Page last updated: 2024-11-12

prasugrel hydrochloride

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Description

Prasugrel Hydrochloride: A piperazine derivative and PLATELET AGGREGATION INHIBITOR that is used to prevent THROMBOSIS in patients with ACUTE CORONARY SYNDROME; UNSTABLE ANGINA and MYOCARDIAL INFARCTION, as well as in those undergoing PERCUTANEOUS CORONARY INTERVENTIONS. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

prasugrel hydrochloride : A racemate comprising equal amounts of (R)- and (S)-prasugrel hydrochloride. Used to prevent blood clots in people with acute coronary syndrome who are undergoing a procedure after a recent heart attack or stroke, and in people with certain disorders of the heart or blood vessels. [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Cross-References

ID SourceID
PubMed CID10158453
CHEMBL ID1201773
CHEBI ID87697
SCHEMBL ID246128
MeSH IDM000603803

Synonyms (75)

Synonym
ly640315
ly 640315
effient (tn)
D05597
389574-19-0
prasugrel hydrochloride (jan/usan)
CHEMBL1201773
prasugrel hcl
prasu doc
prasugrel hydrochloride
2-[2-(acetyloxy)-6,7-dihydrothieno[3,2-c]pyridin-5(4h)-yl]-1-cyclopropyl-2-(2-fluorophenyl)ethanone hydrochloride
FT-0656362
NCGC00188690-01
dtxcid6028993
tox21_113621
dtxsid1049067 ,
cas-389574-19-0
S4637
prasugrel hydrochloride [usan]
ethanone, 2-(2-(acetyloxy)-6,7-dihydrothieno(3,2-c)pyridin-5(4h)-yl)-1-cyclopropyl-2-(2-fluorophenyl)-, hydrochloride
5-((1rs)-2-cyclopropyl-1-(2-fluorophenyl)-2-oxoethyl)-4,5,6,7-tetrahydrothieno(3,2-c)pyridin-2-yl acetate hydrochloride
g89jq59i13 ,
unii-g89jq59i13
JALHGCPDPSNJNY-UHFFFAOYSA-N
2-acetoxy-5-(alpha-cyclopropylcarbonyl-2-fluorobenzyl)-4,5,6,7-tetrahydrothieno[3,2-c]pyridine hydrochloride
SCHEMBL246128
2-acetoxy-5-(.alpha.-cyclopropylcarbonyl-2-fluorobenzyl)-4,5,6,7-tetrahydrothieno(3,2-c)pyridine hydrochloride
prasugrel hydrochloride [ep monograph]
ethanone, 2-(2-(acetyloxy)-6,7-dihydrothieno(3,2-c)pyridin-5(4h)-yl)-1-cyclopropyl-2-(2-fluorophenyl)-, hydrochloride (1:1)
prasugrel hydrochloride [mi]
prasugrel hydrochloride [who-dd]
prasugrel hydrochloride [vandf]
ethanone, 2-(2-(acetyloxy)-6,7-dihydrothieno(3,2-c)pyridin-5(4h)-yl)-1-cyclopropyl-2-(2-fluorophenyl), hydrochloride
prasugrel hydrochloride [orange book]
prasugrel hydrochloride [mart.]
prasugrel hydrochloride [usp monograph]
prasugrel hydrochloride [usp-rs]
prasugrel hydrochloride [jan]
HY-15284A
CS-1785
prasugrel (hydrochloride)
AKOS022185568
AM20090719
ethanone, 2-[2-(acetyloxy)-6,7-dihydrothieno[3,2-c]pyridin-5(4h)-yl]-1-cyclopropyl-2-(2-fluorophenyl)-, hydrochloride (1:1)
NCGC00188690-02
tox21_113621_1
AC-24004
hydrochloride, prasugrel
hcl, prasugrel
5-(2-cyclopropyl-1-(2-fluorophenyl)-2-oxoethyl)-4,5,6,7-tetrahydrothieno[3,2-c]pyridin-2-yl acetate hydrochloride
mfcd11867705
[5-[2-cyclopropyl-1-(2-fluorophenyl)-2-oxoethyl]-6,7-dihydro-4h-thieno[3,2-c]pyridin-2-yl] acetate;hydrochloride
BCP16928
EX-A2645
AS-35081
pcr 4099 (hydrochloride)
effient hydrochloride
ly 640315 hydrochloride
CCG-268764
Q27278929
prasugrenhydrochloride
prasugren hcl
prasugrel hydrochloride (ep monograph)
prasugrel hydrochloride (usp monograph)
(+-)-prasugrel hydrochloride
prasugrel hydrochloride (mart.)
rac-2-(acetyloxy)-5-(2-cyclopropyl-1-(2-fluorophenyl)-2-oxoethyl)-4,5,6,7-tetrahydrothieno(3,2-c)pyridin-5-ium chloride
2-acetoxy-5-(alpha-cyclopropylcarbonyl-2-fluorobenzyl)-4,5,6,7-tetrahydrothieno(3,2-c)pyridine hydrochloride
rac-prasugrel hydrochloride
5-((1rs)-2-cyclopropyl-1-(2-fluorophenyl)-2-oxoethyl)-4,5,6,7-tetrahydrothieno(3,2-c)pyridin-2-yl acetate monohydrochloride
prasugrel hydrochloride (usp-rs)
racemic prasugrel hydrochloride
(rs)-prasugrel hydrochloride
chebi:87697
rac-5-(2-cyclopropyl-1-(2-fluorophenyl)-2-oxoethyl)-4,5,6,7-tetrahydrothieno(3,2-c)pyridin-2-yl acetate hydrochloride

Research Excerpts

Overview

Prasugrel Hydrochloride (PHCl) is an antiplatelet drug.

ExcerptReferenceRelevance
"Prasugrel Hydrochloride (PHCl) is an antiplatelet drug. "( Solid self nano-emulsifying system for the enhancement of dissolution and bioavailability of Prasugrel HCl:
Al-Nimry, S; Attar, S; Khanfar, M, 2021
)
2.06

Toxicity

ExcerptReferenceRelevance
" The drug is associated with rare adverse effects such as thrombotic thrombocytopenia purpura, acute hepatotoxicity, and neutropenia."( Prasugrel as a safe alternative for clopidogrel-induced polyarthralgias.
Coulter, CJ; Montandon, SV, 2012
)
0.38
"To examine whether prasugrel is a safe and effective alternative to clopidogrel for neurointerventional procedures, especially in those patients who are either non-responders or allergic to clopidogrel."( Prasugrel is effective and safe for neurointerventional procedures.
Chaudhary, N; Gemmete, JJ; Maher, CO; Pandey, AS; Stetler, WR; Thompson, BG, 2013
)
0.39
" The CP-load group experienced more in-hospital major adverse cardiac events (5."( Safety of reloading prasugrel in addition to clopidogrel loading in patients with acute coronary syndrome undergoing percutaneous coronary intervention.
Chen, F; Kent, KM; Kitabata, H; Loh, JP; Pendyala, LK; Pichard, AD; Satler, LF; Suddath, WO; Torguson, R; Waksman, R, 2013
)
0.39
" However, the comparative risks of gastrointestinal (GI) adverse events during DAPT are not clear."( Gastrointestinal adverse events after dual antiplatelet therapy: clopidogrel is safer than ticagrelor, but prasugrel data are lacking or inconclusive.
Can, MM; Dinicolantonio, JJ; Kuliczkowski, W; Pershukov, IV; Serebruany, VL, 2013
)
0.39
" Other adverse events observed in patients treated with this platelet inhibitor are discussed, including hematological complications, and cutaneous and hepatic idiosyncratic reactions."( Efficacy and safety of prasugrel in acute coronary syndrome patients.
Delzor, F; Nanau, RM; Neuman, MG, 2014
)
0.4
" The primary efficacy endpoint was the incidence of major adverse cardiovascular events (MACE) at 24 weeks, defined as a composite of cardiovascular death, nonfatal myocardial infarction, and nonfatal ischemic stroke."( Efficacy and safety of adjusted-dose prasugrel compared with clopidogrel in Japanese patients with acute coronary syndrome: the PRASFIT-ACS study.
Isshiki, T; Kimura, T; Kitagawa, K; Miyazaki, S; Nakamura, M; Nanto, S; Nishikawa, M; Ogawa, H; Saito, S; Takayama, M; Yokoi, H, 2014
)
0.4
" Prasugrel is at least as effective and safe as clopidogrel in patients with ACS undergoing early invasive management."( Efficacy and Safety of Prasugrel Compared With Clopidogrel for Patients With Acute Coronary Syndrome Undergoing Percutaneous Coronary Intervention.
Brener, SJ; Lella, LK; Wang, A,
)
0.13
"7, p NS], and in adverse cardiac or cerebrovascular events (MACCE) (5 vs."( Safety and efficacy of in-hospital clopidogrel-to-prasugrel switching in patients with acute coronary syndrome. An analysis from the 'real world'.
Almendro-Delia, M; Blanco Ponce, E; Caballero-Garcia, A; Cruz-Fernandez, MJ; Garcia-Rubira, JC; Gomez-Domínguez, R; Gonzalez-Matos, C; Hidalgo-Urbano, R; Lobo-Gonzalez, M, 2015
)
0.42
"Biodegradable-polymer drug-eluting stents (BP-DES) were developed to be as effective as second-generation durable-polymer drug-eluting stents (DP-DES) and as safe >1 year as bare-metal stents (BMS)."( Long-term efficacy and safety of biodegradable-polymer biolimus-eluting stents: main results of the Basel Stent Kosten-Effektivitäts Trial-PROspective Validation Examination II (BASKET-PROVE II), a randomized, controlled noninferiority 2-year outcome tria
Alber, H; Buser, P; Conen, D; Eberli, F; Galatius, S; Gilgen, N; Hoffmann, A; Jeger, R; Kaiser, C; Kurz, DJ; Moccetti, T; Müller, C; Naber, C; Pedrazzini, G; Pfisterer, M; Rickenbacher, P; Rickli, H; Skov Jensen, J; Steiner, M; Vogt, DR; Von Felten, S; Vuillomenet, A; Wadt Hansen, K; Wanitschek, M; Weilenmann, D, 2015
)
0.42
" Safety assessments include incidence of hemorrhagic events requiring medical intervention and treatment-emergent adverse events."( Design of the DOVE (Determining Effects of Platelet Inhibition on Vaso-Occlusive Events) trial: A global Phase 3 double-blind, randomized, placebo-controlled, multicenter study of the efficacy and safety of prasugrel in pediatric patients with sickle cell
Brown, PB; Heath, LE; Heeney, MM; Hoppe, CC; Jakubowski, JA; Rees, DC; Styles, L; Winters, KJ; Zhou, C, 2016
)
0.43
" Outcome measures were overall bleeding, major bleeding, and major adverse cardiac events (MACE)."( Safety and Efficacy of Switching From Clopidogrel to Prasugrel in Patients Undergoing Percutaneous Coronary Intervention: A Study-level Meta-analysis From 15 Studies.
Cavallari, I; De Luca, L; Patti, G; Ricottini, E, 2016
)
0.43
" The secondary endpoints were a composite of major adverse cardiovascular events (MACE) consisting of cardiovascular death, non-fatal myocardial infarction, non-fatal stroke, a new target vessel revascularisation and all-cause mortality at 30 days."( Safety of the primary percutaneous coronary intervention strategy combining pre-hospital prasugrel, enoxaparin and in-hospital bivalirudin in acute ST-segment elevation myocardial infarction.
Laine, M; Nieminen, T; Tierala, I; Viikilä, J, 2016
)
0.43
"Using data on 11 955 acute myocardial infarction (MI) patients treated with percutaneous coronary intervention at 233 hospitals and enrolled in the TRANSLATE-ACS study, we compared whether discharge PPI use altered the association of 1-year adjusted risks of major adverse cardiovascular events (MACE; death, MI, stroke, or unplanned revascularization) and Global Use of Strategies To Open Occluded Arteries (GUSTO) moderate/severe bleeding between prasugrel- and clopidogrel-treated patients."( Impact of Proton Pump Inhibitor Use on the Comparative Effectiveness and Safety of Prasugrel Versus Clopidogrel: Insights From the Treatment With Adenosine Diphosphate Receptor Inhibitors: Longitudinal Assessment of Treatment Patterns and Events After Acu
Baker, BA; Cohen, DJ; Effron, MB; Faries, DE; Jackson, LR; Ju, C; McCoy, LA; Messenger, JC; Peterson, ED; Wang, TY; Zettler, M, 2016
)
0.43
" Outcomes were evaluated for major adverse cardiovascular events (MACE) and bleeding at 1 year."( Comparative Effectiveness and Safety Analysis of Dual Antiplatelet Therapies Within an Integrated Delivery System.
Boyd, A; Chambers, A; Chanas, T; Coons, JC; Eckardt, J; Ensor, CR; Iasella, CJ; Lemon, LS; Lyons, J; Merkel, A; Rihtarchik, L; Smith, R; Wang, N; Williams, K, 2017
)
0.46
"The US Food and Drug Administration Adverse Event Reporting System (FAERS) is a global passive surveillance database that relies on voluntary reporting by health care professionals and consumers as well as required mandatory reporting by pharmaceutical manufacturers."( Filing Sources after Oral P2Y12 Platelet Inhibitors to the Food and Drug Administration Adverse Event Reporting System (FAERS).
Cabrera-Fuentes, HA; Cherepanov, V; Kim, MH; Litvinov, O; Marciniak, TA; Serebruany, VL,
)
0.13
"From the FAERS database we extracted and examined adverse event cases coreported with oral P2Y12 platelet inhibitors."( Filing Sources after Oral P2Y12 Platelet Inhibitors to the Food and Drug Administration Adverse Event Reporting System (FAERS).
Cabrera-Fuentes, HA; Cherepanov, V; Kim, MH; Litvinov, O; Marciniak, TA; Serebruany, VL,
)
0.13
"Overall, 2015 annual adverse events were more commonly coreported with clopidogrel (n = 13,234) with known source filers (n = 12,818, or 96."( Filing Sources after Oral P2Y12 Platelet Inhibitors to the Food and Drug Administration Adverse Event Reporting System (FAERS).
Cabrera-Fuentes, HA; Cherepanov, V; Kim, MH; Litvinov, O; Marciniak, TA; Serebruany, VL,
)
0.13
" Patients filed most adverse events for clopidogrel and prasugrel, while physicians originated most ticagrelor complaints."( Filing Sources after Oral P2Y12 Platelet Inhibitors to the Food and Drug Administration Adverse Event Reporting System (FAERS).
Cabrera-Fuentes, HA; Cherepanov, V; Kim, MH; Litvinov, O; Marciniak, TA; Serebruany, VL,
)
0.13
" We theorized that Prasugrel with a lower incidence of resistance may be a safe suitable alternative to clopidogrel in patients treated with a flow diverter (FD)."( Safety of Prasugrel loading in ruptured blister like aneurysm treated with a Pipeline device.
Gupta, A; Gupta, V; Parthasarathy, R, 2018
)
0.48
" Major adverse cardiac and cerebrovascular events (MACCE) [death, myocardial infarction (MI), stroke, and unplanned reintervention] and thrombolysis in myocardial infarction (TIMI) bleeding (major/minor) were registered during hospitalization and follow-up."( Safety and Efficacy in Prasugrel- Versus Ticagrelor-Treated Patients With ST-Elevation Myocardial Infarction.
Dannenberg, L; Dimitroulis, D; Golabkesh, M; Helten, C; Jung, C; Kelm, M; Knoop, B; Naguib, D; Pöhl, M; Polzin, A; Zeus, T, 2018
)
0.48
"To describe and evaluate the bleeding-related adverse events associated with use of P2Y12 inhibitors utilizing data from the FDA Adverse Event Reporting System (FAERS) database."( Evaluation of adverse events involving bleeding associated with oral P2Y12 inhibitors use in the Food and Drug Administration adverse event reporting system.
Abou-Ali, A; Fahmy, AI; Mekkawy, MA, 2019
)
0.51
"We identified 2,252, 2,450, and 549 adverse event reports attributed to clopidogrel, ticagrelor, and prasugrel use, respectively."( Evaluation of adverse events involving bleeding associated with oral P2Y12 inhibitors use in the Food and Drug Administration adverse event reporting system.
Abou-Ali, A; Fahmy, AI; Mekkawy, MA, 2019
)
0.51
" Secondary outcomes were adverse bleeding events (safety outcome)."( Efficacy and safety of alternative oral administrations of P2Y12-receptor inhibitors: Systematic review and meta-analysis.
Bilotta, F; Campo, G; Parodi, G; Pavasini, R; Serenelli, M; Tonet, E; Vitali, F, 2019
)
0.51
" Compared with nonsmokers within the first year of follow-up, the reductions of stroke and major adverse cardiovascular event rate were 18% ( P=0."( Effectiveness and Safety of Platelet ADP -P2Y12 Receptor Inhibitors Influenced by Smoking Status: A Systematic Review and Meta-Analysis.
Chen, S; Cui, Y; Gong, Y; Hu, K; Jiang, J; Liu, Z; Mu, G; Wang, Z; Xiang, Q; Xie, Q; Zhou, S, 2019
)
0.51
" The incidences of bleeding (TIMI major and minor) and major adverse cerebrocardiovascular events (MACCE; all-cause death, nonfatal myocardial infarction, stent thrombosis, unplanned revascularization, and stroke) were evaluated."( Safety and Efficacy of Low-Dose Prasugrel as Part of Triple Therapy With Aspirin and Oral Anticoagulants in Patients With Atrial Fibrillation Undergoing Percutaneous Coronary Intervention - From the TWMU-AF PCI Registry.
Arashi, H; Ebihara, S; Fujii, S; Hagiwara, N; Honda, A; Jujo, K; Kawamoto, T; Mori, F; Nakao, M; Ota, Y; Otsuki, H; Saito, K; Takagi, A; Tanaka, H; Tanaka, K; Yamaguchi, J; Yoshikawa, M, 2019
)
0.51
" The primary endpoint was major adverse cardiovascular events (MACE), including cardiovascular (CV) death, all-cause death, myocardial infarction (MI), stent thrombosis and stroke."( Efficacy and safety of clopidogrel versus prasugrel and ticagrelor for coronary artery disease treatment in patients with CYP2C19 LoF alleles: a systemic review and meta-analysis.
Gwak, HS; Lee, N; Seong, JM; Yoon, HY, 2020
)
0.56
" Data on adverse events (AEs) and composite events such as cardiovascular (CV) death, myocardial infarction (MI), and stroke were recorded and summarized to assess efficacy."( Incidence of Cardiovascular Events and Safety Profile of Prasugrel in Korean Patients With Acute Coronary Syndrome.
Choi, JH; Chon, MK; Chun, KJ; Hwang, KW; Jung, SM; Kim, JH; Kim, JS; Lee, SH; Lee, SY; Park, YH, 2020
)
0.56
" Random-effects model was used to calculate an unadjusted odds ratio (OR) for major adverse cardiovascular and cerbrovascular events (MACCE) and its components."( Meta-Analysis Comparing the Safety and Efficacy of Prasugrel and Ticagrelor in Acute Coronary Syndrome.
Ali, Z; Fischman, DL; Khan, S; Mamas, MA; Rafiq, A; Sabouret, P; Sadiq, U; Ullah, W, 2020
)
0.56
"Prasugrel/ticagrelor, compared to clopidogrel, reduces risk of major adverse cardiovascular event (MACE) in Hong Kong ACS population."( Efficacy and safety comparing prasugrel/ticagrelor and clopidogrel in Hong Kong post-acute coronary syndrome patients-A 10-year cohort study.
Lam, ASM; Lee, VWY; Yan, BPY, 2021
)
0.62
"To assess the efficacy and safety of low-dose prasugrel compared to clopidogrel based on the occurrence of major adverse cardiac events (MACEs) and major bleeding in patients with acute coronary syndromes (ACS) undergoing percutaneous coronary intervention (PCI)."( Efficacy and Safety of Low-Dose Prasugrel Versus Clopidogrel in Patients with Acute Coronary Syndrome Undergoing Percutaneous Coronary Intervention: a Systematic Review and Meta-analysis.
Kengkla, K; Kumtep, W; Saokaew, S; Senthong, V; Ungsriwong, S; Wongsalap, Y, 2022
)
0.72
" The primary endpoint was net adverse clinical event, defined as the primary efficacy endpoint of death, myocardial infarction, or cerebrovascular accident and the primary safety endpoint of any bleeding event."( Safety and Efficacy of Triple Therapy With Ticagrelor or Prasugrel Versus Clopidogrel After Percutaneous Coronary Intervention for ST-Elevation Myocardial Infarction.
Flahive, J; Fraielli, K; Gill, K; Servati, N, 2021
)
0.62
"This small cohort study suggests, in patients with ST-elevation myocardial infarction undergoing percutaneous coronary intervention, the net adverse clinical event rate does not differ between clopidogrel and potent P2Y12 inhibitors in the setting of triple antithrombotic therapy."( Safety and Efficacy of Triple Therapy With Ticagrelor or Prasugrel Versus Clopidogrel After Percutaneous Coronary Intervention for ST-Elevation Myocardial Infarction.
Flahive, J; Fraielli, K; Gill, K; Servati, N, 2021
)
0.62
"To establish the safety and efficacy of different dual antiplatelet therapy (DAPT) combinations in patients with acute coronary syndrome (ACS) according to their baseline ischaemic and bleeding risk estimated with a machine learning derived model [machine learning-based prediction of adverse events following an acute coronary syndrome (PRAISE) score]."( Safety and efficacy of different P2Y12 inhibitors in patients with acute coronary syndromes stratified by the PRAISE risk score: a multicentre study.
Abu-Assi, E; Bruno, F; Cerrato, E; Chieffo, A; Conrotto, F; D'Ascenzo, F; De Ferrari, GM; De Filippo, O; Dominguez-Rodriguez, A; Elia, E; Gallone, G; Henriques, JPS; Iannaccone, M; Kinnaird, T; Leonardi, S; Liebetrau, C; Manzano-Fernández, S; Omedè, P; Patti, G; Piroli, F; Raposeiras-Roubin, S; Wańha, W, 2022
)
0.72
" Net adverse clinical events were identified as the composite end point, which was defined as a composite of cardiovascular death, myocardial infarction, revascularization, stroke, and bleeding at 12 months after acute coronary syndromes."( Efficacy and Safety of De-escalation of Antiplatelet Therapy After Percutaneous Coronary Intervention in Patients With Acute Coronary Syndrome: A Meta-Analysis of Randomized Clinical Trials.
Bai, N; Ma, Y; Niu, Y; Shang, YS; Wang, ZL; Zhong, PY, 2022
)
0.72
"The implantation of a p64 MW HPC FD with prasugrel SAPT is safe and results in rapid, reliable and effective aneurysmal occlusion."( Use of a p64 MW Flow Diverter with Hydrophilic Polymer Coating (HPC) and Prasugrel Single Antiplatelet Therapy for the Treatment of Unruptured Anterior Circulation Aneurysms: Safety Data and Short-term Occlusion Rates.
Aguilar Pérez, M; Bäzner, H; Donauer, E; Ganslandt, O; Hellstern, V; Henkes, E; Henkes, H; Wendl, C, 2022
)
0.72
" Safety endpoints included bleeding events and adverse events (AEs)."( Efficacy and Safety of Prasugrel vs Clopidogrel in Thrombotic Stroke Patients With Risk Factors for Ischemic Stroke Recurrence: A Double-blind, Phase III Study (PRASTRO-III).
Kamouchi, M; Kimura, K; Kitazono, T; Koyama, N; Matsumaru, Y; Matsuo, H; Nakamura, M; Tsutsumi, J; Umemura, K, 2023
)
0.91
" The effectiveness outcome was major adverse cardiovascular events (MACE) defined as a composite of recurrent myocardial infarction, repeat revascularization, stroke, or cardiovascular death at 12 months."( Effectiveness and safety of P2Y12 inhibitors in patients with ST-segment elevation myocardial infarction undergoing percutaneous coronary intervention: a nationwide registry-based study.
Bhatt, DL; Butt, JH; Christensen, MK; Fosbøl, EL; Gislason, G; Godtfredsen, SJ; Jørgensen, SH; Kragholm, KH; Køber, L; Leutscher, P; Pareek, M; Sessa, M; Torp-Pedersen, C, 2022
)
0.72
"Immature or reticulated platelets are associated with impaired efficacy of antiplatelet drugs and adverse events in cardiovascular patients."( Immature Platelet Fraction Predicts Adverse Events in Patients With Acute Coronary Syndrome: the ISAR-REACT 5 Reticulated Platelet Substudy.
Anetsberger, A; Angiolillo, DJ; Bernlochner, I; Bongiovanni, D; Fegers-Wustrow, I; Gosetti, R; Holdenrieder, S; Kastrati, A; Laugwitz, KL; Mayer, K; Schreiner, N; Schunkert, H; Schüpke, S; Sibbing, D; von Scheidt, M, 2023
)
0.91
"Independently from drug treatment, IPF was associated with the primary end point and therefore is a promising biomarker for the prediction of adverse cardiovascular events in patients with acute coronary syndrome treated with prasugrel or ticagrelor."( Immature Platelet Fraction Predicts Adverse Events in Patients With Acute Coronary Syndrome: the ISAR-REACT 5 Reticulated Platelet Substudy.
Anetsberger, A; Angiolillo, DJ; Bernlochner, I; Bongiovanni, D; Fegers-Wustrow, I; Gosetti, R; Holdenrieder, S; Kastrati, A; Laugwitz, KL; Mayer, K; Schreiner, N; Schunkert, H; Schüpke, S; Sibbing, D; von Scheidt, M, 2023
)
0.91
" Outcomes included major adverse cardiovascular events, all cause death, major bleeding and myocardial infarction."( Comparison efficacy and safety of different antiplatelet or anticoagulation drugs in chronic coronary syndromes patients: A Bayesian network meta-analysis.
Liu, C; Ma, L, 2023
)
0.91
" In head-to-head comparison, no significant difference was observed between all antithrombotic treatment strategies with respect to primary endpoint of major adverse cardiovascular events."( Comparison efficacy and safety of different antiplatelet or anticoagulation drugs in chronic coronary syndromes patients: A Bayesian network meta-analysis.
Liu, C; Ma, L, 2023
)
0.91

