, LDL-C/HDL-C, TC/HDL-C, TG/HDL-
familial hypercholesterolaemia received C, non-HDL-C/HDL-C, ApoB, ApoB/ApoA-1.
rosuvastatin 5, 10 or 20 mg or placebo daily for These changes were each in the direction of
12 weeks and then all received rosuvastatin daily improved lipid responses and were sustained
for 40 weeks. At study entry, approximately over 2 years.
30% of the patients were 10-13 years and
No effect on growth, weight, BMI or sexual
approximately 17%, 18%, 40%, and 25% were
Tanner stage II, III, IV, and V, respectively. maturation was detected after 24 months of
treatment (see Section 4.4).
LDL-C was reduced 38.3%, 44.6%, and 50.0%
by rosuvastatin 5, 10 and 20 mg, respectively, Rosuvastatin was studied in a randomised,
compared to 0.7% for placebo. double-blind, placebo-controlled, multicenter,
cross-over study with 20 mg once daily versus
At the end of the 40-week, open-label, titration placebo in 14 children and adolescents (aged
to goal, dosing up to a maximum of 20 mg once from 6 to 17 years) with homozygous familial
daily, 70 of 173 patients (40.5%) had achieved hypercholesterolaemia. The study included an
the LDL-C goal of less than 2.8 mmol/l. active 4-week dietary lead-in phase during
which patients were treated with rosuvastatin 10
After 52 weeks of study treatment, no effect on mg, a cross-over phase that consisted of a 6-
growth, weight, BMI or sexual maturation was week treatment period with rosuvastatin 20 mg
detected (see section 4.4). This trial (n=176) was preceded or followed by a 6-week placebo
not suited for comparison of rare adverse drug treatment period, and a 12-week maintenance
events.
phase during which all patients were treated with
Rosuvastatin was also studied in a 2-year open- rosuvastatin 20 mg. Patients who entered the
label, titration-to-goal study in 198 children with study on ezetimibe or apheresis therapy
heterozygous familial hypercholesterolaemia continued the treatment throughout the entire
aged 6 to 17 years (88 male and 110 female, study.
Tanner stage <II-V). The starting dose for all
A statistically significant (p=0.005) reduction in
patients was 5 mg rosuvastatin once daily. LDL-C (22.3%, 85.4 mg/dL or 2.2 mmol/L) was
Patients aged 6 to 9 years (n=64) could titrate to observed following 6 weeks of treatment with
a maximum dose of 10 mg once daily and rosuvastatin 20 mg versus placebo. Statistically
patients aged 10 to 17 years (n=134) to a significant reductions in Total-C (20.1%,
maximum dose of 20 mg once daily.
p=0.003), nonHDL-C (22.9%, p=0.003), and
After 24 months of treatment with rosuvastatin, ApoB (17.1%, p=0.024) were observed.
the LS mean percent reduction from the baseline Reductions were also seen in TG, LDL-C/HDL-
value in LDL-C was - 43% (Baseline: 236 C, Total-C/HDL-C, nonHDL-C/HDL-C, and
mg/dL, Month 24: 133 mg/dL). For each age ApoB/ApoA-1 following 6 weeks of treatment
group, the LS mean percent reductions from with rosuvastatin 20 mg versus placebo. The
baseline values in LDL-C were -43% (Baseline: reduction in LDL-C after 6 weeks of treatment
234 mg/dL, Month 24: 124 mg/dL), -45% with rosuvastatin 20 mg following 6 weeks of
(Baseline: 234 mg/dL, 124 mg/dL), and -35% treatment with placebo was maintained over 12
(Baseline: 241 mg/dL, Month 24: 153 mg/dL) in weeks of continuous therapy. One patient had a
the 6 to <10, 10 to <14, and 14 to <18 age further reduction in LDL-C (8.0%), Total-C
groups, respectively.
(6.7%) and non-HDL-C (7.4%) following 6 P450-based metabolism. CYP2C9 was the
weeks of treatment with 40 mg after up-titration. principal is enzyme involved, with 2C19, 3A4
and 2D6 involved to a lesser extent. The main
During an extended open-label treatment in 9 of metabolites identified are the N-desmethyl and
these patients with 20 mg rosuvastatin for up to lactone metabolites. The N-desmethyl
90 weeks, the LDL-C reduction was maintained metabolite is approximately 50% less active than
in the range of -12.1% to -21.3%.
Rosuvastatin whereas the lactone form is
In the 7 evaluable children and adolescent considered clinically inactive. Rosuvastatin
patients (aged from 8 to 17 years) from the accounts for greater than 90% of the circulating
force-titration open label study with HMG-CoA reductase inhibitor activity.
homozygous familial hypercholesterolaemia (see
Excretion
above), the percent reduction in LDL-C (21.0%),
Total-C (19.2%), and non-HDL-C (21.0%) from Approximately 90% of the rosuvastatin dose is
baseline following 6 weeks of treatment with excreted unchanged in the faeces (consisting of
rosuvastatin 20 mg was consistent with that absorbed and non-absorbed active substance)
observed in the aforementioned study in children and the remaining part is excreted in urine.
and adolescents with homozygous familial Approximately 5% is excreted unchanged in
hypercholesterolaemia. urine. The plasma elimination half-life is
approximately 19 hours. The elimination half-
The European Medicines Agency has waived the
life does not increase at higher doses. The
obligation to submit the results of studies with geometric mean plasma clearance is
rosuvastatin in all subsets of the paediatric approximately 50 liters/hour (coefficient of
population in the treatment of homozygous variation 21.7%). As with other HMG-CoA
familial hypercholesterolaemia, primary reductase inhibitors, the hepatic uptake of
combined (mixed) dyslipidaemia and in the rosuvastatin involves the membrane transporter
prevention of cardiovascular events (see Section
OATP-C. This transporter is important in the
4.2 for information on paediatric use).
hepatic elimination of rosuvastatin.
5.2 Pharmacokinetic properties Linearity
Absorption
Systemic exposure of rosuvastatin increases in
Maximum rosuvastatin plasma concentrations proportion to dose. There are no changes in
are achieved approximately 5 hours after oral
pharmacokinetic parameters following multiple
administration. The absolute bioavailability is daily doses.
approximately 20%.
Special populations
Distribution
Age and sex: There was no clinically relevant
Rosuvastatin is taken up extensively by the liver effect of age or sex on the pharmacokinetics of
which is the primary site of cholesterol synthesis rosuvastatin in adults. The exposure in children
and LDL-C clearance. The volume of and adolescents with heterozygous familial
distribution of rosuvastatin is approximately 134 hypercholesterolemia appears to be similar to or
L. Approximately 90% of rosuvastatin is bound lower than that in adult patients with
to plasma proteins, mainly to albumin.
dyslipidaemia (see “Paediatric population”
Metabolism below).
Rosuvastatin undergoes limited metabolism Race: Pharmacokinetic studies show an
(approximately 10%). In vitro metabolism approximate 2-fold elevation in median AUC
studies using human hepatocytes indicate that and Cmax in Asian subjects (Japanese, Chinese,
rosuvastatin is a poor substrate for cytochrome Filipino, Vietnamese and Koreans) compared
with Caucasians; Asian-Indians show an Two pharmacokinetic studies with rosuvastatin

