Corestin Tablet 10mg10 tablets
Corestin 5 mg Tablet: Pink, round shaped film-coated tablet each tablet contains Rosuvastatin calcium BP equivalent to
Rosuvastatin 5 mg.
Corestin 10 mg Tablet: Pink, shield-shaped, scored on one side, a [https://unimedunihealth.com/wp-content/uploads/2014/04/a.jpg]
[https://unimedunihealth.com/wp-content/uploads/2014/04/a.jpg] engraved on another side film-coated tablet; each tablet contains
Rosuvastatin calcium BP equivalent to Rosuvastatin 10 mg.
Corestin 20 mg Tablet: Pink, diamond-shaped, scored film coated tablet; each tablet contains Rosuvastatin calcium BP equivalent to
Rosuvastatin 20 mg.
Corestin is indicated for patients with primary hypercholesterolaemia (type lla including heterozygous familial
hypercholesterolaemia) or mixed dyslipidaemia (type llb) as an adjunct to diet when the response to diet and exercise are
Corestin reduces elevated LDL-cholesterol, total cholesterol, triglycerides, and ApoB, and increases HDL-cholesterol
Corestin is also indicated in patients with homozygous familial hypercholesterolaemia, either alone or as an adjunct to diet and
other lipid-lowering treatments (e.g. LDL apheresis)
Dosage & administration
Before initiating treatment with Corestin, the patient should be placed on a standard cholesterol-lowering diet that should
continue during treatment. The dose of Corestin should be individualised according to the goal of therapy and patient response,
using current consensus guidelines.
The usual start dose is Corestin 10 mg once daily and the majority of patients are controlled at this dose. A dose adjustment to
20 mg can be made after 4 weeks if necessary Corestin at a dose of 40 mg should only be used in patients with severe
hypercholesterolaemia (including those with familial hypercholesterolaemia) who do not achieve their treatment goal on 20 mg.
Corestin may be given at any time of day, with or without food.
Use in children
Paediatric experience is limited to a small number of children (aged 8 years or above) with homozygous familial
hypercholesterolaemia. Use in children should be supervised by specialists.
Use in the elderly
No dose adjustment is necessary
Dosage in patients with renal insufficiency
No dose adjustment is necessary for patients with mild to moderate renal impairment. For patients with severe renal impairment
(CrCl <30 m/min) the dose of Corestin should not exceed 10 mg once daily
Dosage in patients with hepatic impairment
No dose adjustment is necessary for patients with mild to moderate hepatic impairment Increased systemic exposure to rosuvastatin
has been observed in patients with severe hepatic impairment, therefore, the dose of Corestin should not exceed 20 mg once daily.
Interactions requiring dose adjustments
Gemfibrozil: Increased systemic exposure to rosuvastatin has been observed in subjects taking concomitant Corestin and
gemfibrozil. Patients taking this combination should not exceed a dose of Corestin 10 mg once daily.
Contra indications, warnings etc.
Contra indications: Rosuvastatin is contraindicated in patients:-
* with hypersensitivity to any component of this product.
* with active liver disease including unexplained, persistent elevations of serum transaminases and any serum transaminase
elevation exceeding 3 x the upper limit of normal.
* with myopathy.
* receiving concomitant cyclosporin.
Warnings and Precautions
As with other HMG-CoA reductase inhibitors, Corestin 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 with Rosuvastatin. Rosuvastatin should be discontinued or the dose reduced it the level of
serum transaminases is greater than 3 times the upper limit of normal.
Patients should be asked to report inexplicable muscle pain or weakness immediately, particularly if associated with malaise or
fever. CK levels should be measured in these patients. Rosuvastatin therapy should be discontinued if CK levels are markedly
elevated (10xULN) or, If on clinical grounds, myopathy is diagnosed or suspected.
In Rosuvastatin trials there was no evidence of increased skeletal muscle effects in the small number of patients dosed with
Corestin and concomitant therapy.
Corestin 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).
Proteinuria, detected by dipstick testing and mostly tubular in origin has been observed in patients treated with renal disease.