Pharmacokinetics

ExcerptReferenceRelevance
" The pharmacokinetic data indicate that exposure to prasugrel metabolites occurs rapidly after dosing and is consistent with dose proportionality."( The platelet inhibitory effects and pharmacokinetics of prasugrel after administration of loading and maintenance doses in healthy subjects.
Brandt, JT; Farid, NA; Jakubowski, JA; Li, GY; Naganuma, H; Payne, CD; Small, DS; Weerakkody, GJ; Winters, KJ, 2006
)
0.33
" Ketoconazole decreased R-138727 and clopidogrel active metabolite Cmax (maximum plasma concentration) 34-61% after prasugrel and clopidogrel dosing."( Cytochrome P450 3A inhibition by ketoconazole affects prasugrel and clopidogrel pharmacokinetics and pharmacodynamics differently.
Brandt, JT; Darstein, C; Ernest, CS; Farid, NA; Jakubowski, JA; Payne, CD; Salazar, DE; Small, DS; Winters, KJ, 2007
)
0.34
" The pharmacodynamic response to clopidogrel is more variable than the response to prasugrel, but the reasons for variation in response to clopidogrel are not well characterized."( Common polymorphisms of CYP2C19 and CYP2C9 affect the pharmacokinetic and pharmacodynamic response to clopidogrel but not prasugrel.
Brandt, JT; Close, SL; Ernest, CS; Farid, NA; Iturria, SJ; Lachno, DR; Payne, CD; Salazar, D; Winters, KJ, 2007
)
0.34
"Genotyping was performed for CYP1A2, CYP2B6, CYP2C19, CYP2C9, CYP3A4 and CYP3A5 on samples from healthy subjects participating in studies evaluating pharmacokinetic and pharmacodynamic responses to prasugrel (60 mg, n = 71) or clopidogrel (300 mg, n = 74)."( Common polymorphisms of CYP2C19 and CYP2C9 affect the pharmacokinetic and pharmacodynamic response to clopidogrel but not prasugrel.
Brandt, JT; Close, SL; Ernest, CS; Farid, NA; Iturria, SJ; Lachno, DR; Payne, CD; Salazar, D; Winters, KJ, 2007
)
0.34
" Decreased exposure to its active metabolite is associated with a diminished pharmacodynamic response to clopidogrel."( Common polymorphisms of CYP2C19 and CYP2C9 affect the pharmacokinetic and pharmacodynamic response to clopidogrel but not prasugrel.
Brandt, JT; Close, SL; Ernest, CS; Farid, NA; Iturria, SJ; Lachno, DR; Payne, CD; Salazar, D; Winters, KJ, 2007
)
0.34
" Pharmacokinetic parameter estimates (AUC(0-t last), C(max), and t(max)) and inhibition of platelet aggregation (IPA) by light transmission aggregometry were assessed at multiple time points after the LD and final MD."( Effect of ranitidine on the pharmacokinetics and pharmacodynamics of prasugrel and clopidogrel.
Ernest, CS; Farid, NA; Li, YG; Payne, CD; Salazar, DE; Small, DS; Winters, KJ, 2008
)
0.35
" The lack of a clinically meaningful effect of high-dose atorvastatin on the pharmacodynamic response to prasugrel after the loading or maintenance dose indicates that no dosage adjustment should be necessary in patients receiving these drugs concomitantly."( Effect of atorvastatin on the pharmacokinetics and pharmacodynamics of prasugrel and clopidogrel in healthy subjects.
Brandt, JT; Ernest, CS; Farid, NA; Jakubowski, JA; Konkoy, CS; Li, YG; Payne, CD; Salazar, DE; Small, DS; Winters, KJ, 2008
)
0.35
" Among the healthy subjects, no significant attenuation of the pharmacokinetic or the pharmacodynamic response to prasugrel was observed in carriers versus noncarriers of at least 1 reduced-function allele for any of the CYP genes tested (CYP2C19, CYP2C9, CYP2B6, CYP3A5, and CYP1A2)."( Cytochrome P450 genetic polymorphisms and the response to prasugrel: relationship to pharmacokinetic, pharmacodynamic, and clinical outcomes.
Antman, EM; Brandt, JT; Braunwald, E; Close, SL; Hockett, RD; Macias, WL; Mega, JL; Sabatine, MS; Shen, L; Walker, JR; Wiviott, SD, 2009
)
0.35
" We hypothesized that decreased CYP2C19 activity affects the pharmacokinetic and pharmacodynamic response to clopidogrel but not prasugrel."( Genetic variation of CYP2C19 affects both pharmacokinetic and pharmacodynamic responses to clopidogrel but not prasugrel in aspirin-treated patients with coronary artery disease.
Brandt, JT; Braun, OO; Close, SL; Erlinge, D; James, S; Man, M; Siegbahn, A; Varenhorst, C; Walker, J; Wallentin, L; Winters, KJ, 2009
)
0.35
" For prasugrel, there was no statistically significant difference in active metabolite exposure or pharmacodynamic response between CYP2C19 EM and RM."( Genetic variation of CYP2C19 affects both pharmacokinetic and pharmacodynamic responses to clopidogrel but not prasugrel in aspirin-treated patients with coronary artery disease.
Brandt, JT; Braun, OO; Close, SL; Erlinge, D; James, S; Man, M; Siegbahn, A; Varenhorst, C; Walker, J; Wallentin, L; Winters, KJ, 2009
)
0.35
" Since cytochrome P450 enzymes CYP3A4 and CYP2B6 play a major role in prasugrel's active metabolite formation, the effect of potent CYP induction by rifampin on the pharmacokinetics of prasugrel and on the pharmacodynamic response to prasugrel was evaluated in healthy male subjects."( Effect of rifampin on the pharmacokinetics and pharmacodynamics of prasugrel in healthy male subjects.
Brandt, JT; Ernest II, CS; Farid, NA; Jakubowski, JA; Jin, Y; Li, YG; Payne, CD; Salazar, DE; Small, DS; Winters, KJ, 2009
)
0.35
" Blood collection for pharmacokinetic and pharmacodynamic analyses occurred after the LD and fifth MD of prasugrel in both periods."( Effect of rifampin on the pharmacokinetics and pharmacodynamics of prasugrel in healthy male subjects.
Brandt, JT; Ernest II, CS; Farid, NA; Jakubowski, JA; Jin, Y; Li, YG; Payne, CD; Salazar, DE; Small, DS; Winters, KJ, 2009
)
0.35
" A limitation of this study is that while results of the in vitro post hoc study indicate a pharmacodynamic interaction with rifampin, the mechanism underlying this interaction has not been elucidated."( Effect of rifampin on the pharmacokinetics and pharmacodynamics of prasugrel in healthy male subjects.
Brandt, JT; Ernest II, CS; Farid, NA; Jakubowski, JA; Jin, Y; Li, YG; Payne, CD; Salazar, DE; Small, DS; Winters, KJ, 2009
)
0.35
"Serial pharmacokinetic (PK) sampling in 1159 patients from TRITON-TIMI 38 was undertaken."( Population pharmacokinetic analyses to evaluate the influence of intrinsic and extrinsic factors on exposure of prasugrel active metabolite in TRITON-TIMI 38.
Antman, EM; Braunwald, E; Ernest, CS; Li, YG; Macias, WL; Ni, L; Riesmeyer, JR; Rohatagi, S; Salazar, DE; Small, DS; Weerakkody, GJ; Wiviott, SD; Wrishko, RE, 2009
)
0.35
" Median plasma half-life of the active metabolite is approximately 4 hours, and excretion is mainly urinary."( Pharmacokinetics and pharmacodynamics of prasugrel, a thienopyridine P2Y12 inhibitor.
Dobesh, PP, 2009
)
0.35
" Pharmacokinetic parameters (AUC(0-t), C(max) and t(max)) and maximal platelet aggregation (MPA) by light transmission aggregometry were assessed after the LD and final MD."( Pharmacokinetics and pharmacodynamics of prasugrel in subjects with moderate liver disease.
Ernest, CS; Farid, NA; Li, YG; Payne, CD; Salazar, DE; Small, DS; Winters, KJ, 2009
)
0.35
"The pharmacokinetic (PK) and pharmacodynamic (PD) responses to prasugrel were compared in three studies of healthy subjects vs."( Prasugrel pharmacokinetics and pharmacodynamics in subjects with moderate renal impairment and end-stage renal disease.
Borel, AG; Brandt, JT; Ernest, CS; Farid, NA; Kles, KA; Li, YG; Ni, L; Payne, CD; Salazar, DE; Small, DS; Winters, KJ; Wrishko, RE, 2009
)
0.35
" Plasma concentrations of prasugrel's active metabolite were determined and pharmacokinetic parameter estimates were derived."( Prasugrel pharmacokinetics and pharmacodynamics in subjects with moderate renal impairment and end-stage renal disease.
Borel, AG; Brandt, JT; Ernest, CS; Farid, NA; Kles, KA; Li, YG; Ni, L; Payne, CD; Salazar, DE; Small, DS; Winters, KJ; Wrishko, RE, 2009
)
0.35
" Although the approved loading dose is 60 mg, earlier studies of prasugrel suggested that active-metabolite exposure and pharmacodynamic response may be higher in Asian subjects than in white subjects."( Pharmacodynamics and pharmacokinetics of single doses of prasugrel 30 mg and clopidogrel 300 mg in healthy Chinese and white volunteers: an open-label trial.
Farid, NA; Jakubowski, JA; Kelly, R; Kothare, P; Li, YG; Natanegara, F; Ni, L; Payne, CD; Richard Lachno, D; Salazar, DE; Small, DS; Teng Loh, M; Tomlin, M; Winters, KJ; Yuen, E, 2010
)
0.36
"This study compared the pharmacodynamic response to a single 30-mg dose of prasugrel in healthy Chinese and white subjects and the response to a single 30-mg dose of prasugrel and a single 300-mg dose of clopidogrel in healthy Chinese subjects."( Pharmacodynamics and pharmacokinetics of single doses of prasugrel 30 mg and clopidogrel 300 mg in healthy Chinese and white volunteers: an open-label trial.
Farid, NA; Jakubowski, JA; Kelly, R; Kothare, P; Li, YG; Natanegara, F; Ni, L; Payne, CD; Richard Lachno, D; Salazar, DE; Small, DS; Teng Loh, M; Tomlin, M; Winters, KJ; Yuen, E, 2010
)
0.36
"An integrated analysis of pharmacokinetic (PK) parameter estimates for prasugrel, from 16 phase I clinical pharmacology studies, consolidated exposure estimates from 506 healthy male and female participants and evaluated the effect of specific intrinsic and extrinsic factors on exposure to prasugrel's active metabolite (AM, R-138727)."( Integrated analysis of pharmacokinetic data across multiple clinical pharmacology studies of prasugrel, a new thienopyridine antiplatelet agent.
April, JH; Ernest, CS; Farid, NA; Li, YG; Ni, L; Payne, CD; Rohatagi, S; Small, DS; Winters, KJ, 2011
)
0.37
"This study is a phase 3, multi-dose, pharmacodynamic comparison of prasugrel versus clopidogrel in Asian patients with ACS undergoing PCI."( Prasugrel versus clopidogrel in Asian patients with acute coronary syndromes: design and rationale of a multi-dose, pharmacodynamic, phase 3 clinical trial.
Boonbaichaiyapruck, S; Ge, J; Goh, YS; Hong, BK; Hou, CJ; Pinton, P; Zhu, J, 2010
)
0.36
" The aim of this study was to perform serial pharmacodynamic assessments of prasugrel with high-dose clopidogrel in patients with DM."( A pharmacodynamic comparison of prasugrel vs. high-dose clopidogrel in patients with type 2 diabetes mellitus and coronary artery disease: results of the Optimizing anti-Platelet Therapy In diabetes MellitUS (OPTIMUS)-3 Trial.
Angiolillo, DJ; Badimon, JJ; Baker, BA; Effron, MB; Frelinger, AL; Jakubowski, JA; Michelson, AD; Ojeh, CK; Saucedo, JF; Zhu, B, 2011
)
0.37
" This has led to the development of other P2Y12 receptor inhibitors, such as prasugrel and ticagrelor, with different pharmacokinetic characteristics that influence their pharmacodynamics."( Beyond efficacy: pharmacokinetic differences between clopidogrel, prasugrel and ticagrelor.
Cohen Arazi, H; Di Girolamo, G; Giorgi, MA; Gonzalez, CD, 2011
)
0.37
" However, the pharmacokinetic advantages of both prasugrel and ticagrelor allow clinicians to center patient management by selecting the best drug for the appropriate subject."( Beyond efficacy: pharmacokinetic differences between clopidogrel, prasugrel and ticagrelor.
Cohen Arazi, H; Di Girolamo, G; Giorgi, MA; Gonzalez, CD, 2011
)
0.37
" The pharmacokinetic profile of the thienopyridine clopidogrel has resulted in highly variable pharmacokinetics and efficacy responses."( Pharmacokinetics, drug metabolism, and safety of prasugrel and clopidogrel.
Achar, S, 2011
)
0.37
"Prasugrel demonstrated higher active metabolite exposure and more consistent pharmacodynamic response across all three predicted phenotype groups compared with clopidogrel, confirming observations from previous research that CYP2C19 phenotype plays an important role in variability of response to clopidogrel, but has no impact on response to prasugrel."( Pharmacokinetics and pharmacodynamics following maintenance doses of prasugrel and clopidogrel in Chinese carriers of CYP2C19 variants.
Close, SL; Farid, NA; Ho, M; Jakubowski, JA; Kelly, RP; Natanegara, F; Shen, L; Small, DS; Walker, JR; Winters, KJ, 2012
)
0.38
" This study aimed to define pharmacodynamic (PD) profiles, including high platelet reactivity (HPR) rates, among elderly patients on maintenance clopidogrel therapy and to assess the PD effects of prasugrel 5 mg/day in elderly with HPR."( Platelet function profiles in the elderly: results of a pharmacodynamic study in patients on clopidogrel therapy and effects of switching to prasugrel 5 mg in patients with high platelet reactivity.
Angiolillo, DJ; Calvi, V; Capodanno, D; Capranzano, P; D'Urso, L; Miccichè, E; Tamburino, C, 2011
)
0.37
"The purpose of this study is to assess the pharmacodynamic effects of different prasugrel dosing regimens in patients on maintenance prasugrel therapy."( Pharmacodynamic effects of prasugrel dosing regimens in patients on maintenance prasugrel therapy: results of a prospective randomized study.
Angiolillo, DJ; Bass, TA; Box, LC; Charlton, RK; Desai, B; Ferreiro, JL; Guzman, LA; Kodali, M; Seecheran, N; Tello-Montoliu, A; Tomasello, SD; Ueno, M; Zenni, MM, 2012
)
0.38
"This is a prospective pharmacodynamic study in patients (n = 64) receiving maintenance prasugrel therapy who were randomly allocated to a 10 mg, 30 mg, or 60 mg dose of prasugrel."( Pharmacodynamic effects of prasugrel dosing regimens in patients on maintenance prasugrel therapy: results of a prospective randomized study.
Angiolillo, DJ; Bass, TA; Box, LC; Charlton, RK; Desai, B; Ferreiro, JL; Guzman, LA; Kodali, M; Seecheran, N; Tello-Montoliu, A; Tomasello, SD; Ueno, M; Zenni, MM, 2012
)
0.38
" A 10 mg dose was associated with modest pharmacodynamic effects."( Pharmacodynamic effects of prasugrel dosing regimens in patients on maintenance prasugrel therapy: results of a prospective randomized study.
Angiolillo, DJ; Bass, TA; Box, LC; Charlton, RK; Desai, B; Ferreiro, JL; Guzman, LA; Kodali, M; Seecheran, N; Tello-Montoliu, A; Tomasello, SD; Ueno, M; Zenni, MM, 2012
)
0.38
