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1 uding prasugrel, ticagrelor, and intravenous cangrelor.
2 eeding episodes were numerically higher with cangrelor.
3 e similar in both women and men treated with cangrelor (0.3% versus 0.2%, P=0.30 [women]; 0.1% versus
4 clopidogrel group (adjusted odds ratio with cangrelor, 0.78; 95% confidence interval [CI], 0.66 to 0
5 9, 100 micromol/L) and especially P(2)Y(12) (Cangrelor, 10 micromol/L) blunted CXCL16-triggered plate
6 t occurred in 185 of 2654 patients receiving cangrelor (7.0%) and in 210 of 2641 patients receiving p
7 rivative (a specific P2X(1) antagonist), and cangrelor (a specific P2Y(12) antagonist) mitigated the
8 on Triage Strategy criteria) was higher with cangrelor, a difference that approached statistical sign
11 ee trials that assessed the effectiveness of cangrelor against either clopidogrel or placebo in PCI.
12 significantly lower in patients treated with cangrelor alone (0.7% vs 2.4%; OR, 0.29; 95% CI, 0.13-0.
13 were not significantly different between the cangrelor alone and clopidogrel-GPI groups (2.6% vs 3.3%
14 efined severe/life-threatening bleeding with cangrelor alone compared with clopidogrel-GPI (0.3% vs 0
15 analysis from the 3 phase 3 CHAMPION trials, cangrelor alone was associated with similar ischemic ris
16 ssigned to cangrelor but not receiving GPIs (cangrelor alone) and 1211 patients assigned to clopidogr
19 P2Y12 and alphaIIbbeta3 receptor inhibitors cangrelor and abciximab, respectively, both in vitro--by
20 aracteristics were well balanced between the cangrelor and clopidogrel arms in subsets receiving and
21 0.6%) and 54 of 5,469 (1.0%) patients in the cangrelor and clopidogrel arms, respectively (odds ratio
22 11.8% (12 of 102) vs 10.4% (10 of 96) in the cangrelor and placebo groups, respectively (RR, 1.1 [95%
23 of GPR17 by the marketed antiplatelet drugs cangrelor and ticagrelor, previously suggested to antago
24 el P2Y12 antagonists (prasugrel, ticagrelor, cangrelor, and elinogrel) that have advantages over clop
25 triethylammonium salt hydrate (2MeSAMP) and Cangrelor (AR-C69931MX) have been widely used to demonst
26 icipants included 10929 patients assigned to cangrelor but not receiving GPIs (cangrelor alone) and 1
27 ation showed a trend toward a reduction with cangrelor, but it was not significant (0.6% vs. 0.9%; od
28 linical Trial to Demonstrate the Efficacy of Cangrelor), CHAMPION PLATFORM (Cangrelor Versus Standard
29 e primary composite endpoint were lower with cangrelor compared with clopidogrel in patients who did
30 ought to evaluate the efficacy and safety of cangrelor compared with clopidogrel in subgroups that di
32 ention, the efficacy and bleeding profile of cangrelor compared with clopidogrel was similar to that
33 therapy prior to cardiac surgery, the use of cangrelor compared with placebo resulted in a higher rat
34 large global cardiovascular clinical trial, cangrelor consistently reduced rates of ischemic end poi
39 forskolin) of the cAMP pathway, 2MeSAMP and Cangrelor failed to inhibit Ca(2+) mobilization, Akt pho
40 roduction of an intravenous P2Y12 inhibitor (cangrelor) further adds to the multitude of modalities a
41 he primary safety end point was 0.16% in the cangrelor group and 0.11% in the clopidogrel group (odds
42 n the rate of blood transfusion (1.0% in the cangrelor group and 0.6% in the placebo group, P=0.13),
43 e primary efficacy end point was 4.7% in the cangrelor group and 5.9% in the clopidogrel group (adjus
44 t, which occurred in 7.5% of patients in the cangrelor group and 7.1% of patients in the clopidogrel
45 sis developed in 0.8% of the patients in the cangrelor group and in 1.4% in the clopidogrel group (od
46 e primary efficacy end point was 4.3% in the cangrelor group versus 5.3% in the clopidogrel group (od
47 receiving placebo (8.0%) (odds ratio in the cangrelor group, 0.87; 95% confidence interval [CI], 0.7
49 r bleeding on one scale was increased in the cangrelor group, from 3.5% to 5.5% (P<0.001), because of
50 stent thrombosis and death were lower in the cangrelor group, with no significant increase in the rat
51 greater proportion of patients treated with cangrelor had low levels of platelet reactivity througho
53 imary efficacy and safety end point) favored cangrelor in both women (OR, 0.68; 95% CI, 0.50-0.92) an
55 N) PHOENIX trial demonstrated superiority of cangrelor in reducing ischemic events at 48 hours in pat
56 s GUSTO moderate/severe bleeding, the OR for cangrelor in those >/=75 years old was 0.75 (6.4% versus
58 0.4%), or in transfusion (0.7% vs 0.6%), but cangrelor increased GUSTO mild bleeding (16.8% vs 13.0%,
60 evealed that neither 2MeSAMP nor ARC69931MX (cangrelor) increased cAMP through activation of A2a, IP,
61 lucidate the mechanisms by which 2MeSAMP and Cangrelor inhibit platelet activation and thrombosis.
