Corestin Tablet 10mg

Product Information

CORESTIN

Presentation

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.

Indications

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

inadequate.

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.

Drug Interactions

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.

Undesirable effects

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,

myalgia, asthenia.

Overdose

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.

Pharmacokinetic properties

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.

Pharmaceutical precautions

Store in a cool and dry place, protected from light

Packaging quantities

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.

Manufactured by

UniMed UniHealth Pharmaceuticals Limited

B.K. Bari, Gazipur, Bangladesh

Registered Trademark