" Expression of the 3435T/T genetic variant encoding the MDR1 gene for the P-glycoprotein efflux transporter results in a significantly reduced maximum drug concentration and area under the plasma concentration-time curve as intestinal absorption of clopidogrel is reduced; and the expression of the mutant *2 allele of CYP2C19 results in similar pharmacokinetic effects as the two cytochrome P450 (CYP)-mediated steps required for the production of the active metabolite of clopidogrel are impaired."( Comparative pharmacokinetics and pharmacodynamics of platelet adenosine diphosphate receptor antagonists and their clinical implications.
Ferro, A; Floyd, CN; Passacquale, G, 2012
)
0.38
"Previous studies involving a loading dose (LD) of 60 mg prasugrel have suggested that active metabolite exposure and pharmacodynamic responses may be higher in persons of Asian ethnicity than in Caucasian subjects."( Pharmacodynamic comparisons for single loading doses of prasugrel (30 mg) and clopidogrel (600 mg) in healthy Korean volunteers.
Jung, DK; Kim, MH; Zhang, HZ, 2013
)
0.39
"This study assessed pharmacodynamic (PD) response to the reduced prasugrel maintenance dose of 5 mg in very elderly (VE) patients (≥75 years of age)."( Prasugrel 5 mg in the very elderly attenuates platelet inhibition but maintains noninferiority to prasugrel 10 mg in nonelderly patients: the GENERATIONS trial, a pharmacodynamic and pharmacokinetic study in stable coronary artery disease patients.
Angiolillo, DJ; Brown, PB; Erlinge, D; Foley, DP; Gurbel, PA; Jakubowski, JA; James, S; Lindahl, TL; Luo, J; Moser, BA; Small, DS; Svensson, P; Ten Berg, JM; Wagner, H; Winters, KJ; Zhou, C, 2013
)
0.39
"This article is an overview of currently used antithrombotic therapies in the management of ischaemic stroke with special focus on their pharmacokinetic properties and how these properties may influence their clinical utility."( Pharmacokinetic considerations for antithrombotic therapies in stroke.
Apostolakis, S; Lip, GY; Shantsila, E, 2013
)
0.39
"Increased body weight is independently associated with impaired clopidogrel pharmacodynamic (PD) response."( Pharmacodynamic effects of standard dose prasugrel versus high dose clopidogrel in non-diabetic obese patients with coronary artery disease.
Angiolillo, DJ; Bass, TA; Darlington, A; Desai, B; Ferreiro, JL; Guzman, LA; Patel, R; Rollini, F; Tello-Montoliu, A; Ueno, M, 2014
)
0.4
"The goal of this study was to evaluate the pharmacodynamic effects of switching patients from ticagrelor to prasugrel."( Pharmacodynamic evaluation of switching from ticagrelor to prasugrel in patients with stable coronary artery disease: Results of the SWAP-2 Study (Switching Anti Platelet-2).
Angiolillo, DJ; Curzen, N; Effron, MB; Gurbel, P; Jakubowski, JA; Li, W; Lipkin, F; Trenk, D; Vaitkus, P; Zettler, M, 2014
)
0.4
" Pharmacodynamic assessments were defined according to P2Y12 reaction unit (PRU) (P2Y12 assay) and platelet reactivity index (vasodilator-stimulated phosphoprotein phosphorylation assay) at baseline (before and after the run-in phase) and 2, 4, 24, and 48 h and 7 days after randomization."( Pharmacodynamic evaluation of switching from ticagrelor to prasugrel in patients with stable coronary artery disease: Results of the SWAP-2 Study (Switching Anti Platelet-2).
Angiolillo, DJ; Curzen, N; Effron, MB; Gurbel, P; Jakubowski, JA; Li, W; Lipkin, F; Trenk, D; Vaitkus, P; Zettler, M, 2014
)
0.4
"This article focuses on the pharmacokinetics of prasugrel and recently published pharmacodynamic and clinical studies."( Pharmacokinetic evaluation of prasugrel for the treatment of myocardial infarction.
Coons, JC; Harris, J; Schwier, N; Seybert, AL, 2014
)
0.4
"Prasugrel exhibits favorable pharmacokinetic and pharmacodynamic properties compared to clopidogrel."( Pharmacokinetic evaluation of prasugrel for the treatment of myocardial infarction.
Coons, JC; Harris, J; Schwier, N; Seybert, AL, 2014
)
0.4
" Here, we assessed effects of CYP2C19 metaboliser status on pharmacokinetics (PK) and pharmacodynamic (PD) responses to prasugrel 5-mg and 10-mg and clopidogrel 75-mg using data from two PK/PD studies in stable coronary artery disease (CAD) patients (GENERATIONS and FEATHER)."( The effect of CYP2C19 gene polymorphisms on the pharmacokinetics and pharmacodynamics of prasugrel 5-mg, prasugrel 10-mg and clopidogrel 75-mg in patients with coronary artery disease.
Angiolillo, DJ; Bergmeijer, TO; Brown, PB; Duvvuru, S; Erlinge, D; Gurbel, PA; Jakubowski, JA; James, S; Lindahl, TL; Moser, BA; Small, D; Sundseth, S; Svensson, P; Tantry, US; ten Berg, JM; Walker, JR; Winters, KJ, 2014
)
0.4
"The aim of this study was to determine the impact of cangrelor and prasugrel on the pharmacodynamic effects of each agent."( Pharmacodynamic effects during the transition between cangrelor and prasugrel.
Gogo, P; Keating, FK; Raza, SS; Schneider, DJ; Seecheran, N, 2015
)
0.42
" Pharmacodynamic effects (light transmission platelet aggregation in response to 20 μmol/l ADP, VerifyNow, and flow cytometry) were assessed during and after the cangrelor infusion."( Pharmacodynamic effects during the transition between cangrelor and prasugrel.
Gogo, P; Keating, FK; Raza, SS; Schneider, DJ; Seecheran, N, 2015
)
0.42
"12 mg/kg) based on VN pharmacodynamic measurements at the start of 2 dosing periods, each 14±4 days."( Prasugrel in children with sickle cell disease: pharmacokinetic and pharmacodynamic data from an open-label, adaptive-design, dose-ranging study.
Heath, LE; Heeney, MM; Heiselman, D; Jakubowski, JA; Kanter, J; Moser, BA; Quinn, CT; Rana, SR; Redding-Lallinger, R; Small, DS; Styles, L; Winters, KJ; Zhou, C, 2015
)
0.42
" The aim of this study was to evaluate the pharmacodynamic profile of 5 different anti-platelet treatments in the acute phase of STEMI in patients undergoing primary PCI."( A pharmacodynamic comparison of 5 anti-platelet protocols in patients with ST-elevation myocardial infarction undergoing primary PCI.
Andell, P; Björnsson, S; Erlinge, D; Götberg, M; Harnek, J; Koul, S; Martinsson, A; Norström, E; Scherstén, F; Smith, JG, 2014
)
0.4
" In this study, we compared the pharmacodynamic efficacy of prasugrel and ticagrelor in East Asian patients with acute coronary syndrome (ACS)."( A pharmacodynamic study of the optimal P2Y12 inhibitor regimen for East Asian patients with acute coronary syndrome.
Ahn, MS; Ahn, SG; Kang, YS; Kim, JY; Lee, JH; Lee, JW; Lee, SH; Park, B; Park, SW; Yoo, BS; Yoon, J; Youn, YJ, 2015
)
0.42
" Pharmacodynamic assessments were conducted using three assays (vasodilator-stimulated phosphoprotein, VerifyNow P2Y12, and light transmittance aggregometry, LTA) at baseline, 30 min, 2, 24 h, and 1 week."( A head-to-head pharmacodynamic comparison of prasugrel vs. ticagrelor after switching from clopidogrel in patients with coronary artery disease: results of a prospective randomized study.
Angiolillo, DJ; Bass, TA; Bhatti, M; Cho, JR; DeGroat, C; Dunn, EC; Ferrante, E; Franchi, F; Guzman, LA; Muniz-Lozano, A; Rollini, F; Singh, K; Wilson, RE; Zenni, MM, 2016
)
0.43
"This study sought to assess the pharmacodynamic (PD) effects of switching to ticagrelor patients who were treated with prasugrel after undergoing percutaneous coronary intervention in the setting of an acute coronary syndrome."( Pharmacodynamic Effects of Switching From Prasugrel to Ticagrelor: Results of the Prospective, Randomized SWAP-3 Study.
Aggarwal, N; Angiolillo, DJ; Antoun, P; Bass, TA; Been, L; Cho, JR; Durairaj, A; Faz, GT; Franchi, F; Guzman, LA; Hu, J; Kureti, M; Park, Y; Rollini, F; Suryadevara, S; Thano, E; Zenni, MM, 2016
)
0.43
"To complete a systematic review evaluating the currently available evidence regarding the pharmacokinetic and pharmacodynamic activity of orally administered clopidogrel, prasugrel and ticagrelor during the acute phase of a myocardial infarction in relation to mechanical reperfusion with primary percutaneous coronary angioplasty."( Pharmacokinetics and pharmacodynamics of oral P2Y12 inhibitors during the acute phase of a myocardial infarction: A systematic review.
Cotton, JM; Cox, AR; Khan, N, 2016
)
0.43
"Twelve papers were included in our final analysis; seven relating to pharmacodynamic studies, one to a pharmacokinetic study and four to pharmacokinetic/pharmacodynamic studies."( Pharmacokinetics and pharmacodynamics of oral P2Y12 inhibitors during the acute phase of a myocardial infarction: A systematic review.
Cotton, JM; Cox, AR; Khan, N, 2016
)
0.43
"5-10 mg), the pharmacokinetic parameters on Day 1 and Day 7 were similar, and no accumulation attributable to multiple dosing was observed."( Pharmacokinetics and pharmacodynamics of prasugrel in healthy Japanese subjects.
Ikeda, Y; Kondo, K; Umemura, K, 2016
)
0.43
" Whether these findings may be attributed to differences in the pharmacodynamic profiles of these drugs in DM patients remains poorly explored and represented the aim of this study."( Pharmacodynamic Comparison of Prasugrel Versus Ticagrelor in Patients With Type 2 Diabetes Mellitus and Coronary Artery Disease: The OPTIMUS (Optimizing Antiplatelet Therapy in Diabetes Mellitus)-4 Study.
Aggarwal, N; Angiolillo, DJ; Bass, TA; Been, L; Cho, JR; Duarte, VE; Durairaj, A; Franchi, F; Hu, J; Kureti, M; Rollini, F; Zenni, MM, 2016
)
0.43
"In this prospective, randomized, double-blind, double-dummy, crossover pharmacodynamic study, aspirin-treated DM patients (n=50) with coronary artery disease were randomly assigned to receive prasugrel (60 mg loading dose [LD]/10 mg maintenance dose once daily) or ticagrelor (180 mg LD/90 mg maintenance dose twice daily) for 1 week."( Pharmacodynamic Comparison of Prasugrel Versus Ticagrelor in Patients With Type 2 Diabetes Mellitus and Coronary Artery Disease: The OPTIMUS (Optimizing Antiplatelet Therapy in Diabetes Mellitus)-4 Study.
Aggarwal, N; Angiolillo, DJ; Bass, TA; Been, L; Cho, JR; Duarte, VE; Durairaj, A; Franchi, F; Hu, J; Kureti, M; Rollini, F; Zenni, MM, 2016
)
0.43
" Pharmacodynamic assessments measured by vasodilator-stimulated phosphoprotein, light transmittance aggregometry, and Multiplate were similar between prasugrel and ticagrelor at each time point, including at 1 week."( Pharmacodynamic Comparison of Prasugrel Versus Ticagrelor in Patients With Type 2 Diabetes Mellitus and Coronary Artery Disease: The OPTIMUS (Optimizing Antiplatelet Therapy in Diabetes Mellitus)-4 Study.
Aggarwal, N; Angiolillo, DJ; Bass, TA; Been, L; Cho, JR; Duarte, VE; Durairaj, A; Franchi, F; Hu, J; Kureti, M; Rollini, F; Zenni, MM, 2016
)
0.43
" We assessed the pharmacokinetic and pharmacodynamic effects of prasugrel at the clinical dose used in Japan in healthy Japanese elderly subjects compared with non-elderly subjects."( Evaluation of the Pharmacokinetics and Pharmacodynamics of Prasugrel in Japanese Elderly Subjects.
Fukase, H; Hasunuma, T; Miyazaki, A; Nishikawa, Y, 2017
)
0.46
" Plasma concentration of its active metabolite, R-138727, and pharmacokinetic parameters were determined on days 1 and 7 after dosing."( Evaluation of the Pharmacokinetics and Pharmacodynamics of Prasugrel in Japanese Elderly Subjects.
Fukase, H; Hasunuma, T; Miyazaki, A; Nishikawa, Y, 2017
)
0.46
" There was no statistically significant difference in pharmacokinetic parameters between groups: area under the plasma concentration-time curve up to the last quantifiable time and maximum plasma concentration were about 174-175 ng·h/mL and 134-153 ng/mL, respectively, after the loading dose; and about 25-26 ng·h/mL and 25 ng/mL, respectively, after the maintenance dose."( Evaluation of the Pharmacokinetics and Pharmacodynamics of Prasugrel in Japanese Elderly Subjects.
Fukase, H; Hasunuma, T; Miyazaki, A; Nishikawa, Y, 2017
)
0.46
" A physiologically based pharmacokinetic (PBPK) absorption model was constructed to predict pharmacokinetic (PK) profiles of active metabolite after oral administration of prasugrel HCl products containing various fractions of base based on the prasugrel salt and base intrinsic solubility."( Utility of Physiologically Based Pharmacokinetic Absorption Modeling to Predict the Impact of Salt-to-Base Conversion on Prasugrel HCl Product Bioequivalence in the Presence of Proton Pump Inhibitors.
Fan, J; Zhang, X; Zhao, L, 2017
)
0.46
" The impact of LOF alleles on the pharmacodynamic response to half-dose prasugrel in patients with non-ST-elevation acute coronary syndrome (NSTE-ACS) undergoing percutaneous coronary intervention (PCI) is unknown."( Pharmacodynamic study of prasugrel or clopidogrel in non-ST-elevation acute coronary syndrome with CYP2C19 genetic variants undergoing percutaneous coronary intervention (PRAISE-GENE trial).
Ann, SH; Cho, YR; Guo, LZ; Jin, C; Jin, E; Kim, MH; Kim, SJ; Lee, MS; Park, JS; Shin, ES, 2020
)
0.56
" Clopidogrel has long been the gold standard but has major pharmacological limitations such as a slow onset and long duration of effect, as well as weak platelet inhibition with high inter-individual pharmacokinetic and pharmacodynamic variability."( Pharmacokinetics and Pharmacodynamics of Approved and Investigational P2Y12 Receptor Antagonists.
Dingemanse, J; Schilling, U; Ufer, M, 2020
)
0.56
" Pharmacodynamic measurements were performed at 4 time points: before antiplatelet treatment, at the beginning and end of pPCI, and 4 h after study treatment onset."( Pharmacodynamic Effects of Pre-Hospital Administered Crushed Prasugrel in Patients With ST-Segment Elevation Myocardial Infarction.
Alexopoulos, D; Angiolillo, DJ; Delewi, R; Diletti, R; Krucoff, MW; Lemmert, ME; Montalescot, G; Nuis, RJ; Paradies, V; Smits, PC; van der Waarden, NWPL; van Mieghem, NM; van Vliet, R; Vlachojannis, GJ; Vogel, RF; Wilschut, JM; Zijlstra, F, 2021
)
0.62
" A pharmacokinetic model for R-95913 and R-138727, and a pharmacodynamic model between the concentration of R-138727 and maximal platelet aggregation measured by light transmittance were constructed."( Pharmacokinetic and Pharmacodynamic Modeling and Simulation Analysis of Prasugrel in Healthy Male Volunteers.
Choi, HY; Choi, SC; Kim, EH; Kim, H; Kim, MJ; Kim, YH; Lee, SM; Lim, HS; Park, HJ, 2023
)
0.91