approximate 1.3-fold elevation in median AUC (given as tablets) in paediatric patients with
and C max. A population pharmacokinetic heterozygous familial hypercholesterolaemia 10-
analysis revealed no clinically relevant 17 or 6-17 years of age (total of 214 patients)
differences in pharmacokinetics between demonstrated that exposure in paediatric patients
Caucasian and Black groups. appears comparable to or lower than that in adult
patients. Rosuvastatin exposure was predictable
Renal insufficiency: In a study in subjects with with respect to dose and time over a 2-year
varying degrees of renal impairment, mild to period.
moderate renal disease had no influence on
plasma concentration of rosuvastatin or the N- 5.3 Preclinical safety data
desmethyl metabolite. Subjects with severe Preclinical data reveal no special hazard for
impairment (CrCl<30 ml/min) had a 3-fold humans based on conventional studies of safety
increase in plasma concentration and a 9-fold pharmacology, genotoxicity and carcinogenicity
increase in the N desmethyl metabolite potential. Specific tests for effects on hERG
concentration compared to healthy volunteers. have not been evaluated. Adverse reactions not
Steady-state plasma concentrations of observed in clinical studies, but seen in animals
rosuvastatin in subjects undergoing at exposure levels similar to clinical exposure
haemodialysis were approximately 50% greater levels were as follows: In repeated-dose toxicity
compared to healthy volunteers. studies histopathologic liver changes likely due
to the pharmacologic action of Rosuvastatin
Hepatic insufficiency: In a study with subjects were observed in mouse, rat, and to a lesser
with varying degrees of hepatic impairment extent with effects in the gall bladder in dogs,
there was no evidence of increased exposure to but not in monkeys. In addition, testicular
rosuvastatin in subjects with Child-Pugh scores
toxicity was observed in monkeys and dogs at
of 7 or below. However, two subjects with
higher dosages. Reproductive toxicity was
Child-Pugh scores of 8 and 9 showed an evident in rats, with reduced litter sizes, litter
increase in systemic exposure of at least 2-fold weight and pup survival observed at maternally
compared to subjects with lower Child-Pugh
toxic doses, where systemic exposures were
scores. There is no experience in subjects with several times above the therapeutic exposure
Child-Pugh scores above 9. level.
Genetic polymorphisms: Disposition of HMG-
CoA reductase inhibitors, including rosuvastatin, 6. Pharmaceutical particulars
involves OATP1B1 and BCRP transporter
6.1 List of excipients
proteins. In patients with SLCO1B1 (OATP1B1)
Sodium bicarbonate, Precipitated calcium
and/or ABCG2 (BCRP) genetic polymorphisms
carbonate, Lactose monohydrate,
there is a risk of increased rosuvastatin
Microcrystalline cellulose, Crospovidone,
exposure. Individual polymorphisms of
Povidone, Magnesium stearate,
SLCO1B1 c.521CC and ABCG2 c.421AA are
Opadry,Hypromellose, Titanium dioxide.
associated with a higher Rosuvastatin exposure
(AUC) compared to the SLCO1B1 c.521TT or 6.2 Incompatibilities
ABCG2 c.421CC genotypes. This specific Not applicable
genotyping is not established in clinical practice,
but for patients who are known to have these 6.3 Shelf life
types of polymorphisms, a lower daily dose of 3 years
Rosuvastatin is recommended. 6.4 Special precautions for storage
Paediatric population: Blister pack: Store in the original blister packs to
protect from moisture
Container pack: Keep the plastic container

