CLOPID
-
Chemical Name:
Clopidogrel (Bisulfate) -
Therapeutic Category:
Cardiovascular drugs -
Pharmacologic Category:
Antiplatelet Agent, Thienopyridine -
Pharmaceutical Form:
Tablets -
Composition:
Clopidogrel (Bisulfate) 75mg
CLOPID
Film Coated Tablets
Clopidogrel (Bisulfate)
1. CLINICAL PHARMAGOLOGY:
CLOPID (Clopidogrel Bisulfate) is an inhibitor of ADP-induced platelet aggregation acting by direct inhibition of adenosine diphosphate (ADP) binding to its receptor and of the subsequent ADP-mediated activation of the glycoprotein GPIIb/IIIa complex.
Clopidogrel is an inhibitor of platelet aggregation. A variety of drugs that inhibit platelet function have been shown to decrease morbid events in people with established atherosclerotic cardiovascular disease as evidenced by stroke or transient ischemic attacks, myocardial infarction, or need for bypass or angioplasty. This indicates that platelets participate in the initiation and/or evolution of these events and that inhibiting them can reduce the event rate.
2. PHARMACOKINETICS:
Clopidogrel is extensively metabolized by the liver. The main circulating metabolite is the carboxylic acid derivative, and it too has no effect on platelet aggregation. It represents about 85% of the circulating drug-related compounds in plasma.
Following an oral dose of 14C-labeled clopidogrel in humans, approximately 50% was excreted in the urine and approximately 46% in the feces in the 5 days after dosing. The elimination half-life of the main circulating metabolite was 8 hours after single and repeated administration.
Effect of Food: Administration of CLOPID with meals did not significantly modify the bioavailability of clopidogrel as assessed by the pharmacokinetics of the main circulating metabolite.
Absorption and Distribution: Clopidogrel is rapidly absorbed after oral administration of repeated doses of 75 mg clopidogrel, with peak plasma levels (@3 mg/L) of the main circulating metabolite occurring approximately 1 hour after dosing. The pharmacokinetics of the main circulating metabolite are linear (plasma concentrations increased in proportion to dose) in the dose range of 50 to 150 mg of clopidogrel. Absorption is at least 50% based on urinary excretion of clopidogrel-related metabolites.
Clopidogrel and the main circulating metabolite bind reversibly in vitro to human plasma proteins (98 % and 94 % respectively).
Metabolism and Elimination: In vitro and in vivo, clopidogrel undergoes rapid hydrolysis into its carboxylic acid derivative. In plasma and urine, the glucuronide of the carboxylic acid derivative is also observed.
3. INDICATIONS:
CLOPID is indicated for the reduction of atherosclerotic events (myocardial infarction, stroke, and vascular death) in patients with atherosclerosis documented by recent stroke, recent myocardial infarction, or established peripheral arterial disease.
4. CONTRAINDICATIONS:
The use of CLOPID is contraindicated in the following conditions:
- Hypersensitivity to the drug substance or any component of the product.
- Active pathological bleeding such as peptic ulcer or intracranial hemorrhage.
5. PRECAUTIONS:
As with other anti-platelet agents, CLOPID should be used with caution in patients who may be at risk of increased bleeding from trauma, surgery, or other pathological conditions. If a patient is to undergo elective surgery and an antiplatelet effect is not desired, CLOPID should be discontinued 7 days prior to surgery.
6. PREGNANCY & NURSING MOTHERS:
Pregnancy: Category B. Do not use during pregnancy only if clearly needed.
Nursing mothers: Should not be given to nursing mothers.
If the drug is very important, decision should be made to discontinue nursing.
7. SIDE EFFECTS:
CLOPID is well tolerated and the overall tolerability of CLOPID was similar to that of aspirin with regards to hemorrhagic, and gastrointestinal events (e.g. dyspepsia, gastritis or constipation).
8. DRUG INTERACTIONS:
Study of specific drug interactions yielded the following results:
- Aspirin: Aspirin did not modify the clopidogrel-mediated inhibition of ADP-induced platelet aggregation. Concomitant administration of 500 mg of aspirin twice a day for 1 day did not significantly increase the prolongation of bleeding time induced by CLOPID.
- Heparin: In a study in healthy volunteers, CLOPID did not necessitate modification of the heparin dose or alter the effect of heparin on coagulation. Coadministration of heparin had no effect on inhibition of platelet aggregation induced by CLOPID.
- Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): In healthy volunteers receiving naproxen, concomitant administration of CLOPID was associated with increased occult gastrointestinal blood loss. NSAIDs and CLOPID should be coadministration with caution.
- Warfarin: Concomitant administration of these two agents should be undertaken with caution.
- Other Concomitant Therapy: No clinically significant pharmacodynamic interactions were observed when CLOPID was coadministered with atenolol, nifedipine, or both atenolol and nifedipine. The pharmacodynamic activity of CLOPID was also not significantly influenced by the coadministration of phenobarbital, cimetidine or estrogen. The pharmacokinetics of digoxin or theophylline was not modified by the coadministration of CLOPID.
9. DOSAGE & ADMINISTRATION:
The recommended dose of CLOPID is 75 mg once daily with or without food.
No dosage adjustment is necessary for elderly patients or patients with renal disease.
10. PACKAGING & COMPOSITION:
CLOPID – F.C.Tablets: A pack of 10 or 30 f.c.tablets. Each film coated tablet contains Clopidogrel Bisulfate equivalent to 75 mg Clopidogrel base.
11. STORAGE CONDITIONS:
Store CLOPID – F.C.Tablets at temperature between (15-30)°C.
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