Compound-Compound Interactions

ExcerptReferenceRelevance
" Moreover, unwanted drug-drug pharmacokinetic interactions influencing CYP2C19 activity and clopidogrel bioactivation such as with proton pump inhibitors remain a matter of intense controversy."( Impact of genetic polymorphisms and drug-drug interactions on clopidogrel and prasugrel response variability.
Ancrenaz, V; Besson, M; Daali, Y; Dayer, P; Desmeules, J; Fontana, P; Samer, C, 2010
)
0.36
" This finding suggests a potential significant drug-drug interaction between these two drugs."( Ritonavir inhibits the two main prasugrel bioactivation pathways in vitro: a potential drug-drug interaction in HIV patients.
Ancrenaz, V; Bosilkovska, M; Daali, Y; Dayer, P; Desmeules, J, 2011
)
0.37
" However, comparative clinical effects of newest-generation DES with biodegradable polymers vs second-generation DES or newest-generation BMS with biocompatible coatings, all combined with a prasugrel-based antiplatelet therapy, on 2-year outcomes are not known."( Newest-generation drug-eluting and bare-metal stents combined with prasugrel-based antiplatelet therapy in large coronary arteries: the BAsel Stent Kosten Effektivitäts Trial PROspective Validation Examination part II (BASKET-PROVE II) trial design.
Alber, H; Eberli, F; Galatius, S; Gilgen, N; Jeger, R; Jensen, JS; Kaiser, C; Naber, C; Pedrazzini, G; Pfisterer, M; Rickli, H; Vuilliomenet, A, 2012
)
0.38
"We evaluated the pharmacokinetics and pharmacodynamics of prasugrel used in combination with aspirin in healthy Japanese subjects."( Platelet Aggregation Inhibitory Effects and Pharmacokinetics of Prasugrel Used in Combination With Aspirin in Healthy Japanese Subjects.
Ikeda, Y; Kondo, K; Matsushima, N; Umemura, K, 2017
)
0.46
"The risk and benefit of GP-IIb/IIIa Inhibition (GPI) in combination with recent antiplatelet regimens in acute coronary syndromes (ACS) remain unassessed."( Safety and efficacy of IIb/IIIa inhibitors in combination with highly active oral antiplatelet regimens in acute coronary syndromes: A meta-analysis of pivotal trials.
Agueznai, M; Ardouin, P; Beygui, F; Blanchart, K; Collet, JP; Lemaître, A; Milliez, P; Montalescot, G; Roule, V; Sabatier, R, 2017
)
0.46

Bioavailability

ExcerptReferenceRelevance
" The relative bioavailability of the active metabolites of prasugrel and clopidogrel calculated by the ratio of active metabolite AUC (prodrug oral administration/active metabolite intravenous administration) were 25% and 7%, respectively, in rats, and 25% and 10%, respectively, in dogs."( Comparison of formation of thiolactones and active metabolites of prasugrel and clopidogrel in rats and dogs.
Farid, NA; Fusegawa, K; Hagihara, K; Ikeda, T; Ikenaga, H; Kazui, M; Kurihara, A; Nanba, T; Okazaki, O; Takahashi, M, 2009
)
0.35
" Prasugrel is more potent than clopidogrel with a better bioavailability and lower pharmacodynamic variability."( Impact of genetic polymorphisms and drug-drug interactions on clopidogrel and prasugrel response variability.
Ancrenaz, V; Besson, M; Daali, Y; Dayer, P; Desmeules, J; Fontana, P; Samer, C, 2010
)
0.36
" In an open-label, randomized, four-period, 2 x two-way crossover study, the relative bioavailability of tablets containing prasugrel free base compared to prasugrel hydrochloride (originator product) both in the presence and in the absence of the proton pump inhibitor lansoprazole (CAS 103577-45-3) was investigated."( Relative bioavailability of prasugrel free base in comparison to prasugrel hydrochloride in the presence and in the absence of a proton pump inhibitor.
Doser, K; Salem, I; Seiler, D, 2011
)
0.8
"This study sought to determine whether crushing prasugrel is associated with more favorable drug bioavailability and platelet inhibitory effects compared with whole tablets in STEMI patients undergoing PPCI."( Crushed Prasugrel Tablets in Patients With STEMI Undergoing Primary Percutaneous Coronary Intervention: The CRUSH Study.
Aggarwal, N; Angiolillo, DJ; Antoun, P; Bass, TA; Cox-Alomar, P; Durairaj, A; Franchi, F; Guzman, LA; Hu, J; Kureti, M; Park, Y; Rollini, F; Seawell, M; Suryadevara, S; Zenni, MM, 2016
)
0.43
" Therefore, this novel prasugrel base microsphere-loaded tablet could be a potential alternative for enhancing the stability and bioavailability of prasugrel."( Development of novel prasugrel base microsphere-loaded tablet with enhanced stability: Physicochemical characterization and in vivo evaluation in beagle dogs.
Choi, HG; Jin, SG; Kim, DS; Kim, DW; Kim, JC; Kim, JO; Kim, KS; Oh, KT; Woo, JS; Yong, CS; Youn, YS, 2016
)
0.43
"Prasugrel exhibits beneficial mid-term effects on endothelial nitric oxide bioavailability and inflammatory markers."( Prasugrel as opposed to clopidogrel improves endothelial nitric oxide bioavailability and reduces platelet-leukocyte interaction in patients with unstable angina pectoris: A randomized controlled trial.
Baldus, S; Friedrichs, K; Fuchs, A; Hellmich, M; Klinke, A; Mollenhauer, M; Rudolph, TK; Rudolph, V; Schlichting, A; Schwedhelm, E, 2017
)
0.46
" A model based on assumptions of the fraction of a dose absorbed remaining unchanged for formulations containing different fractions of base over predicted the reduction of bioavailability upon conversion to the base."( Utility of Physiologically Based Pharmacokinetic Absorption Modeling to Predict the Impact of Salt-to-Base Conversion on Prasugrel HCl Product Bioequivalence in the Presence of Proton Pump Inhibitors.
Fan, J; Zhang, X; Zhao, L, 2017
)
0.46
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019
)
0.51
" However, oral antiplatelet agents, such as prasugrel or ticagrelor, are characterized by slow gastrointestinal drug absorption in the acute phase of STEMI, leading to decreased bioavailability and therefore delayed onset of platelet inhibition."( COMPARison of pre-hospital CRUSHed vs. uncrushed Prasugrel tablets in patients with STEMI undergoing primary percutaneous coronary interventions: Rationale and design of the COMPARE CRUSH trial.
Alexopoulos, D; Angiolillo, DJ; Delewi, R; Diletti, R; Krucoff, MW; Lemmert, ME; Montalescot, G; Nuis, RJ; Paradies, V; Smits, PC; van der Waarden, N; Van Mieghem, NM; van Vliet, R; Vlachojannis, GJ; Vogel, RF; Wilschut, JM; Zijlstra, F, 2020
)
0.56
" The objective of this work was to enhance the solubility and hence the bioavailability and efficacy of PHCl."( Solid self nano-emulsifying system for the enhancement of dissolution and bioavailability of Prasugrel HCl:
Al-Nimry, S; Attar, S; Khanfar, M, 2021
)
0.62

