|Place of Origin:||China|
|Model Number:||Film-coated tablets, 75mg|
|Minimum Order Quantity:||300, 000 tablets|
|Payment Terms:||L/C, T/T|
|Supply Ability:||One million pills per day|
|Product:||Clopidogrel Hydrogen Sulphate Tablets||Specification:||Film-coated Tablets, 75mg|
Clopidogrel Hydrogen Sulphate Tablets Film-coated tablets, 75mg Oral Medications
Product : Clopidogrel Hydrogen Sulphate Tablets
Specification : Film-coated tablets, 75mg
Standard : BP, USP
Packing : 7’s/blister
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 tablets, USP 75 mg for oral administration contain 97.875 mg of clopidogrel bisulfate, which is the molar equivalent of 75 mg of clopidogrel base.
Indications and Usage :
1. Acute Coronary Syndrome
Clopidogrel tablets can be administered with or without food.
For patients with non-ST-elevation ACS (UA/NSTEMI), initiate clopidogrel tablets with a single 300 mg oral loading dose and then continue at 75 mg once daily. Initiate aspirin (75 to 325 mg once daily) and continue in combination with clopidogrel tablets.
For patients with STEMI, the recommended dose of clopidogrel is 75 mg once daily orally, administered in combination with aspirin (75 to 325 mg once daily), with or without thrombolytics. Clopidogrel may be initiated with or without a loading dose.
2. Recent MI, Recent Stroke, or Established Peripheral Arterial Disease
The recommended daily dose of clopidogrel is 75 mg once daily orally, with or without food.
4. CYP2C19 Poor Metabolizers
5. CYP2C19 poor metabolizer status is associated with diminished antiplatelet response to clopidogrel. Although a higher dose regimen in poor metabolizers increases antiplatelet response, an appropriate dose regimen for this patient population has not been established.
6. Use with Proton Pump Inhibitors (PPI)
Avoid using omeprazole or esomeprazole with clopidogrel. Omeprazole and esomeprazole significantly reduce the antiplatelet activity of clopidogrel. When concomitant administration of a PPI is required, consider using another acid-reducing agent with minimal or no CYP2C19 inhibitory effect on the formation of clopidogrel active metabolite.
Since clopidogrel is a prodrug, it must be metabolized by CYP450 enzymes to produce the active metabolite that inhibits platelet aggregation. This active metabolite selectively inhibits adenosine diphosphate (ADP) binding to its platelet P2Y12 receptor and subsequently the ADP-mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.
Mechanism of action
The active metabolite of clopidogrel prevents binding of adenosine diphosphate (ADP) to its platelet receptor, impairing the ADP-mediated activation of the glycoprotein GPIIb/IIIa complex. It is proposed that the inhibition involves a defect in the mobilization from the storage sites of the platelet granules to the outer membrane. he drug specifically and irreversibly inhibits the P2Y12 subtype of ADP receptor, which is important in aggregation of platelets and cross-linking by the protein fibrin. No direct interference occurs with the GPIIb/IIIa receptor. As the glycoprotein GPIIb/IIIa complex is the major receptor for fibrinogen, its impaired activation prevents fibrinogen binding to platelets and inhibits platelet aggregation. By blocking the amplification of platelet activation by released ADP, platelet aggregation induced by agonists other than ADP is also inhibited by the active metabolite of clopidogrel.