Xpectedly low in both AMN-107 Nilotinib groups. Headache, diarrhea, palpitations, dizziness and palpitations were h More often with cilostazol than aspirin, leading to a level almost twice the judgment of cilostazol. Thienopyridines 4.0 ticlopidine, clopidogrel, prasugrel and repr sentieren Three generations of oral thienopyridine that selectively inhibit ADP-induced platelet aggregation. Ticlopidine fi rstgeneration Agent of toxicity T and bone marrow Descr Nkt was largely of clopidogrel, which has become a standard treatment for the entire spectrum of ACS patients and those who has a percutaneous coronary intervention replaced. However, clopidogrel Descr Website will, Such as fluctuating variable absorption Antipl Ttchen effects related, at least in part, to polymorphisms in genes that regulate the metabolic activation of clopidogrel, and a galvanized GERTES onset and offset action. Prasugrel, a third generation thienopyridine, has a more consistent rapidproduces platelet inhibition. All three thienopyridines are prodrugs, the metabolic activation of hepatic CYP450 system to active metabolites, platelet P2Y12 receptor inhibition generate undergoing. The inhibition of platelet P2Y12 receptor by thienopyridines is consistent with the function of time, cumulative inhibition of ADP-induced aggregation, with repeated t Glicher administration of ticlopidine action thienopyridines clopidogrel and slower and occurs with the slow recovery of platelet function after discontinuation of the drug. 160 Although thienopyridines and L Between, the platelet aggregation induced by arachidonic Acid, collagen, and thrombin-induced, these inhibitory effects 161 162 attenuated Cht or by increasing Increase eliminated the agonist concentration and are probably explained by the blockade of cations ADP amplification Mediated utert the reaction of Blutpl ttchen to other agonists. Ticlopidine 4.1 4.1.1 Pharmacokinetics: Up to 90% is a single oral dose of ticlopidine is rapidly absorbed. The maximum plasma concentration of 160 1 to 3 h after a single oral dose of 250 mg. over 98% of ticlopidine is absorbed fa Reversibly bound to plasma proteins, principally Chlich albumin. Ticlopidine is metabolized rapidly and extensively. A total of 13 metabolites were underscored in humans. Of these, only the two keto derivative of ticlopidine st Stronger than the parent compound in inhibiting ADP-induced PI Ttchenaggregation. 160 The life of the elimination half-life of ticlopidine is 24 to 36 h after oral single dose and up to 96 h after 14 days of repeat dosing. 160 The current standard therapy with ticlopidine 250 mg twice t Possible. 4.1.2 Efficiency and Safety: As a single agent was ticlopidine in patients with stroke, TIA 163, 164, 165 unstable angina pectoris, MI, 166 and 167, 169, and intermittent claudication evaluated in those undergoing CABG. 170 Ticlopidine was more effective than aspirin in reducing isch stroke in patients Valproate with transient Mix attacks or minor stroke 164 was as effective as aspirin in the treatment of patients with acute MI 166 was more effective than placebo in reducing the risk of the combined endpoint stroke, myocardial infarction or stroke rer death in patients with stroke, thromboembolism 163 was more effective than the convention.