Dosage Studied

ExcerptRelevanceReference
" Patients were randomized to either standard dosing with clopidogrel or 1 of 3 prasugrel regimens."( Randomized comparison of prasugrel (CS-747, LY640315), a novel thienopyridine P2Y12 antagonist, with clopidogrel in percutaneous coronary intervention: results of the Joint Utilization of Medications to Block Platelets Optimally (JUMBO)-TIMI 26 trial.
Antman, EM; Behounek, BD; Braunwald, E; Carney, RJ; Lazzam, C; McCabe, CH; McKay, RG; Murphy, SA; Weerakkody, G; Winters, KJ; Wiviott, SD, 2005
)
0.33
" The aims of this double-blind, double-dummy, placebo-controlled, randomized, parallel group phase 1 study were to investigate the antiplatelet effects of prasugrel after oral administration of a loading dose (LD) and subsequent 20 days of once-daily maintenance dosing (MD), to characterize the pharmacokinetics of prasugrel metabolites with an LD/MD regimen, and to assess the safety and tolerability of prasugrel in healthy subjects."( The platelet inhibitory effects and pharmacokinetics of prasugrel after administration of loading and maintenance doses in healthy subjects.
Brandt, JT; Farid, NA; Jakubowski, JA; Li, GY; Naganuma, H; Payne, CD; Small, DS; Weerakkody, GJ; Winters, KJ, 2006
)
0.33
"At the dosing regimens chosen in the JUMBO trial, it seems that prasugrel is a more potent antiplatelet agent than clopidogrel."( Platelet inhibition with prasugrel (CS-747) compared with clopidogrel in patients undergoing coronary stenting: the subset from the JUMBO study.
Lowry, DR; Malinin, AI; Meilman, H; Midei, MG; Serebruany, VL, 2006
)
0.33
"This double-blind, placebo-controlled trial evaluated the safety, pharmacodynamics, and pharmacokinetics of prasugrel (CS-747, LY640315), a novel thienopyridine P2Y12 ADP receptor antagonist, during multiple oral dosing in healthy subjects."( Platelet inhibitory activity and pharmacokinetics of prasugrel (CS-747) a novel thienopyridine P2Y12 inhibitor: a multiple-dose study in healthy humans.
Asai, F; Brandt, JT; Freestone, S; Hirota, T; Jakubowski, JA; Matsushima, N; Naganuma, H; Winters, KJ, 2006
)
0.33
"This double-blind, placebo-controlled trial was designed to evaluate the pharmacodynamics, pharmacokinetics, safety, and tolerability of prasugrel (CS-747, LY640315), a novel thienopyridine P2Y(12) ADP receptor antagonist compared with clopidogrel, during multiple oral dosing in healthy subjects."( A multiple dose study of prasugrel (CS-747), a novel thienopyridine P2Y12 inhibitor, compared with clopidogrel in healthy humans.
Asai, F; Brandt, JT; Freestone, S; Hirota, T; Jakubowski, JA; Matsushima, N; Naganuma, H; Winters, KJ, 2007
)
0.34
" Within the limitations of the study, prasugrel was found to be well tolerated when dosed as LD followed by MD in the presence of ASA and provided greater platelet inhibition than ASA alone."( Dose-dependent inhibition of human platelet aggregation by prasugrel and its interaction with aspirin in healthy subjects.
Brandt, JT; Farid, NA; Jakubowski, JA; Lachno, DR; Li, YG; Naganuma, H; Payne, CD; Weerakkody, GJ; Winters, KJ, 2007
)
0.34
"Prasugrel is converted to the pharmacologically active metabolite after oral dosing in vivo."( Absorption, distribution and excretion of the new thienopyridine agent prasugrel in rats.
Farid, NA; Hagihara, K; Ikeda, T; Kawabata, K; Kawai, K; Kazui, M; Kurihara, A; Takahashi, M, 2007
)
0.34
"Antiplatelet and antithrombotic activity of multiple oral dosing of prasugrel were evaluated in several animal species."( Repeat oral dosing of prasugrel, a novel P2Y12 receptor inhibitor, results in cumulative and potent antiplatelet and antithrombotic activity in several animal species.
Asai, F; Hashimoto, M; Isobe, T; Jakubowski, JA; Niitsu, Y; Ogawa, T; Otsuguro, K; Sugidachi, A, 2008
)
0.35
" Prasugrel is orally more potent and acts more rapidly than clopidogrel, allowing lower oral dosing despite of similar in vitro activity of the active metabolites."( [Prasugrel, a new thienopyridine].
Huber, K; Schrör, K, 2007
)
0.34
" Despite the unambiguous clinical benefit associated with clopidogrel, accumulating experience with this drug has also led to identification of some of its drawbacks, which are related to inadequate platelet inhibition with standard dosage regimens as well as to its irreversible antiplatelet effects."( ADP receptor antagonism: what's in the pipeline?
Angiolillo, DJ, 2007
)
0.34
"Platelet inhibition as measured by vasodilator-stimulated phosphoprotein (VASP) and light transmission aggregometry (LTA) have shown concordance following dosing of clopidogrel."( A comparison of the antiplatelet effects of prasugrel and high-dose clopidogrel as assessed by VASP-phosphorylation and light transmission aggregometry.
Brandt, JT; Farid, NA; Jakubowski, JA; Li, YG; Payne, CD; Salazar, DE; Small, DS; Winters, KJ, 2008
)
0.35
" Since prasugrel is still under investigation, an official recommended dosage regimen has yet to be determined."( Prasugrel: a novel antiplatelet agent.
Haber, SL; Riley, AB; Tafreshi, MJ, 2008
)
0.35
" Future studies with prasugrel should determine its optimal dosage regimen to minimize bleeding risks and evaluate its outcomes in ACS and safety profile in special patient populations."( Prasugrel: a novel antiplatelet agent.
Haber, SL; Riley, AB; Tafreshi, MJ, 2008
)
0.35
" Currently, efficiency, dosing and indications of established antiplatelet substances are being re-evaluated, whilst new, so far unrecognized molecular targets for inhibition of platelet activity come up front."( Antiplatelet drugs in cardiological practice: established strategies and new developments.
Klauss, V; Krötz, F; Sohn, HY, 2008
)
0.35
" The drug was given as monotherapy for 10 days, and after a 6-day run-in period with atorvastatin 80 mg/day, the same dosage of atorvastatin was continued with the respective thienopyridine for 10 days."( Effect of atorvastatin on the pharmacokinetics and pharmacodynamics of prasugrel and clopidogrel in healthy subjects.
Brandt, JT; Ernest, CS; Farid, NA; Jakubowski, JA; Konkoy, CS; Li, YG; Payne, CD; Salazar, DE; Small, DS; Winters, KJ, 2008
)
0.35
"Blood samples were collected before and at various time points after dosing on days 1 and 11 for determination of plasma concentrations of metabolites and for measurement of platelet aggregation induced by adenosine 5'-diphosphate 20 microM and vasodilator-stimulated phosphoprotein (VASP)."( Effect of atorvastatin on the pharmacokinetics and pharmacodynamics of prasugrel and clopidogrel in healthy subjects.
Brandt, JT; Ernest, CS; Farid, NA; Jakubowski, JA; Konkoy, CS; Li, YG; Payne, CD; Salazar, DE; Small, DS; Winters, KJ, 2008
)
0.35
" The lack of a clinically meaningful effect of high-dose atorvastatin on the pharmacodynamic response to prasugrel after the loading or maintenance dose indicates that no dosage adjustment should be necessary in patients receiving these drugs concomitantly."( Effect of atorvastatin on the pharmacokinetics and pharmacodynamics of prasugrel and clopidogrel in healthy subjects.
Brandt, JT; Ernest, CS; Farid, NA; Jakubowski, JA; Konkoy, CS; Li, YG; Payne, CD; Salazar, DE; Small, DS; Winters, KJ, 2008
)
0.35
" Recent data have demonstrated limitations with the currently approved dosing regimen of clopidogrel (loading dose, 300 mg; maintenance dose, 75 mg daily) in a significant number of patients during the first few hours-days of treatment (Gurbel et al, Circulation."( Antiplatelet therapy in percutaneous coronary intervention: integration of prasugrel into clinical practice.
Giugliano, RP; Thomas, D, 2009
)
0.35
" The steady-state trough MPA to ADP 20 micromol/L during 10-mg maintenance dosing was 30."( Effect of age on the pharmacokinetics and pharmacodynamics of prasugrel during multiple dosing: an open-label, single-sequence, clinical trial.
Ernest, CS; Farid, NA; Li, YG; Ni, L; Payne, CD; Salazar, DE; Small, DS; Winters, KJ; Wrishko, RE, 2009
)
0.35
" These results characterize prasugrel's PK across a range of studies and highlight body weight as the most influential covariate on prasugrel AM exposure, with implications for prasugrel maintenance dosing in clinical practice."( Integrated analysis of pharmacokinetic data across multiple clinical pharmacology studies of prasugrel, a new thienopyridine antiplatelet agent.
April, JH; Ernest, CS; Farid, NA; Li, YG; Ni, L; Payne, CD; Rohatagi, S; Small, DS; Winters, KJ, 2011
)
0.37
" The large clinical trials COAG and EU-PACT will define the extent to which pharmacogenetic dosing affects the safety and efficacy of warfarin and coumarin derivatives."( Implementing genotype-guided antithrombotic therapy.
Duconge, J; Ruaño, G; Seip, RL, 2010
)
0.36
" We review the recent data on efficacy and safety of dosing strategies for antiplatelet therapy in PCI."( Dosing strategies for antiplatelet therapy in percutaneous coronary intervention.
Bauters, C; Bonello, L; Delhaye, C; Lablanche, JM; Lemesle, G; Maluenda, G; Sudre, A, 2010
)
0.36
" No dosage adjustments need to be made for renal or hepatic impairment."( Thienopyridine antiplatelet agents: focus on prasugrel.
Freeman, MK, 2010
)
0.36
" East and Southeast Asian patients (N = 715) with moderate- to high-risk ACS undergoing PCI will be randomized to one of three prasugrel dosing regimens (60 mg LD/10 mg MD; 30 mg LD/7."( Prasugrel versus clopidogrel in Asian patients with acute coronary syndromes: design and rationale of a multi-dose, pharmacodynamic, phase 3 clinical trial.
Boonbaichaiyapruck, S; Ge, J; Goh, YS; Hong, BK; Hou, CJ; Pinton, P; Zhu, J, 2010
)
0.36
" However, different degrees of resistance to clopidogrel have been the subject of many recent studies that led to higher dosing regimens of clopidogrel."( A new era for antiplatelet therapy in patients with acute coronary syndrome.
Abu-Fadel, MS; Dib, C; Hanna, EB, 2010
)
0.36
" The serum thromboxane levels in mice (n = 3) dosed with clopidogrel and prasugrel were decreased by 83."( Antagonism of P2Y₁₂ reduces physiological thromboxane levels.
Bhavaraju, K; Gartner, TK; Georgakis, A; Jin, J; Kunapuli, SP; Nurden, A; Nurden, P; Tomiyama, Y, 2010
)
0.36
" The present article reviews data on the clinical impact of enhanced P2Y12 inhibition with either higher clopidogrel dosing or new oral antiplatelet agents, including prasugrel and ticagrelor, in the setting of STEMI, focusing on results in the setting of primary PCI."( Clinical impact of enhanced inhibition of P2Y12-mediated platelet aggregation in patients with ST-segment elevation myocardial infarction undergoing percutaneous coronary intervention.
Capranzano, P; Dangas, G; Mehran, R; Stone, GW; Tamburino, C, 2010
)
0.36
"The precise risk/benefit of thienopyridine pretreatment and the optimal dosage and timing of a thienopyridine loading dose (LD) for patients presenting with non-ST-segment elevation (NSTE) acute coronary syndromes are still being debated."( A comparison of prasugrel at the time of percutaneous coronary intervention or as pretreatment at the time of diagnosis in patients with non-ST-segment elevation myocardial infarction: design and rationale for the ACCOAST study.
Bolognese, L; Dudek, D; Goedicke, J; Goldstein, P; Hamm, C; Luo, J; Miller, DL; Montalescot, G; Tanguay, JF; ten Berg, J; Widimsky, P, 2011
)
0.37
" Further study is required to determine optimal dosing and proper patient selection with prasugrel treatment."( Emerging antiplatelet therapies in percutaneous coronary intervention: a focus on prasugrel.
Martin, MT; Nutescu, EA; Spinler, SA, 2011
)
0.37
"In HD patients exhibiting HTPR following standard clopidogrel treatment, prasugrel 10 mg day(-1) is significantly more efficient than doubling the clopidogrel dosage in achieving adequate platelet inhibition."( Antiplatelet effects of prasugrel vs. double clopidogrel in patients on hemodialysis and with high on-treatment platelet reactivity.
Alexopoulos, D; Davlouros, P; Fourtounas, C; Goumenos, D; Kassimis, G; Komninakis, D; Panagiotou, A; Xanthopoulou, I, 2011
)
0.37
" Whether this is worth both the risk of non-compliance with twice-a-day dosing in real-life patients lacking the same motivation as their trial-volunteer counterparts, and the 2000-fold difference in incremental cost, is the remaining matter for debate."( Quantitative comparison of clopidogrel 600 mg, prasugrel and ticagrelor, against clopidogrel 300 mg on major adverse cardiovascular events and bleeding in coronary stenting: synthesis of CURRENT-OASIS-7, TRITON-TIMI-38 and PLATO.
Davies, JE; Francis, DP; Nijjer, SS, 2012
)
0.38
" In the management of bleeding ulcer patients with high-risk stigmata of recent hemorrhage, resuming antiplatelet agents at 3-5 days after the last dosing is a reasonable strategy."( New look at antiplatelet agent-related peptic ulcer: an update of prevention and treatment.
Hsu, PI, 2012
)
0.38
"The purpose of this study is to assess the pharmacodynamic effects of different prasugrel dosing regimens in patients on maintenance prasugrel therapy."( Pharmacodynamic effects of prasugrel dosing regimens in patients on maintenance prasugrel therapy: results of a prospective randomized study.
Angiolillo, DJ; Bass, TA; Box, LC; Charlton, RK; Desai, B; Ferreiro, JL; Guzman, LA; Kodali, M; Seecheran, N; Tello-Montoliu, A; Tomasello, SD; Ueno, M; Zenni, MM, 2012
)
0.38
"There are a growing number of patients on chronic prasugrel therapy regimens, leading to questions about the dosing regimen of prasugrel to administer if percutaneous coronary intervention is required."( Pharmacodynamic effects of prasugrel dosing regimens in patients on maintenance prasugrel therapy: results of a prospective randomized study.
Angiolillo, DJ; Bass, TA; Box, LC; Charlton, RK; Desai, B; Ferreiro, JL; Guzman, LA; Kodali, M; Seecheran, N; Tello-Montoliu, A; Tomasello, SD; Ueno, M; Zenni, MM, 2012
)
0.38
"For patients on maintenance prasugrel therapy, a 60 mg dosing strategy is associated with faster and higher platelet inhibition compared with lower doses, as assessed by P2Y(12) specific assays."( Pharmacodynamic effects of prasugrel dosing regimens in patients on maintenance prasugrel therapy: results of a prospective randomized study.
Angiolillo, DJ; Bass, TA; Box, LC; Charlton, RK; Desai, B; Ferreiro, JL; Guzman, LA; Kodali, M; Seecheran, N; Tello-Montoliu, A; Tomasello, SD; Ueno, M; Zenni, MM, 2012
)
0.38
" However, the reversible binding of ticagrelor to the P2Y(12) receptor requires a twice-daily dosing regimen."( Comparative pharmacokinetics and pharmacodynamics of platelet adenosine diphosphate receptor antagonists and their clinical implications.
Ferro, A; Floyd, CN; Passacquale, G, 2012
)
0.38
" The comparator was standard dosage of clopidogrel."( Comparing newer oral anti-platelets prasugrel and ticagrelor in reduction of ischemic events-evidence from a network meta-analysis.
Chatterjee, S; Frankel, R; Ghose, A; Guha, G; Mukherjee, D; Sharma, A, 2013
)
0.39
" Although further guidance will be provided by a recently completed phase 3 study, these preliminary data suggest that dosing strategies approved for white patients with acute coronary syndromes are applicable to Asian patients."( Pharmacokinetic and pharmacodynamic effects of prasugrel in healthy Korean males.
Choi, HC; Gu, N; Kawakatsu, E; Kelly, RP; Park, KW; Payne, C; Pinton, P; Small, DS; Yu, KS, 2013
)
0.39
" However, the increased risk of bleeding has been associated with a greater antiplatelet effect and dosing profile; this is especially the case in those patients who are at a higher risk of bleeding complications."( The discovery and development of prasugrel.
Shan, J; Sun, H, 2013
)
0.39
"Different aspirin dosing regimens have been suggested to impact outcomes when used in combination with adenosine diphosphate (ADP) P2Y12 receptor antagonists."( Impact of aspirin dose on adenosine diphosphate-mediated platelet activities. Results of an in vitro pilot investigation.
Angiolillo, DJ; Bass, TA; Darlington, A; Desai, B; Franchi, F; Guzman, LA; Muñiz-Lozano, A; Patel, R; Rollini, F; Tello-Montoliu, A; Thano, E; Wilson, RE, 2013
)
0.39
" In contrast, on an oral dosage basis (mg/kg), prasugrel showed more potent platelet inhibition compared to ticagrelor on ex vivo aggregation and VASP phosphorylation assays in monkeys."( Comparison of antiplatelet effects of prasugrel and ticagrelor in cynomolgus monkeys by an ELISA-based VASP phosphorylation assay and platelet aggregation.
Jakubowski, JA; Mizuno, M; Ohno, K; Sugidachi, A; Tomizawa, A, 2013
)
0.39
" Dans certaines situations de risque par contre, une adaption du dosage est conseillée pour minimiser les effets secondaires négatifs: Chez les patients de plus de 75 ans, et/ou d'un poids corporel de moins de 60 kg, une réduction du dosage de prasugrel est conseillée en raison d'un risque élevé d'hémorragie."( [Thrombocyte aggregation inhibitors: what are the risks?].
Curkovic, I; Egbring, M; Kullak-Ublick, GA, 2013
)
0.39
" In this situation, a number of alternatives to conventional dosing of clopidogrel have been investigated, including increasing the dosage of clopidogrel, switching from clopidogrel to either prasugrel or ticagrelor, or adding cilostazol to clopidogrel therapy."( Treatment options for patients with poor clopidogrel response.
Nawarskas, JJ; Roberts, DI,
)
0.13
"Optimal aspirin dosing after acute coronary syndromes remains uncertain."( Discharge aspirin dose and clinical outcomes in patients with acute coronary syndromes treated with prasugrel versus clopidogrel: an analysis from the TRITON-TIMI 38 study (trial to assess improvement in therapeutic outcomes by optimizing platelet inhibit
Antman, EM; Braunwald, E; Cannon, CP; Kohli, P; Murphy, SA; Udell, JA; Wiviott, SD, 2014
)
0.4
" In conclusion, in non-diabetic obese patients with CAD, standard prasugrel dosing achieved more potent PD effects than high-dose clopidogrel in the acute phase of treatment, but this was not sustained during maintenance phase treatment."( Pharmacodynamic effects of standard dose prasugrel versus high dose clopidogrel in non-diabetic obese patients with coronary artery disease.
Angiolillo, DJ; Bass, TA; Darlington, A; Desai, B; Ferreiro, JL; Guzman, LA; Patel, R; Rollini, F; Tello-Montoliu, A; Ueno, M, 2014
)
0.4
"Clinicians may need to switch between more potent P2Y12 inhibitors because of adverse effects or switch to the use of a once-daily dosing regimen due to compliance issues."( Pharmacodynamic evaluation of switching from ticagrelor to prasugrel in patients with stable coronary artery disease: Results of the SWAP-2 Study (Switching Anti Platelet-2).
Angiolillo, DJ; Curzen, N; Effron, MB; Gurbel, P; Jakubowski, JA; Li, W; Lipkin, F; Trenk, D; Vaitkus, P; Zettler, M, 2014
)
0.4
" The PRASugrel For Japanese PatIenTs with Coronary Artery Diseases Undergoing Elective PCI (PRASFIT-Elective) study investigated the efficacy and safety of different prasugrel dosing regimens in Japanese patients undergoing elective PCI."( Prasugrel, a third-generation P2Y12 receptor antagonist, in patients with coronary artery disease undergoing elective percutaneous coronary intervention.
Ikeda, Y; Isshiki, T; Kimura, T; Kitagawa, K; Miyazaki, S; Nakamura, M; Nanto, S; Nishikawa, M; Ogawa, H; Saito, S; Takayama, M; Yokoi, H, 2014
)
0.4
"These results support the risk-benefit profile of an adjusted dosing regimen of prasugrel in Japanese patients undergoing PCI."( Prasugrel, a third-generation P2Y12 receptor antagonist, in patients with coronary artery disease undergoing elective percutaneous coronary intervention.
Ikeda, Y; Isshiki, T; Kimura, T; Kitagawa, K; Miyazaki, S; Nakamura, M; Nanto, S; Nishikawa, M; Ogawa, H; Saito, S; Takayama, M; Yokoi, H, 2014
)
0.4
"12 mg/kg) based on VN pharmacodynamic measurements at the start of 2 dosing periods, each 14±4 days."( Prasugrel in children with sickle cell disease: pharmacokinetic and pharmacodynamic data from an open-label, adaptive-design, dose-ranging study.
Heath, LE; Heeney, MM; Heiselman, D; Jakubowski, JA; Kanter, J; Moser, BA; Quinn, CT; Rana, SR; Redding-Lallinger, R; Small, DS; Styles, L; Winters, KJ; Zhou, C, 2015
)
0.42
"The prasugrel dosing regimen of 20/3."( Randomized, Double-Blind, Dose-Finding, Phase II Study of Prasugrel in Japanese Patients Undergoing Elective Percutaneous Coronary Intervention.
Ikeda, Y; Isshiki, T; Kimura, T; Ogawa, H; Yamaguchi, T; Yokoi, H, 2015
)
0.42
" Ex vivo platelet aggregation was analyzed on Day 1 (1 and 4h after administration), Day 4 (4h), and Day 7 (4h) under three different prasugrel dosing regimens: LD0/MD1 (1mg/kg/day), LD0/MD3 (3mg/kg/day), and LD10/MD1 (10mg/kg loading dose and 1mg/kg/day maintenance dose)."( Characterization of platelet aggregation responses in microminipigs: Comparison with miniature pigs and the influence of dual antiplatelet administration of aspirin plus prasugrel.
Jakubowski, JA; Mizuno, M; Ohno, K; Sugidachi, A; Tomizawa, A, 2015
)
0.42
" Point-of-care genetic testing for CYP2C19*2, ABCB1 TT and CYP2C19*17 was performed with carriers of either the CYP2C19*2 allele or ABCB1 TT genotype randomly assigned to a strategy of prasugrel 10 mg daily or an augmented dosing strategy of clopidogrel (150 mg daily for 6 days then 75 mg daily)."( A prospective randomized evaluation of a pharmacogenomic approach to antiplatelet therapy among patients with ST-elevation myocardial infarction: the RAPID STEMI study.
Bernick, J; Dick, AJ; Froeschl, M; Glover, C; Gollob, MH; Hibbert, B; Labinaz, M; Le May, MR; Marquis, JF; McPherson, R; Roberts, JD; So, DY; Tran, L; Wells, GA, 2016
)
0.43
" Study results suggest that there is no benefit to dosing clopidogrel twice daily when compared to either prasugrel or once daily clopidogrel dosing."( Comparing prasugrel to twice daily clopidogrel post percutaneous coronary intervention in a Veterans Affairs population.
Khatri, S; Pierce, T, 2015
)
0.42
" Platelet activation markers were measured by flow cytometry on unstimulated or stimulated (adenosine diphosphate (ADP) 20 μM) platelets, before and after each dosing period."( Prasugrel 5 mg inhibits platelet P-selectin and GPIIb-IIIa expression in very elderly and non elderly: results from the GENERATIONS trial, a pharmacodynamic study in stable CAD patients.
Borna, C; Brown, P; Erlinge, D; Gidlöf, O; Jakubowski, JA; Lood, C; Truedsson, L; Wagner, H; Winters, K; Zhou, C, 2016
)
0.43
" Although there was no effect on the patency rate before R-138727 dosing (P=0."( The active metabolite of prasugrel, R-138727, improves cerebral blood flow and reduces cerebral infarction and neurologic deficits in a non-human primate model of acute ischaemic stroke.
Jakubowski, JA; Mizuno, M; Ohno, K; Sugidachi, A; Tomizawa, A, 2016
)
0.43
"5-10 mg), the pharmacokinetic parameters on Day 1 and Day 7 were similar, and no accumulation attributable to multiple dosing was observed."( Pharmacokinetics and pharmacodynamics of prasugrel in healthy Japanese subjects.
Ikeda, Y; Kondo, K; Umemura, K, 2016
)
0.43
" The time interval from ADP receptor blocker loading dosing to the blood sampling was similar in T2D and ND patients in both examinations."( The Impact of Type 2 Diabetes on the Efficacy of ADP Receptor Blockers in Patients with Acute ST Elevation Myocardial Infarction: A Pilot Prospective Study.
Bolek, T; Fedor, M; Fedorová, J; Galajda, P; Kovář, F; Kubisz, P; Mokáň, M; Samoš, M; Stančiaková, L; Staško, J, 2016
)
0.43
"The dosing regimen of prasugrel adjusted for Japanese patients was compared with that of clopidogrel by analyzing the pharmacokinetics and pharmacodynamics in 40 healthy Japanese subjects in a randomized, single-blind crossover study."( The Pharmacokinetics and Pharmacodynamics of Prasugrel and Clopidogrel in Healthy Japanese Volunteers.
Iwaki, T; Umemura, K, 2016
)
0.43
"The optimal dosing of novel oral P2Y12 receptor platelet inhibitors such as prasugrel or ticagrelor is unclear and especially challenging in East Asians."( A Prospective, Randomized, Open-Label, Blinded, Endpoint Study Exploring Platelet Response to Half-Dose Prasugrel and Ticagrelor in Patients with the Acute Coronary Syndrome: HOPE-TAILOR Study.
Bang, J; Jin, C; Kim, MH; Serebruany, V,
)
0.13
"Long-term evidence supports a clustering of cardiovascular events in the early morning and smaller mechanistic studies in aspirin-treated patients have shown increased platelet reactivity at the end of the dosing interval."( Diurnal Variability of On-Treatment Platelet Reactivity in Clopidogrel versus Prasugrel Treated Acute Coronary Syndrome Patients: A Pre-Specified TROPICAL-ACS Sub-Study.
Aradi, D; Dézsi, DA; Freynhofer, MK; Geisler, T; Gross, L; Haller, PM; Hein-Rothweiler, R; Huber, K; Huczek, Z; Massberg, S; Orban, M; Sibbing, D; Toth-Gayor, GG; Trenk, D, 2019
)
0.51
" Oral dosing with vehicle, ticagrelor (300mg/kg/d), aspirin (20mg/kg/d), their combination or prasugrel (15mg/kg/d) started 7days after infarction."( Ticagrelor Improves Remodeling, Reduces Apoptosis, Inflammation and Fibrosis and Increases the Number of Progenitor Stem Cells After Myocardial Infarction in a Rat Model of Ischemia Reperfusion.
Birnbaum, Y; Chen, H; Nylander, S; Sampaio, LC; Tran, D; Ye, Y, 2019
)
0.51
" To improve adherence to DAPT, the FDC (fixed dose combination) of Acetylsalicylic acid (ASA) and clopidogrel was developed into a single pill instead of two separate pills thus facilitating the dosage and administration of the therapy and increasing compliance."( Adherence and persistence analysis in patients treated with double antiplatelet therapy (DAPT) at two years in real life.
Costantini, A; Romagnoli, A; Santoleri, F, 2021
)
0.62
" This modified dosage regimen has been established in studies conducted in Japan; however, the efficacy and safety of switching from clopidogrel to prasugrel DAPT among Taiwanese patients remain to be explored."( Prasugrel switching from clopidogrel after percutaneous coronary intervention for acute coronary syndrome in Taiwanese patients: an analysis of safety and efficacy.
Cheng, LC; Chu, PH; Huang, CL; Kuo, FY; Lan, WR; Lee, CH; Lee, WL; Lin, WS; Liu, PY; Lo, PH; Lu, TM; Nikolajsen, C; Rafael, V; Su, CH; Tsukiyama, S; Wang, YC; Yang, WC; Yin, WH, 2022
)
0.72
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Protein Targets (7)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
GLI family zinc finger 3Homo sapiens (human)Potency11.67220.000714.592883.7951AID1259369; AID1259392
AR proteinHomo sapiens (human)Potency10.22220.000221.22318,912.5098AID1259243; AID1259247
glucocorticoid receptor [Homo sapiens]Homo sapiens (human)Potency26.83250.000214.376460.0339AID720692
retinoic acid nuclear receptor alpha variant 1Homo sapiens (human)Potency25.49050.003041.611522,387.1992AID1159552; AID1159555
retinoid X nuclear receptor alphaHomo sapiens (human)Potency9.52050.000817.505159.3239AID1159527
pregnane X nuclear receptorHomo sapiens (human)Potency26.60320.005428.02631,258.9301AID1346982
Histone H2A.xCricetulus griseus (Chinese hamster)Potency1.38650.039147.5451146.8240AID1224845
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Bioassays (6)

Assay IDTitleYearJournalArticle
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (1,741)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's0 (0.00)18.2507
2000's195 (11.20)29.6817
2010's1148 (65.94)24.3611
2020's398 (22.86)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 37.29

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index37.29 (24.57)
Research Supply Index7.70 (2.92)
Research Growth Index6.91 (4.65)
Search Engine Demand Index52.90 (26.88)
Search Engine Supply Index1.97 (0.95)