tightly closed to protect from moisture
6.5 Nature and contents of container
Rosuvastatin Tablets are available in Alu-Alu
blister.
Pack sizes: 7, 14, 28, 30, 50, 60, 90, 100 and 500
Tablets.
Not all pack sizes may be marketed.
6.6 Special precautions for disposal and other
handling
No special requirements for disposal.
7. Manufactured In India By:
TAJ PHARMACEUTICALS LTD.
Mumbai, India
Unit No. 214.Old Bake House,
Maharashtra chambers of Commerce Lane,
Fort, Mumbai - 400001
at:Gujarat, INDIA.
Customer Service and Product Inquiries:
1-800-TRY-FIRST (1-800-222-434 & 1-800-
222-825)
Monday through Saturday 9:00 a.m. to 7:00 p.m.
EST
E-mail: tajgroup@tajpharma.com

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Ros uvastatin 10mg, 20mg, 40mg Ta blets TajPhar ma : U ses, Side E ffe cts, Intera ctions , Picture s, Warni

Rosuvastatin Calcium Tablets diet and other non-pharmacological treatments

2. Qualitative and quantitative Prevention of major cardiovascular events in

Prevention of cardiovascular events paediatric treatment recommendations (see

Race - in patients with hypersensitivity to rosuvastatin

The 40 mg dose is contraindicated in some of - moderate renal impairment (creatinine

inhibitors. Therefore, the combination of It is recommended that liver function tests be

Interstitial lung disease 4.5 Interaction with other medicinal products

vitamin K antagonists (e.g. warfarin or another Pregnancy

Digoxin: Based on data from specific interaction Fertility

following table presents the adverse reaction ding

media experience to date has not identified a causal

Reporting of suspected adverse reactions Dose N LD Tota HD T Non Apo Apo

homozygous familial hypercholesterolaemia Study participants were randomly assigned to

with Caucasians; Asian-Indians show an Two pharmacokinetic studies with rosuvastatin

Container pack: Keep the plastic container

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