Each EXTRAC 75mg film coated tablet contains 97.875 mg of clopidogrel bisulfate which is the molar equivalent of 75 mg of clopidogrel base.
http://u6831577.isp.regruhosting.ru/i/known/huz-stop-worrying-get.php CLINICAL PHARMACOLOGY
logiciel espion fleximobile Mechanism Of Action
EXTRAC (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 acts by irreversibly modifying the platelet ADP receptor. Consequently, platelets exposed to clopidogrel are affected for the remainder of their lifespan (about 7-10 days).
Variety of drugs that inhibit platelet function have been shown to decrease morbid events in people with established cardiovascular atherosclerotic disease as evidenced by stroke or transient ischemic attacks, myocardial infarction, unstable angina or the need for vascular 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.
http://www.provisionalprocedure.com/sites/default/files/secret/the-new-android-phone-monitoring-without-installing-application.html Pharmacodynamic Properties
Clopidogrel is a prodrug, one of whose metabolites is an inhibitor of platelet aggregation. Dose dependent inhibition of platelet aggregation can be seen 2 hours after single oral doses of EXTRAC. Repeated doses of 75 mg EXTRAC per day inhibit ADP-induced platelet aggregation on the first day, and inhibition reaches steady state between Day 3 and Day 7. Platelet aggregation and bleeding time gradually return to baseline values after treatment is discontinued, generally in about 5 days.
http://magalink.ru/themes/2018-12-06/spiare-iphone.php Absorption: EXTRAC is rapidly absorbed after oral administration of single & repeated doses of 75 mg clopidogrel (base). Mean peak plasma levels of unchanged clopidogrel (approximately 2.2-2.5 ng/ml after a single 75 mg oral dose) occurred approximately 45 minutes after dosing. Absorption is at least 50%, based on urinary excretion of clopidogrel metabolites. Administration of EXTRAC (clopidogrel bisulfate) with meals did not significantly modify the bioavailability of clopidogrel.
Distribution: Clopidogrel and the main circulating metabolite bind reversibly in vitro to human plasma proteins (98% and 94%, respectively).
Metabolism: Clopidogrel is extensively metabolized by the liver. In vitro and in vivo, clopidogrel is metabolized according to two main metabolic pathways: one mediated by esterases and leading to hydrolysis into its inactive carboxylic acid derivative (85% of circulating metabolites), and one mediated by multiple cytochromes P450. Cytochromes metabolism results in formation of the active metabolite, a thiol derivative of clopidogrel.
Elimination: Following an oral dose of 14C-labeled clopidogrel in humans, approximately 50% of total radioactivity was excreted in urine and approximately 46% in feces over the 5 days post dosing. After a single, oral dose of 75 mg, clopidogrel has a half-life of approximately 6 hours. The elimination half-life of the inactive acid metabolite was 8 hours after single and repeated administration. Covalent binding to platelets accounted for 2% of radiolabel with a half-life of 11 days. In plasma and urine, the glucuronide of the carboxylic acid derivative is also observed.
The pharmacokinetics of clopidogrel's active metabolite is not known in these special populations.
Geriatric Patients: In elderly ( 75 years) volunteers compared to young healthy volunteers, there were no differences in platelet aggregation and bleeding time. No dosage adjustment is needed for the elderly.
Renally-Impaired Patients: After repeated doses of 75 mg EXTRAC per day in patients with severe renal impairment (creatinine clearance from 5 to 15 ml/min), inhibition of ADP-induced platelet aggregation was lower (25%) than that observed in healthy volunteers; however, the prolongation of bleeding time was similar to healthy volunteers receiving 75 mg of EXTRAC per day.
Hepatically-Impaired Patients: After repeated doses of 75 mg EXTRAC per day for 10 days in patients with severe hepatic impairment, inhibition of ADP-induced platelet aggregation was similar to that observed in healthy subjects. The mean bleeding time prolongation was also similar in the two groups.
Gender: In a small study comparing men and women, less inhibition of ADP-induced platelet aggregation was observed in women, but there was no difference in prolongation of bleeding time.
EXTRAC (clopidogrel bisulfate) is indicated for the reduction of atherothrombotic events as follows:
Recent MI, Recent Stroke or Established Peripheral Arterial Disease: For patients with a history of recent myocardial infarction (MI), recent stroke, or established peripheral arterial disease.
Acute Coronary Syndrome: For patients with non-ST-segment elevation acute coronary syndrome (unstable angina/non-Q-wave MI) including patients who are to be managed medically and those who are to be managed with percutaneous coronary intervention (with or without stent) or CABG.
For patients with ST-segment elevation acute myocardial infarction.