This Compound (37.29)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials396 (21.96%)5.53%
Reviews397 (22.02%)6.00%
Case Studies69 (3.83%)4.05%
Observational112 (6.21%)0.25%
Other829 (45.98%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (170)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
A Pharmacodynamic Comparison of Prasugrel (LY640315) Versus Clopidogrel in Subjects With Acute Coronary Syndrome Who Are Receiving Clopidogrel [NCT00356135]Phase 2139 participants (Actual)Interventional2006-07-31Completed
Phase III Study, Multivessel Percutaneous Treatment During Myocardial Infarction [NCT01160900]Phase 3180 participants (Anticipated)Interventional2010-07-31Active, not recruiting
ReAssessment of Anti-Platelet Therapy Using an InDividualized Strategy Based on GENetic Evaluation (The RAPID GENE Study) [NCT01184300]Phase 2/Phase 3200 participants (Actual)Interventional2010-08-31Completed
Comparison of Multiple Oral and/or Intravenous Anti-platelet Strategies in Patients With ST-segment Elevation Myocardial Infarction Undergoing Primary PCI [NCT01336348]Phase 3100 participants (Anticipated)Interventional2010-04-30Completed
[NCT01346800]Phase 110 participants (Actual)Interventional2011-02-28Completed
The Role of the P2Y12 Receptor in Tissue Factor Induced Coagulation [NCT01099566]Phase 420 participants (Actual)Interventional2009-11-30Completed
Phase 3 Study of Prasugrel vs High Dose (150 mg) Clopidogrel in Clopidogrel Resistant Patients Post Coronary Angioplasty. [NCT01109784]Phase 370 participants (Anticipated)Interventional2010-04-30Completed
Bivalirudin Plus Prasugrel vs Abciximab Plus Clopidogrel. Optimizing Ischemic Protection and Bleeding Risk in Patients With ST Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention [NCT01158846]Phase 4800 participants (Anticipated)Interventional2010-08-31Not yet recruiting
Prasugrel Versus High Dose Clopidogrel in Patients With Stable Coronary Artery Disease and High Platelet Reactivity While on Chronic Clopidogrel Treatment [NCT01304472]Phase 325 participants (Anticipated)Interventional2011-02-28Completed
Low-dose Prasgurel Versus Clopidogrel on the Dual Antiplatelet Regimen for Intracranial Stenting or Flow Diverter Treatment for Unruptured Cerebral Aneurysms: a Multi-center Randomized Controlled Trial [NCT05359224]Phase 4406 participants (Anticipated)Interventional2022-06-13Recruiting
Prasugrel in Comparison to High Clopidogrel Dose for Inhibition of Platelet Reactivity as Assessed With a Point-of-Care Platelet Function Assay in Patients Undergoing Chronic Hemodialysis Presenting Resistance to the Usual Clopidogrel Dose [NCT01155765]Phase 370 participants (Anticipated)Interventional2010-05-31Completed
Prasugrel in Comparison to Clopidogrel for Inhibition of Platelet Reactivity in Patients With ST-elevation Myocardial Infarction (STEMI), Undergoing Primary Percutaneous Coronary Intervention (PCI)and Presenting With High Platelet Reactivity, as Assessed [NCT01338909]Phase 335 participants (Anticipated)Interventional2011-04-30Completed
Reducing Micro Vascular Dysfunction In Revascularized ST-elevation Myocardial Infarction Patients by Off-target Properties of Ticagrelor [NCT02422888]Phase 4110 participants (Actual)Interventional2015-05-31Active, not recruiting
Time to Thrombocytic Inhibition After Supine and Upright Ingestion of Efient [NCT01365741]20 participants (Actual)Interventional2011-02-28Completed
Ticagrelor in Comparison to Prasugrel for Inhibition of Platelet Reactivity, in Patients With Acute Coronary Syndrome (ACS) Presenting Resistance to the Usual Clopidogrel Dose After PCI [NCT01360437]Phase 344 participants (Actual)Interventional2011-05-31Completed
Pharmacodynamic Comparison of Prasugrel Versus Ticagrelor in Patients With CYP2C19 Loss-of-function Genotype: a Validation Study in Patients With Stable Coronary Artery Disease [NCT03489863]Phase 414 participants (Actual)Interventional2018-05-30Completed
Switching From Ticagrelor to Prasugrel in Patients With Acute Coronary Syndrome-a Stepped Wedge Cluster Randomized Evaluation in the SWEDEHEART-registry [NCT05183178]Phase 416,000 participants (Anticipated)Interventional2022-02-01Recruiting
The Effect of Prasugrel on Bronchial Hyperreactivity and on Markers of Inflammation in Patients With Chronic Asthma: a Pilot Randomised Controlled Trial (PRINA Study) [NCT01305369]Phase 426 participants (Actual)Interventional2011-03-31Completed
Tailored Versus Coventional AntiPlaTelet Strategy Intended After OPTIMIZEd Drug [NCT05418556]Phase 43,944 participants (Anticipated)Interventional2022-10-21Recruiting
Aspirin and a Potent P2Y12 Inhibitor Versus Aspirin and Clopidogrel Therapy in Patients Undergoing Elective Percutaneous Coronary Intervention for Complex Lesion Treatment (SMART-ATTEMPT) [NCT04014803]Phase 43,500 participants (Anticipated)Interventional2020-01-13Recruiting
SWITCH 600/60: The Effect of Reloading Prasugrel in a Patient Who Has Already Received a Loading Dose (LD) of Clopidogrel [NCT01365221]Phase 477 participants (Actual)Interventional2010-10-31Completed
Double the Dose of Clopidogrel or Switch to Prasugrel to Antagonize Proton Pump Inhibitor Interaction. A Prospective, Mono-center, Placebo- and Active Treatment-controlled, Randomized, Cross Over Study. [NCT01175200]82 participants (Actual)Interventional2010-09-30Completed
Prospective, Randomized Trial of Ticagrelor Versus Prasugrel in Patients With Acute Coronary Syndrome - Intracoronary Stenting and Antithrombotic Regimen: Rapid Early Action for Coronary Treatment (ISAR-REACT) 5 [NCT01944800]Phase 44,018 participants (Actual)Interventional2013-09-15Completed
COMPARison of Pre-hospital CRUSHed vs. Uncrushed Prasugrel Tablets in Patients With STEMI Undergoing Primary Percutaneous Coronary Interventions [NCT03296540]Phase 4729 participants (Actual)Interventional2017-11-28Completed
"High on Treatment Platelet Reactivity in the Intensive Care Unit" [NCT02285751]Phase 2200 participants (Anticipated)Interventional2012-11-30Recruiting
[NCT02032303]Phase 488 participants (Anticipated)Interventional2014-02-28Not yet recruiting
Evaluation of the Safety and Efficacy of an Edoxaban-based Compared to a Vitamin K Antagonist-based Antithrombotic Regimen in Subjects With Atrial Fibrillation Following Successful Percutaneous Coronary Intervention (PCI) With Stent Placement. [NCT02866175]Phase 31,506 participants (Actual)Interventional2017-02-24Completed
An Open Label, Single Dose Study to Characterize the Pharmacokinetics and Pharmacodynamics of Prasugrel in Healthy Male Adult Subjects [NCT02075268]Phase 18 participants (Anticipated)Interventional2014-01-31Recruiting
The Laboratory AntiPlatelet Efficacy and Clinical Outcome Registry [NCT02264912]2,016 participants (Actual)Observational [Patient Registry]2008-07-31Completed
Differential Effect of Ticagrelor vs Prasugrel or Clopidogrel Loading on Fractional Flow Reserve [NCT02108808]Phase 476 participants (Actual)Interventional2014-04-30Completed
Randomized Evaluation of Short-term DUal Anti Platelet Therapy in Patients With Acute Coronary Syndrome Treated With the COMBO Dual-therapy stEnt [NCT02118870]Phase 41,500 participants (Actual)Interventional2014-06-10Completed
PANDDA Study: Pharmacokinetics of Antiplatelet Drugs in Diabetic pAtients [NCT02302508]Phase 40 participants (Actual)Interventional2019-09-01Withdrawn(stopped due to Funding)
ASET Clinical Investigational Plan Acetyl Salicylic Elimination Trial: The ASET Pilot Study [NCT03469856]200 participants (Anticipated)Interventional2018-02-22Recruiting
ST-segment Elevation Myocardial infArction Treated With a Polymer-free Sirolimus-based nanocarrieR Eluting Stent and a P2Y12 Inhibitor-based Aspirin-free Single Antiplatelet Strategy Versus Conventional Dual AntiPlatelet Therapy [NCT05785897]350 participants (Anticipated)Interventional2024-06-01Not yet recruiting
A Prospective Randomized Double Blind Study to Evaluate the Effect of Ticagrelor on Endothelial Function [NCT02261922]Phase 420 participants (Anticipated)Interventional2014-10-31Recruiting
Effect of Lower Loading Dose of Prasugrel Compared With Conventional Loading Dose of Clopidogrel and Prasugrel in Korean Coronary Artery Disease Patients Undergoing Coronary Angiography [NCT02070159]Phase 343 participants (Actual)Interventional2011-12-31Completed
GORE® CARDIOFORM Septal Occluder Migraine Clinical Study: A Study to Evaluate the Safety and Efficacy of Transcatheter Closure of Patent Foramen Ovale for Relief of Migraine Headaches [NCT04100135]150 participants (Anticipated)Interventional2021-02-05Recruiting
Ticagrelor or Prasugrel Versus Clopidogrel in Elderly Patients With an Acute Coronary Syndrome and a High Bleeding Risk: Optimization of Antiplatelet Treatment in High-risk Elderly [NCT02317198]Phase 41,011 participants (Actual)Interventional2013-06-30Active, not recruiting
PPD Trial Pilot Study: Plavix, Prasugrel and Drug Eluting Stents [NCT01103843]1,000 participants (Anticipated)Interventional2010-04-30Recruiting
Thrombocytes And IndividuaLization of ORal Antiplatelet Treatment After Percutaneous Coronary Intervention [NCT01135667]Phase 4106 participants (Actual)Interventional2010-09-30Completed
A Randomized, Pharmacodynamic Comparison of Low Dose Ticagrelor (60mg Bid) to Low Dose Prasugrel (5mg od) in Patients With Prior Myocardial Infarction [NCT03387826]Phase 420 participants (Actual)Interventional2018-01-11Completed
Phase IV, Non-comparative, Open Label, Multicenter, 28-Week Switching Study of Prasugrel Maintenance Dose From Clopidogrel in Patients With Acute Coronary Syndrome (ACS) Who Underwent a Percutaneous Coronary Intervention (PCI) in Taiwan [NCT03672097]Phase 4204 participants (Actual)Interventional2018-10-16Completed
Evaluating the Benefit of Additional Platelet Inhibition in Acute Coronary Syndrome Patients With High Platelet Reactivity Undergoing PCI [NCT01339026]Phase 444 participants (Actual)Interventional2012-02-29Terminated(stopped due to Change in guidelines favouring newer antiplatelet drugs in ACS)
A Prospective, Randomized, Multi-Center, Double-Blind Trial to Assess the Effectiveness and Safety of Different Durations of Dual Anti-Platelet Therapy (DAPT) in Subjects Undergoing Percutaneous Coronary Intervention With the CYPHER® Sirolimus-eluting Cor [NCT00954707]Phase 42,509 participants (Actual)Interventional2009-08-31Active, not recruiting
Harmonizing Optimal Strategy for Treatment of Coronary Artery Diseases Trial - Comparison of REDUCTION of PrasugrEl Dose & POLYmer TECHnology in ACS Patients (HOST REDUCE POLYTECH RCT Trial) Comparison of the Efficacy and Safety of Biostable Polymer DES ( [NCT02193971]Phase 43,384 participants (Anticipated)Interventional2014-07-31Active, not recruiting
Clopidogrel Monotherapy in High Bleeding Risk Patients Undergoing Percutaneous Coronary Interventions: A Safety Assessment, Pilot Study to Reduce Post-Discharge Bleeding [NCT05223335]Phase 4121 participants (Actual)Interventional2022-03-29Completed
Effects of Combinated Administration of Lysine Acetylsalicylate Versus Prasugrel and Aspirin on Platelet Aggregation in Healthy Volunteers [NCT02243137]Phase 130 participants (Actual)Interventional2013-05-31Completed
XIENCE V® Everolimus Eluting Coronary Stent System USA Post- Approval Study (XIENCE V® USA DAPT Cohort) (XVU-AV DAPT) [NCT01106534]Phase 4870 participants (Actual)Interventional2009-08-31Completed
Randomized Trial of Prasugrel Plus Bivalirudin vs. Clopidogrel Plus Heparin in Patients With Acute STEMI [NCT00976092]Phase 4548 participants (Actual)Interventional2009-09-30Active, not recruiting
A Comparison of CS-747 and Clopidogrel in Acute Coronary Syndrome Subjects Who Are to Undergo Percutaneous Coronary Intervention [NCT00097591]Phase 313,619 participants (Actual)Interventional2004-11-30Completed
A Double-Blind, Randomized, Multicenter, Dose-Ranging Trial of CS-747 Compared With Clopidogrel in Subjects Undergoing Percutaneous Coronary Intervention [NCT00059215]Phase 2905 participants (Actual)Interventional2003-04-30Completed
ETAMI-Study: Early Thienopyridine Treatment to Improve Primary Percutaneous Coronary Intervention in Patients With Acute Myocardial Infarction [NCT01327534]Phase 363 participants (Actual)Interventional2011-05-31Completed
Comparison of Prasugrel and Ticagrelor in the Treatment of Acute Myocardial Infarction [NCT02808767]Phase 41,226 participants (Actual)Interventional2013-01-31Completed
Double Randomization of a Monitoring Adjusted Antiplatelet Treatment Versus a Common Antiplatelet Treatment for DES Implantation, and a Interruption Versus Continuation of Double Antiplatelet Therapy, One Year After Stenting [NCT00827411]Phase 42,500 participants (Actual)Interventional2009-01-31Completed
Prasugrel Versus Adjusted High-dose Clopidogrel to TREAT High On-clopidogrel Platelet Reactivity in Acute Coronary Syndrome Patients After PCI [NCT01493999]Phase 4147 participants (Actual)Interventional2011-09-30Completed
Hunting for the Off-Target Properties of Ticagrelor on Endothelial Function and Other Circulating Biomarkers in Humans [NCT02587260]Phase 454 participants (Actual)Interventional2015-12-17Completed
A Comparison of Platelet Inhibition Following Prasugrel or Clopidogrel Administration in Asian Acute Coronary Syndrome Subjects Who Are to Undergo Percutaneous Coronary Intervention [NCT00830960]Phase 3720 participants (Actual)Interventional2009-02-28Completed
A Pharmacokinetic and Pharmacodynamic Assessment of Prasugrel in Healthy Adults and Adults With Sickle Cell Disease [NCT01178099]Phase 126 participants (Actual)Interventional2010-07-31Completed
A Double-Blind, Randomized, Multicenter Study of Prasugrel Compared to Placebo in Adult Patients With Sickle Cell Disease [NCT01167023]Phase 262 participants (Actual)Interventional2010-07-31Completed
Atrial Fibrillation and Ischemic Events With Rivaroxaban in Patients With Stable Coronary Artery Disease Study (AFIRE Study) [NCT02642419]Phase 42,200 participants (Anticipated)Interventional2015-01-31Recruiting
A Pharmacokinetic and Pharmacodynamic Comparison of Prasugrel and Clopidogrel in Very Elderly Versus Non-Elderly Aspirin-Treated Subjects With Stable Coronary Artery Disease [NCT01107912]Phase 1155 participants (Actual)Interventional2010-03-31Completed
A Comparison of Prasugrel and Clopidogrel in Acute Coronary Syndrome Subjects With Unstable Angina/Non-ST-Elevation Myocardial Infarction Who Are Medically Managed [NCT00699998]Phase 39,326 participants (Actual)Interventional2008-06-30Completed
Intensified Loading With Prasugrel Versus Standard Loading With Clopidogrel in Invasive-treated Patients With Biomarker-Negative Angina Pectoris [NCT02548611]Phase 4795 participants (Actual)Interventional2015-09-30Terminated(stopped due to Due to low recruitment)
Recovery of Platelet Function After a Loading Dose of Prasugrel or Clopidogrel in Aspirin-Treated Subjects Presenting With Symptoms of Acute Coronary Syndromes [NCT01107899]Phase 129 participants (Actual)Interventional2009-10-31Terminated(stopped due to Terminated due to Enrollment futility)
Recovery of Platelet Function Following Discontinuation of Prasugrel or Clopidogrel Maintenance Dosing in Aspirin-Treated Subjects With Stable Coronary Disease [NCT01014624]Phase 456 participants (Actual)Interventional2010-02-28Completed
COMPARE STEMI ONE- Comparison Of Reduced DAPT Followed by P2Y12 Inhibitor Monotherapy With Prasugrel vs stAndard Regimen in STEMI Patients Treated With OCT-guided vs aNgio-guided completE Revascularization [NCT05491200]Phase 41,608 participants (Anticipated)Interventional2022-07-22Recruiting
Harmonizing Optimal Strategy for Treatment of Coronary Artery Stenosis - Coronary Intervention With Next Generation Drug-Eluting Stent Platforms and Abbreviated Dual Antiplatelet Therapy (HOST-IDEA) Trial [NCT02601157]Phase 42,173 participants (Actual)Interventional2016-01-18Completed
A Pharmacodynamic Comparison of Prasugrel (LY640315) Versus High Dose Clopidogrel in Subjects With Type 2 Diabetes Mellitus and Coronary Artery Disease. [NCT00642174]Phase 235 participants (Actual)Interventional2008-04-30Completed
Optical Coherence Tomography-Guided PCI With Single-Antiplatelet Therapy [NCT04766437]Phase 275 participants (Actual)Interventional2021-02-19Completed
Reassessment of Anti-Platelet Therapy Using InDividualized Strategies - Modifying Acute CoroNary Syndrome Algorithms Based on Genetic and Demographic Evaluation: The RAPID-MANAGE Study [NCT02044146]Phase 2/Phase 3120 participants (Actual)Interventional2014-09-30Completed
An Open-label, Randomized, Prospective Study Exploring Half Dose of Prasugrel and Ticagrelor in Platelet Response After Acute Coronary Syndromes [NCT02944123]Phase 3120 participants (Actual)Interventional2016-09-30Completed
A Randomized Double-Blind Cross-Over Study Comparing the Pharmacodynamic (PD)Response in Subjects With ACS Receiving 14 Days 10-mg Maintenance Dose (MD) Prasugrel vs 14 Days 150-mg MD Clopidogrel After Using a 900-mg Loading Dose (LD) of Clopidogrel to Re [NCT00385944]Phase 256 participants (Actual)Interventional2007-03-31Completed
Protocol H7T-MC-TABL(a) PRasugrel IN Comparison to Clopidogrel for Inhibition of PLatelet Activation and AggrEgation (PRINCIPLE) - TIMI 44 [NCT00357968]Phase 2201 participants (Actual)Interventional2006-08-31Completed
A Single Dose, Open-label, One Sequence, 2-period, Crossover Study to Characterize the Pharmacokinetics and Pharmacodynamics of Ticagrelor and Prasugrel in Healthy Male Adult Subjects [NCT01876797]Phase 112 participants (Actual)Interventional2013-07-31Completed
Fixed-dose vs. Phenotype-based PrAsugrel Dose to MATCH Therapeutic Zone in Asians With Acute Coronary Syndrome [NCT01951001]Phase 4255 participants (Actual)Interventional2013-07-31Completed
Differential Effect of Ticagrelor Versus Prasugrel Maintenance Dose on Endothelial Function of Peripheral Vessels in Patients With Coronary Artery Disease [NCT01957540]Phase 422 participants (Actual)Interventional2014-06-30Completed
Platelet Function Guided Prasugrel Therapy in ACS Patients Undergoing PCI [NCT01959451]Phase 42,600 participants (Actual)Interventional2013-09-30Completed
The Influence of Smoking Status on the Pharmacokinetics and Pharmacodynamics of Prasugrel and Clopidogrel in Aspirin-treated Subjects With Stable Coronary Artery Disease [NCT01260584]Phase 4110 participants (Actual)Interventional2010-11-30Completed
Phase 3 Study Comparing the Efficacy and Safety of Prasugrel and Clopidogrel in Acute Coronary Syndrome Patients With CYP2C19 Polymorphism Who Undergo Percutaneous Coronary Intervention. [NCT01641510]Phase 370 participants (Actual)Interventional2013-10-31Completed