62 e data together demonstrate that 2MeSAMP and Cangrelor inhibit platelet function through the P2Y(12)-
74 r total MIs (n=134); however, the effects of cangrelor on MI remained significant (OR, 0.65; 95% CI,
75 ere seen in the evaluation of the effects of cangrelor on MIs with peak creatinine kinase-MB >/=10 ti
77 total of 11 145 patients were randomized to cangrelor or clopidogrel in the CHAMPION PHOENIX trial (
81 dine awaiting CABG surgery to receive either cangrelor or placebo after an initial open-label, dose-f
82 n treated with clopidogrel to receive either cangrelor or placebo at the time of PCI, followed by 600
83 were stopped and patients were administered cangrelor or placebo for at least 48 hours, which was di
84 d therapy to receive a bolus and infusion of cangrelor or to receive a loading dose of 600 mg or 300
85 linical Trial to Demonstrate the Efficacy of Cangrelor [PCI]: NCT00305162; Cangrelor Versus Standard
86 recent study reported that both 2MeSAMP and Cangrelor raise intra-platelet cAMP levels and inhibit p
87 pared with control (clopidogrel or placebo), cangrelor reduced PCI periprocedural thrombotic complica
98 e Percutaneous Coronary Intervention) trial, cangrelor significantly reduced periprocedural and 30-da
100 intravenous adenosine diphosphate antagonist cangrelor substantially reduced IPST, contributing to it
102 d CHAMPION PHOENIX (Clinical Trial Comparing Cangrelor to Clopidogrel Standard of Care Therapy in Sub
104 RM]: NCT00385138; A Clinical Trial Comparing Cangrelor to Clopidogrel Standard Therapy in Subjects Wh
105 CHAMPION PHOENIX (A Clinical Trial Comparing Cangrelor to Clopidogrel Standard Therapy in Subjects Wh
106 rence in GUSTO moderate/severe bleeding with cangrelor versus clopidogrel (1.1% versus 1.0%; OR, 1.07
107 he Efficacy of Cangrelor [PCI]: NCT00305162; Cangrelor Versus Standard Therapy to Achieve Optimal Man
109 e Efficacy of Cangrelor), CHAMPION PLATFORM (Cangrelor Versus Standard Therapy to Achieve Optimal Man
110 r clopidogrel in the CHAMPION PHOENIX trial (Cangrelor versus Standard Therapy to Achieve Optimal Man
113 d, patient-level analysis of the 3 CHAMPION (Cangrelor versus Standard Therapy to Achieve Optimal Man
114 odds of the primary outcome by 19% (3.8% for cangrelor vs 4.7% for control; odds ratio [OR] 0.81, 95%
115 pooled patient-level data from the 3 phase 3 Cangrelor vs Standard Therapy to Achieve Optimal Managem
116 , double-blind, double-dummy trials in which cangrelor was compared with clopidogrel during percutane
121 a large-scale international trial comparing cangrelor with 600 mg of oral clopidogrel administered b
122 ION-PLATFORM, and CHAMPION-PHOENIX) compared cangrelor with control (clopidogrel or placebo) for prev
124 t P2Y12 inhibitor (ticagrelor, prasugrel, or cangrelor) without the planned use of glycoprotein IIb/I
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