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10.1161/ATVBAHA.114.303724 http://scihub22266oqcxt.onion/10.1161/ATVBAHA.114.303724 C4180209!4180209!25147334     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Arterioscler+Thromb+Vasc+Biol 2014 ; 34 (10): 2321-9 Nephropedia Template TP {{tp|p=25147334|t=2014. RUC-4: A Novel ?IIb?3 Antagonist for Pre-hospital Therapy of Myocardial Infarction |pdf=|usr=}}{{25147334}} gab.com Text RUC-4: A Novel IIb 3 Antagonist for Pre-hospital Therapy of Myocardial Infarction JO: Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=25147334 #FOAvip Objective: Treatment of myocardial infarction (MI) within the first 1?2 hours with a thrombolytic agent, percutaneous coronary intervention, or an ?IIb?3 antagonist decreases mortality and the later development of heart failure. We previously reported on a novel small molecule ?IIb?3 antagonist, RUC-2, that has a unique mechanism of action. We have now developed a more potent and more soluble congener of RUC-2, RUC-4, designed to be easily administered intramuscularly (IM) by autoinjector to facilitate its use in the pre-hospital setting. Here we report the properties of RUC-4 and the antiplatelet and antithrombotic effects of RUC-2 and RUC-4 in animal models. Approach and Results: RUC-4 was ~20% more potent than RUC-2 in inhibiting human ADP-induced platelet aggregation and much more soluble in aqueous solutions (60?80 mg/ml). It shared RUC-2?s specificity for ?IIb?3 vs ?V?3, did not prime the receptor to bind fibrinogen, or induce changes in ?3 identified by a conformation-specific monoclonal antibody. Both RUC-2 and RUC-4 prevented FeCl3-induced thrombotic occlusion of the carotid artery in mice and decreased microvascular thrombi in response to laser injury produced by human platelets infused into transgenic mice containing a mutated von Willebrand factor that reacts with human, but not mouse platelets. IM injection of RUC-4 in non-human primates at 1.9 and 3.85 mg/kg led to complete inhibition of platelet aggregation within 15 minutes, with dose-dependent return of platelet aggregation after 4.5?24 hours. Conclusions: RUC-4 has favorable biochemical, pharmacokinetic, pharmacodynamic, antithrombotic, and solubility properties as a pre-hospital therapy of MI, but the possibility of increased bleeding with therapeutic doses remains to be evaluated. Twit Text FOAVip RUC-4: A Novel IIb 3 Antagonist for Pre-hospital Therapy of Myocardial Infarction ????Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=25147334 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25147334 #FOAvip English Wikipedia <ref>{{Cite pmid|25147334}}</ref> RUC-4: A Novel ?IIb?3 Antagonist for Pre-hospital Therapy of Myocardial Infarction #MMPMID25147334 Li J; Vootukuri S; Shang Y; Negri A; Jiang Jk; Nedelman M; Diacovo TG; Filizola M; Thomas CJ; Coller BS Arterioscler Thromb Vasc Biol 2014[Oct]; 34 (10): 2321-9 PMID25147334show ga Objective: Treatment of myocardial infarction (MI) within the first 1?2 hours with a thrombolytic agent, percutaneous coronary intervention, or an ?IIb?3 antagonist decreases mortality and the later development of heart failure. We previously reported on a novel small molecule ?IIb?3 antagonist, RUC-2, that has a unique mechanism of action. We have now developed a more potent and more soluble congener of RUC-2, RUC-4, designed to be easily administered intramuscularly (IM) by autoinjector to facilitate its use in the pre-hospital setting. Here we report the properties of RUC-4 and the antiplatelet and antithrombotic effects of RUC-2 and RUC-4 in animal models. Approach and Results: RUC-4 was ~20% more potent than RUC-2 in inhibiting human ADP-induced platelet aggregation and much more soluble in aqueous solutions (60?80 mg/ml). It shared RUC-2?s specificity for ?IIb?3 vs ?V?3, did not prime the receptor to bind fibrinogen, or induce changes in ?3 identified by a conformation-specific monoclonal antibody. Both RUC-2 and RUC-4 prevented FeCl3-induced thrombotic occlusion of the carotid artery in mice and decreased microvascular thrombi in response to laser injury produced by human platelets infused into transgenic mice containing a mutated von Willebrand factor that reacts with human, but not mouse platelets. IM injection of RUC-4 in non-human primates at 1.9 and 3.85 mg/kg led to complete inhibition of platelet aggregation within 15 minutes, with dose-dependent return of platelet aggregation after 4.5?24 hours. Conclusions: RUC-4 has favorable biochemical, pharmacokinetic, pharmacodynamic, antithrombotic, and solubility properties as a pre-hospital therapy of MI, but the possibility of increased bleeding with therapeutic doses remains to be evaluated. äRUC-4: A Novel ?IIb?3 Antagonist for Pre-hospital Therapy of Myocardia(epmc).pdf DeepDyve Pubget Overpricing