Τicagrelor Versus Prasugrel in Diabetic Patients: a Pharmacodynamic Study [NCT01642940]Phase 430 participants (Actual)Interventional2012-06-30Completed
Comparison of Prasugrel and Clopidogrel Reloading on High Platelet Reactivity in Clopidogrel-loaded Patients Undergoing Percutaneous Coronary Intervention [NCT01609647]Phase 376 participants (Actual)Interventional2012-09-30Completed
A Pharmacokinetic and Pharmacodynamic Comparison of Prasugrel and Clopidogrel in Low Body Weight Versus Higher Body Weight Aspirin-Treated Subjects With Stable Coronary Artery Disease [NCT01107925]Phase 172 participants (Actual)Interventional2010-03-31Completed
A Comparison of Prasugrel at the Time of Percutaneous Coronary Intervention (PCI) Or as Pretreatment At the Time of Diagnosis in Patients With Non-ST-Elevation Myocardial Infarction (NSTEMI): The ACCOAST Study [NCT01015287]Phase 34,033 participants (Actual)Interventional2009-12-31Completed
TAXUS Libertē Post Approval Study: A U.S. Post-Approval Study of the TAXUS® Liberté® Paclitaxel-Eluting Coronary Stent System [NCT00997503]4,199 participants (Actual)Observational2009-12-31Completed
A Prospective, Multi-center, Randomized, Double-blind Trial to Assess the Effectiveness and Safety of 12 Versus 30 Months of Dual Antiplatelet Therapy in Subjects Undergoing Percutaneous Coronary Intervention With Either Drug-eluting Stent or Bare Metal S [NCT00977938]Phase 425,682 participants (Actual)Interventional2009-10-31Completed
Prasugrel Or Ticagrelor De-escalation in Non-ST-elevation Acute Coronary Syndrome [NCT05779059]Phase 350 participants (Anticipated)Interventional2023-04-01Not yet recruiting
TRansferring From ClopIdogrel Loading Dose to Prasugrel Loading Dose in Acute Coronary Syndrome PatiEnTs: TRIPLET [NCT01115738]Phase 2282 participants (Actual)Interventional2010-05-31Completed
Effectiveness of Prasugrel Versus Clopidogrel in Subjects With High Platelet Reactivity on Clopidogrel Following Elective Percutaneous Coronary Intervention With Implantation of Drug-Eluting Stent [NCT00910299]Phase 2423 participants (Actual)Interventional2009-07-31Terminated(stopped due to Due to the low rate of primary endpoint events experienced in the study to date)
Bless Study (BLeeding Events and Maintenance DoSe of PraSugrel) [NCT01790854]Phase 4195 participants (Actual)Interventional2012-11-30Terminated(stopped due to Low events rate. Scarce economical resources)
PhaRmacodynamic Effects of Switching thErapy in paTients With High on Treatment Platelet Reactivity and Genotype Variation: High Clopidogrel Dose Versus Prasugrel RESET GENE Trial [NCT01465828]Phase 330 participants (Actual)Interventional2011-10-31Completed
Overcoming High On-Treatment Platelet Reactivity (HPR) During Prasugrel Therapy [NCT01869309]Phase 4400 participants (Anticipated)Interventional2014-01-31Recruiting
Pharmacokinetic/Pharmacodynamic Effects of add-on Antiplatelet Therapy With Parenteral Cangrelor as Compared to Standard Dual Antiplatelet Treatment in Patients With ST-elevation Myocardial Infarction Complicated by Out-of-hospital Cardiac Arrest and Trea [NCT03273075]Phase 460 participants (Anticipated)Interventional2017-09-30Recruiting
Effects of Ticagrelor Versus Prasugrel on Coronary Microcirculation in Patients Undergoing Elective Percutaneous Coronary Intervention: Results of the PROtecting MICROcirculation During Coronary Angioplasty (PROMICRO)-3 Randomised Study [NCT05643586]Phase 450 participants (Actual)Interventional2017-12-01Completed
Comparison of Circadian Variability of Platelet Inhibition in Patients With Myocardial Infarction Treated With Prasugrel and Ticagrelor [NCT03454841]73 participants (Actual)Observational2018-02-26Completed
[NCT03016611]Phase 4100 participants (Anticipated)Interventional2017-02-28Not yet recruiting
Platelet Function Evaluation in Patients With Acute Coronary Syndromes on Potent P2Y12 Inhibitor Monotherapy Versus Dual Antiplatelet Therapy With Aspirin and a Potent P2Y12 Inhibitor [NCT05767723]Phase 448 participants (Anticipated)Interventional2023-02-06Recruiting
Platelet Reactivity With Clopidogrel Versus Prasugrel in Patients With Systolic Heart Failure [NCT01765400]Phase 430 participants (Actual)Interventional2013-05-15Completed
Switching From Standard of Care Dual Antiplatelet Treatment (DAPT) Regimens With Aspirin Plus a P2Y12 Inhibitor to Dual Pathway Inhibition (DPI) With Low-dose Rivaroxaban in Adjunct to Aspirin in Patients With Coronary Artery Disease: The Switching Anti-P [NCT04006288]Phase 490 participants (Actual)Interventional2019-09-06Completed
Facilitation Through Aggrastat or Cangrelor Bolus and Infusion Over prasugreL: a mUlticenter Randomized Open-label Trial in patientS With ST-elevation Myocardial inFarction Referred for primAry percutaneouS inTERvention.FABOLUS FASTER Trial [NCT02978040]Phase 4122 participants (Actual)Interventional2017-07-04Completed
Effect of Antiplatelet Therapies in Patients With Depression and Coronary Disease [NCT05821062]400 participants (Anticipated)Observational2022-04-14Recruiting
Individualizing Dual Antiplatelet Therapy After Percutaneous Coronary Intervention - The IDEAL-PCI Registry [NCT01515345]Phase 31,008 participants (Actual)Interventional2011-07-31Completed
Single and Multiple Dose Pharmacokinetics and Pharmacodynamics of Prasugrel (LY640315) in Korean Healthy Male Subjects [NCT01591317]Phase 130 participants (Actual)Interventional2009-03-31Completed
Prasugrel Or Ticagrelor In ST-Elevation Myocardial Infarction Patients With Diabetes Mellitus [NCT01531114]Phase 350 participants (Actual)Interventional2013-05-31Completed
The ANTARCTIC Study - Assessment of a Normal Versus Tailored Dose of Prasugrel After Stenting in Patients Aged > 75 Years to Reduce the Composite of Bleeding, Stent Thrombosis and Ischemic Complications [NCT01538446]Phase 4880 participants (Actual)Interventional2012-03-31Completed
Comparison of Therapy With TICAGRELOR, Prasugrel and High Clopidogrel Dose in PCI Patients With High on Treatment Platelet Reactivity and Genotype Variation [NCT01543932]Phase 381 participants (Actual)Interventional2012-07-31Completed
Efficacy, Safety and Tolerability of PrasugrEl 5mg or TIcagrelor 60mg in COmplex and Higher-Risk Indicated PCI/PatieNts: The Prospective, Randomized, Open-labeled, Blinded Endpoint (PROBE), Multi-center E5TION Trial [NCT04734353]Phase 4492 participants (Anticipated)Interventional2020-01-15Recruiting
Rapid Activity of Platelet Inhibitor Drugs Study (RAPID 2) [NCT01805570]Phase 450 participants (Actual)Interventional2012-11-30Completed
A Study of the Transition From Cangrelor to Clopidogrel or Prasugrel in Patients With Coronary Artery Disease. [NCT01979445]Phase 215 participants (Actual)Interventional2013-12-02Completed
A Pharmacodynamic Study Comparing Prasugrel Versus Ticagrelor in Patients With Coronary Artery Disease Undergoing PCI With CYP2C19 Loss-of-function Genotypes: A Feasibility Study With Point-of-care Pharmacodynamic and Genetic Testing [NCT02065479]Phase 465 participants (Actual)Interventional2014-03-31Completed
High (100mg) Versus Standard (60mg) Loading Dose of Prasugrel in Patients With ST-elevation Myocardial Infarction (STEMI), Undergoing Primary Percutaneous Coronary Intervention (PCI) [NCT01835353]Phase 382 participants (Actual)Interventional2012-06-30Completed
Antiplatelet Therapy Guided by Thrombelastography in Patients With Acute Coronary Syndromes (TEGCOR Study) [NCT01612884]Phase 467 participants (Actual)Interventional2011-08-31Terminated(stopped due to Slow enrollment)
A Pharmacodynamic Evaluation of Switching From Ticagrelor to Prasugrel in Subjects With Stable Coronary Artery Disease: 2nd Switching Antiplatelet Agents [NCT01587651]Phase 4110 participants (Actual)Interventional2012-03-31Completed
Platelet Aggregation and Adenosine Levels Among Patients With Stable Chronic Coronary Artery Disease Taking Ticagrelor or Prasugrel [NCT05247385]Phase 487 participants (Actual)Interventional2017-03-20Completed
Sampling P2Y12 Receptor Inhibition With Prasugrel and Ticagrelor in Patients Submitted to Thrombolysis After Loading Dose of Clopidogrel [NCT02215993]Phase 450 participants (Actual)Interventional2013-07-31Completed
Differential Effect of Ticagrelor Versus Prasugrel on the Adenosine-induced Coronary Vasodilatory Responses in Patients With Acute Coronary Syndrome Undergoing Percutaneous Coronary Intervention. [NCT01642966]Phase 456 participants (Actual)Interventional2012-09-30Completed
Impact of Clopidogrel Dose Adjustment According to Platelet Reactivity Monitoring in Patients With High on Treatment Platelet Reactivity Undergoing Percutaneous Coronary Intervention [NCT01505790]Phase 3187 participants (Actual)Interventional2011-07-31Completed
Rapid Activity of Platelet Inhibitor Drugs Study [NCT01510171]Phase 450 participants (Actual)Interventional2012-01-31Completed
Escalated Single Platelet Inhibition for One Month Plus Direct Oral Anticoagulation in Patients With Atrial Fibrillation and acUte coRonary Syndrome Undergoing percutaneoUS Coronary Intervention [NCT04981041]Phase 42,334 participants (Anticipated)Interventional2021-12-16Recruiting
A Randomized Study With Loading Dose of Prasugrel Opposed to the Standard Dose of Clopidogrel in Type 2 Diabetic Patients in Acute Coronary Syndrome, Revascularized Through Drug-eluting Stent. [NCT01684813]Phase 465 participants (Anticipated)Interventional2012-10-31Completed
Effects of Clopidogrel vs Prasugel vs Ticagrelor on Endothelial Function, Inflammatory and Oxidative Stress Parameters and Platelet Function in Patients Undergoing Coronary Artery Stenting. A Randomised, Prospective Study. [NCT01700322]Phase 4126 participants (Actual)Interventional2012-08-31Completed
Smart Angioplasty Research Team: Safety of 6-month Duration of Dual Antiplatelet Therapy After Percutaneous Coronary Intervention in Patients With Acute Coronary Syndromes (SMART-DATE) [NCT01701453]2,712 participants (Actual)Interventional2012-08-31Active, not recruiting
Vasoactive and Anti-inflammatory Effects of Prasugrel in Acute Coronary Syndrome [NCT01774838]Phase 349 participants (Actual)Interventional2014-10-31Completed
Phase IV: A Comparison of Reduced-dose Prasugrel and Clopidogrel in Elderly Patients With Acute Coronary Syndrome Undergoing Early Percutaneous Coronary Intervention (PCI) [NCT01777503]Phase 42,000 participants (Anticipated)Interventional2012-11-30Recruiting
PhaRmacodynamic Effect of Antiplatelet Agents in Elderly Patients: Standard Clopidogrel Versus prasugrEl Low Dose Therapy. [NCT01778842]Phase 368 participants (Anticipated)Interventional2013-03-31Not yet recruiting
Bedside Testing of the CYP2C19 Gene to Asses Effectiveness of Clopidogrel in Coronary Artery Disease Patients Treated With Percutaneous Coronary Intervention : Individualized Antiplatelet Drugs Treatment to Improve Prognosis [NCT01823185]Phase 41,500 participants (Anticipated)Interventional2013-03-31Recruiting
Impact of Prasugrel Re-load on Platelet Aggregation in Patients on Chronic Prasugrel Therapy [NCT01201772]Phase 465 participants (Actual)Interventional2010-08-31Completed
A Study of the Transition From IV Cangrelor to Oral Prasugrel, and Prasugrel to Cangrelor, in Patients With Coronary Artery Disease. [NCT01852019]Phase 212 participants (Actual)Interventional2013-06-30Completed
A head-to Head Comparison of the Pharmacodynamic Effects of Prasugrel Compared With Ticagrelor in Patients With Coronary Artery Disease [NCT01852175]110 participants (Actual)Interventional2012-01-31Completed
Comparison of Dual-Antiplatelet and Triple-Antiplatelet Preparation Using P2Y12 Assay in Patients With High On-Treatment Platelet Reactivity Undergoing Stent-Assisted Coil Embolization for An Unruptured Intracranial Aneurysm [NCT03581409]Phase 4198 participants (Actual)Interventional2018-10-24Completed
Pharmacodynamic and Pharmacokinetic Profiles of Prasugrel in Patients With ST Elevation Myocardial Infarction: A Randomized Comparison of Standard Versus Crushed Formulation [NCT02212028]Phase 452 participants (Actual)Interventional2014-10-31Completed
A U.S. Post-Approval Study of the PROMUS Element™ Plus Everolimus-Eluting Platinum Chromium Coronary Stent System [NCT01589978]Phase 42,681 participants (Actual)Interventional2012-05-31Completed
The Effect of Prasugrel as Compared to Clopidogrel on Platelet Function Immediately Following the Termination of Intravenous Bivalirudin in Patients Undergoing Percutaneous Coronary and Structural Cardiac Intervention [NCT01789814]Phase 424 participants (Actual)Interventional2013-07-31Completed
Prasugrel for Prevention of Early Saphenous Vein Graft Thrombosis [NCT01560780]Phase 384 participants (Actual)Interventional2013-02-01Completed
Tailoring Bleeding Reduction Approaches in Patients Undergoing Percutaneous Coronary Interventions: Comparative Pharmacodynamic Effects of Potent P2Y12 Inhibitor Monotherapy Versus Dual Antiplatelet Therapy De-escalation [NCT05681702]Phase 490 participants (Anticipated)Interventional2023-02-15Recruiting
Replication of the ISAR-REACT 5 Antiplatelet Trial in Healthcare Claims Data [NCT05086081]28,389 participants (Actual)Observational2020-10-10Completed
Replication of the TRITON-TIMI Antiplatelet Trial in Healthcare Claims Data [NCT04237922]43,864 participants (Actual)Observational2019-09-22Completed
Prasugrel 5mg Versus High Dose Clopidogrel in Clopidogrel Resistant Patients Aged ≥75 Years and/or Weighing <60 kg Post Percutaneous Coronary Intervention (PCI) [NCT01463150]Phase 427 participants (Actual)Interventional2011-10-31Completed
Ticagrelor in Comparison to Prasugrel for Early Inhibition of Platelet Reactivity in Patients With ST-elevation Myocardial Infarction (STEMI), Undergoing Primary Percutaneous Coronary Intervention (PCI) [NCT01463163]Phase 450 participants (Actual)Interventional2011-10-31Completed
Prospective, Randomized Study of the Platelet Inhibitory Efficacy of Ticagrelor Versus Prasugrel in Clopidogrel Low Responders After Percutaneous Coronary Intervention [NCT01456364]Phase 470 participants (Anticipated)Interventional2011-09-30Recruiting
Single-center, Double-blind (ACT-246475), Open-label (Clopidogrel, Prasugrel, and Ticagrelor), Placebo-controlled, Randomized, Two-way Crossover Study to Investigate the Pharmacodynamics, Safety, and Tolerability of a Single Oral Dose of Clopidogrel or, P [NCT03430661]Phase 177 participants (Actual)Interventional2018-01-24Completed
ReAssessment of Anti-Platelet Therapy Using an InDividualized Strategy in Patients With ST-segment Elevation Myocardial Infarction [NCT01452139]Phase 2/Phase 3102 participants (Actual)Interventional2011-09-30Completed
Prospective, Randomized, Open Label Trial of 6 Months vs. 12 Months Dual Antiplatelet Therapy After Drug-Eluting Stent Implantation In ST-elevation Myocardial Infarction [NCT01459627]Phase 41,100 participants (Anticipated)Interventional2011-12-31Completed
Relative Bioavailability of a Prasugrel Paediatric Orally Disintegrating Tablet Formulation Compared to the Tablet in Healthy Adult Subjects [NCT01430091]Phase 118 participants (Actual)Interventional2011-09-30Completed
Pharmacogenomics of Anti-platelet Intervention-2 (PAPI-2) Study: A Prospective, Multicenter, Randomized Trial of Genotype-directed (G-D)Versus Standard of Care (SOC)Anti-platelet Therapy [NCT01452152]Phase 49 participants (Actual)Interventional2012-02-29Terminated(stopped due to Terminated by study sponsor.)
A Multicenter, Single Arm, Open-label Trial of Prasugrel Monotherapy After PCI With the SYNERGY® Stent in Patients With Chronic Coronary Syndrome or Non-ST-elevation Acute Coronary Syndromes [NCT05117866]400 participants (Anticipated)Interventional2020-09-15Recruiting
The Effect Of Antiplatelets Therapy, Tirafiban, Prasugrel, And Aspirin On Saphenous Vein Coronary Artery Bypass Graft Patency [NCT01598337]Phase 3200 participants (Anticipated)Interventional2011-04-30Recruiting
A Randomized, Pilot, Single-center Study, Investigator-Initiated Study to Look at an Aggressive Therapeutic Approach in Aspirin Resistant Patients Comparing to Standard for Patient Undergoing Percutaneous Coronary Intervention [NCT01103440]Phase 236 participants (Actual)Interventional2007-04-30Completed
Adjunctive Vorapaxar Therapy in Patients With Prior Myocardial Infarction Treated With New Generation P2Y12 Receptor Inhibitors Prasugrel and Ticagrelor (VORA-PRATIC): A Prospective, Randomized, Pharmacodynamic Study [NCT02545933]Phase 4130 participants (Actual)Interventional2016-02-29Completed
Pharmacokinetics and Pharmacodynamics of Platelet P2Y12 Inhibitors in Patients Undergoing Percutaneous Coronary Intervention (PCI) for Acute Myocardial Infarction: A Pilot Study [NCT02376283]Phase 487 participants (Actual)Interventional2015-03-09Completed
Pivotal Study of the AggreGuide A-100 Adenosine Diphosphate (ADP) Assay to Evaluate the Detection of Platelet Dysfunction Due to P2Y12 Antiplatelet Drugs [NCT03111420]280 participants (Actual)Interventional2017-01-09Completed
Impact of Antiretroviral Treatment on Pharmacokinetics and Pharmacodynamics of Thienopyridines in Healthy Volunteers and HIV Patients [NCT03054207]Phase 121 participants (Actual)Interventional2015-06-30Terminated(stopped due to difficulty to recruit)
Effect of Continue vs. Stop P2Y12 Inhibitor on Bleeding in Patient Receiving Dual-antiplatelet Therapy Undergoing Dental Procedure. [NCT03103685]Phase 4428 participants (Anticipated)Interventional2017-05-01Not yet recruiting
Comparison of Prasugrel and Ticagrelor Antiplatelet Effects in Korean Patients Presenting With ST-segment Elevation Myocardial Infarction [NCT02075125]Phase 339 participants (Actual)Interventional2014-01-31Terminated(stopped due to Enrolling participants has halted prematurely and will not resume)
[NCT01839968]32 participants (Actual)Observational2011-09-30Completed
A Pharmacodynamic Comparison of Prasugrel vs. Ticagrelor in Patients With Type 2 Diabetes Mellitus and Coronary Artery Disease [NCT01852214]50 participants (Actual)Interventional2013-02-28Completed
SYNergy Stent® System Implantation With Mandatory Intra-VascularUltra-Sound Guidance to Examine the Safety of Cessation of Dual Anti-Platelet Therapy in High Bleeding Risk Patients at One Month [NCT03606642]Phase 250 participants (Actual)Interventional2018-11-19Active, not recruiting
[NCT02487732]Phase 460 participants (Actual)Interventional2015-07-31Completed
Therapeutic Control of Aspirin-Exacerbated Respiratory Disease (Aspirin) [NCT01597375]Phase 246 participants (Actual)Interventional2012-08-31Completed
Pharmacodynamic and Pharmacokinetic Profiles on Switching From Cangrelor to Prasugrel in Patients With Acute Coronary Syndrome Undergoing Percutaneous Coronary Intervention: The Switching Antiplatelet -6 (SWAP-6) Study [NCT04668144]Phase 477 participants (Actual)Interventional2021-02-09Completed