Vitamin K antagonists: As with other HMG-CoA reductase inhibitors, the initiation of treatment or dosage up-titration of Corestin
in patients treated concomitantly with vitamin K antagonists (e.g. warfarin) may result in an increase in INR. Discontinuation or
down-titration of Corestin may result in a decrease in INR. In such situations, appropriate monitoring of INR is desirable.
Gemfibrozil: Concomitant use of Rosuvastatin and gemfibrozil resulted in a 2-fold increase in rosuvastatin Cmax and AUC.
Cyclosporin: During concomitant treatment with Rosuvastatin and cyclosporin, rosuvastatin plasma levels were on average 7 times
higher than those observed in healthy volunteers. Concomitant administration of Corestin and cyclosporin did not affect plasma
concentrations of cyclosporin. Antacid: The simultaneous dosing of Corestin with an antacid suspension containing aluminum and
magnesium hydroxide resulted in a decrease in rosuvastatin plasma concentration of approximately 50%. This effect was mitigated
when the antacid was dosed 2 hours after Corestin. Cytochrome P450 enzymes: Results from in vitro and in vivo studies show that
rosuvastatin is neither an inhibitor nor an inducer of cytochrome P450 isoenzymes. No interactions have been observed between
rosuvastatin and either fluconazole or ketoconazole. Erythromycin: Concomitant use of Rosuvastatin and erythromycin resulted in a
20% decrease in AUC (0-t) and a 30% decrease in Cmax of rosuvastatin. This interaction may be caused by the increase in gut
motility caused by erythromycin. Oral Contraceptive: Concomitant use of Rosuvastatin and an oral contraceptive resulted in an
increase in ethinyloestradiol and norgestrel AUC of 26% and 34%, respectively. These increased plasma levels should be considered
when selecting oral contraceptive doses. Other medications: There were no clinically relevant interactions with digoxin,
fenofibrate, antihypertensive agents, antidiabetic agents, and hormone replacement therapy.
Use during pregnancy and lactation
Rosuvastatin should not be used during pregnancy or lactation as the safety of Rosuvastatin during pregnancy and whilst
breastfeeding has not been established.
The adverse events seen with Rosuvastatin are generally mild and transient. In controlled clinical trials, less than 4% of
Rosuvastatin treated patients were withdrawn due to adverse events. Headache, dizziness, constipation, nausea, abdominal pain,
There is no specific treatment in the event of an overdose. In the event of overdose, the patient should be treated
symptomatically and supportive measures instituted as required. Liver function and CK levels should be monitored. Haemodialysis is
unlikely to be of benefit.
Mechanism of action
Rosuvastatin is a selective and competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts
3-hydroxy-3-methyIgIutaryI coenzyme A to mevalonate, a precursor for cholesterol. The primary site of action of rosuvastatin is
the liver, the target organ for cholesterol-lowering. Corestin 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. A therapeutic response to Corestin is evident within 1 week of commencing therapy and 90% of the maximum
response is usually achieved in 2 weeks. The maximum response is usually achieved by 4 weeks and is maintained after 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. Approximately 90% of rosuvastatin is bound to plasma proteins, mainly to albumin.
Metabolism: Rosuvastatin undergoes limited metabolism (approximately 10%), mainly to the N- desmethyl metabolite and the lactone
metabolite. The N-desmethyl metabolite is approximately 50% less active than rosuvastatin whereas the lactone form is considered
clinically inactive. Rosuvastatin accounts for greater than 90% of the circulating HMG-CoA reductase inhibitor activity.
Excretion: Approximately 90% of rosuvastatin is excreted as unchanged drug in the faeces and the remaining part is excreted in the
urine. The plasma elimination half-life is approximately 19 hours. The elimination half-life does not increase at higher doses.
Store in a cool and dry place, protected from light
Corestin 5 mg Tablet: Carton containing 30 tablets in Alu-Alu blister.
Corestin 10 mg Tablet Carton containing 30 tablets in Alu-Alu blister.
Corestin 20 mg Tablet Carton containing 10 tablets in Alu-Alu blister.
UniMed UniHealth Pharmaceuticals Limited
B.K. Bari, Gazipur, Bangladesh