A Phase 3, Double-Blind, Randomized, Efficacy and Safety Comparison of Prasugrel and Placebo in Pediatric Patients With Sickle Cell Disease. [NCT01794000]Phase 3341 participants (Actual)Interventional2013-04-30Terminated(stopped due to The study is being terminated for lack of efficacy.)
An Open-Label, Dose-Ranging Study of Prasugrel in Pediatric Patients With Sickle Cell Disease [NCT01476696]Phase 233 participants (Actual)Interventional2011-11-30Completed
Comparison of Prasugrel vs. Ticagrelor on Myocardial Injury in Revascularized ST Elevation Acute Myocardial Infarction Patients [NCT03435133]61 participants (Actual)Interventional2015-11-23Completed
Relative Bioavailability of Prasugrel Orally Disintegrating Tablet Formulations and the Effect of Food on the Bioavailability of the Orally Disintegrating Tablet in Healthy Subjects [NCT01648790]Phase 120 participants (Actual)Interventional2012-07-31Completed
Prasugrel in the Prevention of Severe SARS-CoV2 Pneumonia in Hospitalised Patients [NCT04445623]Phase 3128 participants (Anticipated)Interventional2020-07-31Not yet recruiting
An Open-label, Randomized, Controlled, Multicenter Study Exploring Two Treatment Strategies of Rivaroxaban and a Dose-Adjusted Oral Vitamin K Antagonist Treatment Strategy in Subjects With Atrial Fibrillation Who Undergo Percutaneous Coronary Intervention [NCT01830543]Phase 32,124 participants (Actual)Interventional2013-05-10Completed
Pharmacodynamic Outcomes in Patients With Coronary Artery Disease Undergoing Percutaneous Coronary Intervention Treated With an Individualized Treatment STRATEGY [NCT05773989]Phase 488 participants (Anticipated)Interventional2023-07-01Not yet recruiting
Body Weight Adjusted Clopidogrel Treatment in Patients With Coronary Artery Disease [NCT05657041]Phase 2/Phase 380 participants (Anticipated)Interventional2023-04-26Recruiting
Pharmacodynamic Evaluation of Switching From Prasugrel to Ticagrelor: The SWAP (SWitching Anti Platelet)-3 Study [NCT02016170]82 participants (Actual)Interventional2014-03-31Completed
TIPRIS: Ticagrelor vs. Prasugrel Effects on Infarct Size: A Head to Head Comparison With Prasugrel [NCT02507323]Phase 20 participants (Actual)Interventional2016-02-29Withdrawn(stopped due to collaborator withdrew the study)
A Single Center, Randomized, Open Label, Crossover Study With Ticagrelor and Prasugrel to Evaluate Ticagrelor Mechanism of Action in Inhibiting Juvenile Platelet ADP Response [NCT03027934]Phase 40 participants (Actual)Interventional2017-08-28Withdrawn(stopped due to Study population difficult to recruit)
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00059215 (4) [back to overview]Number of Participants With Major Adverse Cardiovascular Events (MACE)
NCT00059215 (4) [back to overview]Number of Participants With Non-CABG TIMI Major or Minor Bleeding Plus MACE
NCT00059215 (4) [back to overview]Number of Participants With Non-coronary Artery Bypass Graft (Non-CABG) Thrombolysis in Myocardial Infarction (TIMI) Major or Minor Bleeding Events
NCT00059215 (4) [back to overview]Number of Participants With Non-Coronary Artery Bypass Graft (Non-CABG) Thrombolysis in Myocardial Infarction (TIMI) Major Bleeding
NCT00097591 (6) [back to overview]Number of Subjects Reaching the Composite Endpoint of All-Cause Death, Nonfatal Myocardial Infarction (MI), or Nonfatal Stroke
NCT00097591 (6) [back to overview]Number of Treated Subjects With Non-Coronary Artery Bypass Graft (CABG) Related Thrombolysis In Myocardial Infarction (TIMI) Study Group Major and Minor Bleeding Events
NCT00097591 (6) [back to overview]Number of Subjects Reaching the Composite Endpoint of Cardiovascular (CV) Death, Nonfatal Myocardial Infarction (MI), Nonfatal Stroke, or Rehospitalization for Cardiac Ischemic Events
NCT00097591 (6) [back to overview]Number of Subjects Reaching the Composite Endpoint of Cardiovascular (CV) Death, Nonfatal Myocardial Infarction (MI), or Nonfatal Stroke
NCT00097591 (6) [back to overview]Number of Subjects Reaching the Composite Endpoint of Cardiovascular (CV) Death, Nonfatal Myocardial Infarction (MI), or Nonfatal Stroke
NCT00097591 (6) [back to overview]Number of Subjects Reaching the Composite Endpoint of Cardiovascular (CV) Death, Nonfatal Myocardial Infarction (MI), or Urgent Target Vessel Revascularization (UTVR)
NCT00356135 (6) [back to overview]Maximum Platelet Aggregation (MPA) to 20 uM ADP According to Clopidogrel Use at Time of Qualifying Acute Coronary Syndrome (ACS) Event
NCT00356135 (6) [back to overview]Correlation Coefficent of Verify Now™ P2Y12 Assay Values to Maximum Platelet Aggregation (MPA) and Residual Platelet Aggregation (RPA) to 20 uM ADP at 1 Week
NCT00356135 (6) [back to overview]Maximum Platelet Aggregation (MPA) (to 5 and 20 uM ADP) at 2 Hours, 24 Hours, 1 Week and 2 Weeks
NCT00356135 (6) [back to overview]Number of Participants With Bleeding Events by Visit According to Thrombolysis in Myocardial Infarction Study Group (TIMI) Criteria
NCT00356135 (6) [back to overview]Residual Platelet Aggregation (RPA) (to 5 and 20 uM ADP) at 2 Hours, 24 Hours, 1 Week and 2 Weeks
NCT00356135 (6) [back to overview]Maximum Platelet Aggregation (MPA) to 20 Micromolar (uM) Adenosine Diphosphase (ADP)
NCT00357968 (18) [back to overview]Myonecrosis Measure: Creatine Kinase-Myocardial Bands (CK-MB) 18 to 24 Hours After the Loading Dose
NCT00357968 (18) [back to overview]Number of Participants With Major Adverse Cardiac Events During the Crossover Maintenance Dose Phase
NCT00357968 (18) [back to overview]Number of Hyporesponsive Participants at the End of the First Maintenance Dose Phase
NCT00357968 (18) [back to overview]Number of Hyporesponsive Participants at the End of the Crossover Maintenance Dose Phase
NCT00357968 (18) [back to overview]Number of Hyporesponsive Participants at 6 Hours After the Loading Dose
NCT00357968 (18) [back to overview]Myonecrosis Measure: Creatine Kinase-Myocardial Bands (CK-MB) at 6 Hours After the Loading Dose
NCT00357968 (18) [back to overview]Myonecrosis Measure: Cardiac Troponin at 6 Hours After the Loading Dose
NCT00357968 (18) [back to overview]Myonecrosis Measure: Cardiac Troponin 18 to 24 Hours After the Loading Dose
NCT00357968 (18) [back to overview]Inhibition of Platelet Aggregation to 20 μM Adenosine Diphosphate at 2 Hours After the Loading Dose
NCT00357968 (18) [back to overview]Inhibition of Platelet Aggregation to 20 μM Adenosine Diphosphate After 14 Days of Maintenance Dose Treatment
NCT00357968 (18) [back to overview]Inhibition of Platelet Aggregation (IPA) to 20 Micromolar (μM) Adenosine Diphosphate (ADP) at 6 Hours After the Loading Dose
NCT00357968 (18) [back to overview]Platelet Reactivity Index Percent (PRI%) Measured by Vasodilator-stimulated Phosphoprotein (VASP) at 6 Hours After the Loading Dose
NCT00357968 (18) [back to overview]Platelet Reactivity Index Percent (PRI%) Measured by Vasodilator-stimulated Phosphoprotein (VASP) at 2 Hours After the Loading Dose
NCT00357968 (18) [back to overview]Platelet Reactivity Index Percent (PRI%) Measured by Vasodilator-stimulated Phosphoprotein (VASP) After 14 Days of Maintenance Dose Treatment
NCT00357968 (18) [back to overview]Platelet Reactivity Index Percent (PRI%) Measured by Vasodilator-stimulated Phosphoprotein (VASP) 18 to 24 Hours After the Loading Dose
NCT00357968 (18) [back to overview]Number of Participants With Non-Coronary Artery Bypass Graft (CABG) Thrombolysis in Myocardial Infarction (TIMI) Major or Minor Bleeding During the First Maintenance Dose Phase
NCT00357968 (18) [back to overview]Number of Participants With Non-Coronary Artery Bypass Graft (CABG) Thrombolysis in Myocardial Infarction (TIMI) Major or Minor Bleeding During the Crossover Maintenance Dose Phase
NCT00357968 (18) [back to overview]Number of Participants With Major Adverse Cardiac Events (MACE) During the First Maintenance Dose Phase
NCT00385944 (18) [back to overview]Poor Responder of MPA to 20 μM ADP Following Maintenance Dose (MD)
NCT00385944 (18) [back to overview]MPA to 20 μM ADP at 14 Days After the First Maintenance Dose (MD)
NCT00385944 (18) [back to overview]Inhibition of Residual Platelet Aggregation (IRPA) to 20 μM ADP
NCT00385944 (18) [back to overview]MPA to 20 μM ADP at 14 Days After the Second Maintenance Dose (MD)
NCT00385944 (18) [back to overview]Change in MPA to 20 μM ADP From 6-18 Hrs Post Loading Dose (LD) to 14 Days After the First Maintenance Dose (MD)
NCT00385944 (18) [back to overview]Change in MPA to 20 μM ADP From Baseline to 6-18 Hrs Post Loading Dose (LD)
NCT00385944 (18) [back to overview]Correlation of MPA to 20 μM ADP and PRU
NCT00385944 (18) [back to overview]Inhibition of Residual Platelet Aggregation (IRPA) to 5 μM ADP
NCT00385944 (18) [back to overview]Inhibition Platelet Aggregation (IPA) to 20 μM ADP
NCT00385944 (18) [back to overview]Inhibition Platelet Aggregation (IPA) to 5 μM ADP
NCT00385944 (18) [back to overview]Maximum Platelet Aggregation (MPA) to 20 Micromolar (μM) Adenosine Diphosphate (ADP)
NCT00385944 (18) [back to overview]Mean Residual Platelet Aggregation (RPA) to 20 µM ADP
NCT00385944 (18) [back to overview]Mean Residual Platelet Aggregation (RPA) to 5 µM ADP
NCT00385944 (18) [back to overview]MPA to 5 μM ADP
NCT00385944 (18) [back to overview]P2Y12 Reaction Units (PRU)
NCT00385944 (18) [back to overview]Platelet Reactivity Index (PRI)
NCT00385944 (18) [back to overview]Number of Participants With Bleeding Events According to Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO)
NCT00385944 (18) [back to overview]Number of Participants With Bleeding Events According to Thrombolysis in Myocardial Infarction Study Group (TIMI) Criteria
NCT00642174 (5) [back to overview]Inhibition of Platelet Aggregation at 1- and 24-Hours After Loading Dose (LD) and 24-Hours After Last Maintenance Dose (LMD) Assessed by Accumetrics VerifyNow™ P2Y12 Assay
NCT00642174 (5) [back to overview]Inhibition of Platelet Function as Measured by Thromboelastography (TEG)-Platelet Mapping Maximum Amplitude - Adenosine Diphosphate
NCT00642174 (5) [back to overview]Maximum Platelet Aggregation (MPA) as Assessed by Light Transmittance Aggregometry (LTA)
NCT00642174 (5) [back to overview]Platelet Reactivity Index (PRI)
NCT00642174 (5) [back to overview]Inhibition of Platelet Aggregation (IPA) 4 Hours After Loading Dose Assessed by Accumetrics VerifyNow™ P2Y12 Assay
NCT00699998 (10) [back to overview]Biomarker Measurements of Inflammation/Hemodynamic Stress: Brain Natriuretic Peptide (BNP)
NCT00699998 (10) [back to overview]Percentage of Participants With a Composite Endpoint of CV Death, MI, Stroke, or Re-hospitalization for Recurrent Unstable Angina (UA)
NCT00699998 (10) [back to overview]Percentage of Participants With a Composite Endpoint of CV Death and MI
NCT00699998 (10) [back to overview]Percentage of Participants With a Composite Endpoint of Cardiovascular (CV) Death, Myocardial Infarction (MI), or Stroke
NCT00699998 (10) [back to overview]Summary of All Deaths
NCT00699998 (10) [back to overview]Percentage of Participants With a Composite Endpoint of All-cause Death, MI, or Stroke
NCT00699998 (10) [back to overview]Platelet Aggregation Measures
NCT00699998 (10) [back to overview]Economic and Quality of Life Outcomes
NCT00699998 (10) [back to overview]Biomarker Measurements of Inflammation/Hemodynamic Stress: C-Reactive Protein (CRP)
NCT00699998 (10) [back to overview]Genotyping Related to Drug Metabolism
NCT00830960 (11) [back to overview]Risk of All-cause Death in Primary Cohort and Low Weight/Elderly Cohort
NCT00830960 (11) [back to overview]Adenosine Diphosphate (ADP)-Induced P2Y12 Receptor-mediated Platelet Aggregation (P2Y12 Reaction Units; PRU) Using the Accumetrics VerifyNow (VN) P2Y12 Assay at 4 Hours Post-Loading Dose (LD) in Primary Cohort (≥60 kg and <75 Years)
NCT00830960 (11) [back to overview]Adenosine Diphosphate (ADP)-Induced P2Y12 Reaction Units (PRU) Using the Accumetrics VerifyNow (VN) P2Y12 Assay at 30 Days During Maintenance Dose (MD) Administration in Primary Cohort
NCT00830960 (11) [back to overview]Genetic Variation Related to Drug Metabolism and Transport Substudy Result Summary
NCT00830960 (11) [back to overview]Incidence of CABG-related TIMI Major or Minor Bleeding.
NCT00830960 (11) [back to overview]Percent Inhibition of Adenosine Diphosphate (ADP)-Induced P2Y12 Reaction Units (PRU) During the Maintenance Dose (MD) Phase at 30 Days and 90 Days in Primary Cohort and Low Weight/Elderly Cohort
NCT00830960 (11) [back to overview]Percent Inhibition of Adenosine Diphosphate (ADP)-Induced P2Y12 Reaction Units (PRU) at 30 Minutes, 2 Hours, and 4 Hours Post-Loading Dose (LD) in Primary in Primary Cohort and Low Weight/Elderly Cohort
NCT00830960 (11) [back to overview]Incidence of Non-coronary Artery Bypass Graft (CABG) Related Thrombolysis in Myocardial Infarction (TIMI) Life-threatening (a Subset of Non-CABG-related TIMI Major Bleeding), Major, Minor, and Minimal Bleeding
NCT00830960 (11) [back to overview]Summary of Myocardial Infarction (MI), Stroke, Stent Thrombosis and Urgent Target Vessel Revascularization (UTVR) in Primary Cohort and Low Weight/Elderly Cohort
NCT00830960 (11) [back to overview]Adenosine Diphosphate (ADP)-Induced P2Y12 Reaction Units (PRU) Using the Accumetrics VerifyNow (VN) P2Y12 Assay at During Maintenance Dose (MD) Phase at 30 Days and 90 Days in Primary Cohort and Low Weight/Elderly Cohort
NCT00830960 (11) [back to overview]Adenosine Diphosphate (ADP)-Induced P2Y12 Reaction Units (PRU) Using the Accumetrics VerifyNow (VN) P2Y12 Assay at 30 Minutes, 2 and 4 Hours Post-Loading Dose (LD) in Primary (≥60 kg and <75 Years) and Low Weight/Elderly (<60 kg or ≥75 Years) Cohorts.
NCT00910299 (3) [back to overview]Number of Participants With Stent Thrombosis (ST)
NCT00910299 (3) [back to overview]Number of Participants With Composite Endpoint of Cardiovascular Death or Myocardial Infarction (MI)
NCT00910299 (3) [back to overview]Number of Participants With Composite Endpoint of All-Cause Death or Myocardial Infarction (MI)
NCT00954707 (13) [back to overview]Phase I: the Rate of Target Lesion Failure (TLF)
NCT00954707 (13) [back to overview]Rate of Academic Research Consortium (ARC) Defined Stent Thrombosis (ST)
NCT00954707 (13) [back to overview]Rate of Cardiac Death
NCT00954707 (13) [back to overview]Rate of Clinically-driven Target Lesion Revascularization (TVR)
NCT00954707 (13) [back to overview]Rate of Non-cardiac Death
NCT00954707 (13) [back to overview]Rate of Procedure Success
NCT00954707 (13) [back to overview]Rate of Protocol Defined Major Bleeding Complications
NCT00954707 (13) [back to overview]Rate of Protocol Defined Stent Thrombosis (ST)
NCT00954707 (13) [back to overview]Rate of Target Vessel Failure (TVF)
NCT00954707 (13) [back to overview]Rate of Clinically Driven Target Vessel Revascularization (TVR)
NCT00954707 (13) [back to overview]Rate of Lesion Success
NCT00954707 (13) [back to overview]Rate of Major Adverse Cardiac Events (MACE)
NCT00954707 (13) [back to overview]Rate of Device Success
NCT00977938 (14) [back to overview]GUSTO Severe or Moderate Bleeding - Randomized BMS ITT
NCT00977938 (14) [back to overview]Definite or Probable Stent Thrombosis (ST) - Randomized DES ITT
NCT00977938 (14) [back to overview]Definite or Probable Stent Thrombosis (ST) - Randomized DES ITT
NCT00977938 (14) [back to overview]Definite or Probable Stent Thrombosis (ST) - Randomized BMS ITT
NCT00977938 (14) [back to overview]Definite or Probable Stent Thrombosis (ST) - Propensity Matched DES vs. BMS
NCT00977938 (14) [back to overview]MACCE (Death, Myocardial Infarction or Stroke) - Randomized DES ITT
NCT00977938 (14) [back to overview]MACCE (Death, Myocardial Infarction or Stroke) - Randomized DES ITT
NCT00977938 (14) [back to overview]MACCE (Death, Myocardial Infarction or Stroke) - Randomized BMS ITT
NCT00977938 (14) [back to overview]MACCE (Death, Myocardial Infarction or Stroke) - Randomized BMS ITT
NCT00977938 (14) [back to overview]MACCE (Death, Myocardial Infarction or Stroke) - Propensity Matched DES vs. BMS
NCT00977938 (14) [back to overview]GUSTO Severe or Moderate Bleeding - Randomized DES ITT
NCT00977938 (14) [back to overview]GUSTO Severe or Moderate Bleeding - Randomized DES ITT
NCT00977938 (14) [back to overview]GUSTO Severe or Moderate Bleeding - Randomized BMS ITT
NCT00977938 (14) [back to overview]Definite or Probable Stent Thrombosis (ST) - Randomized BMS ITT
NCT00997503 (37) [back to overview]Rate of Major Adverse Cardiac and Cerebrovascular Events (MACCE)
NCT00997503 (37) [back to overview]Rate of Major Adverse Cardiac and Cerebrovascular Events (MACCE)
NCT00997503 (37) [back to overview]Rate of Major Adverse Cardiac and Cerebrovascular Events (MACCE): Study Stent Related
NCT00997503 (37) [back to overview]Rate of Major Adverse Cardiac Events (MACE)
NCT00997503 (37) [back to overview]Rate of Major Adverse Cardiac Events (MACE)
NCT00997503 (37) [back to overview]Rate of Major Adverse Cardiac Events (MACE): Study Stent Related
NCT00997503 (37) [back to overview]Rate of Major Adverse Cardiac Events (MACE): Study Stent Related
NCT00997503 (37) [back to overview]Rate of Major Bleeding
NCT00997503 (37) [back to overview]Rate of Major Bleeding
NCT00997503 (37) [back to overview]Rate of Myocardial Infarction (MI)
NCT00997503 (37) [back to overview]Rate of Myocardial Infarction (MI)
NCT00997503 (37) [back to overview]Rate of Myocardial Infarction (MI): Study Stent Related
NCT00997503 (37) [back to overview]Rate of Myocardial Infarction (MI): Study Stent Related
NCT00997503 (37) [back to overview]Rate of Stent Thrombosis (ARC Definite + Probable)
NCT00997503 (37) [back to overview]Rate of Stent Thrombosis (ARC Definite + Probable)
NCT00997503 (37) [back to overview]Rate of Stent Thrombosis (Protocol Definition)
NCT00997503 (37) [back to overview]Rate of Stent Thrombosis (Protocol Definition)
NCT00997503 (37) [back to overview]Rate of Stroke
NCT00997503 (37) [back to overview]Rate of Stroke
NCT00997503 (37) [back to overview]Rate of Target Vessel Failure (TVF)
NCT00997503 (37) [back to overview]Rate of Target Vessel Failure (TVF)
NCT00997503 (37) [back to overview]Rate of Target Vessel Reintervention (TVR)
NCT00997503 (37) [back to overview]Rate of Target Vessel Reintervention (TVR)
NCT00997503 (37) [back to overview]Rate of Target Vessel Reintervention (TVR): Study Stent Related
NCT00997503 (37) [back to overview]Rate of Target Vessel Reintervention (TVR): Study Stent Related
NCT00997503 (37) [back to overview]Target Vessel Failure (TVF) for the Medically-Treated Diabetic Population
NCT00997503 (37) [back to overview]Cardiac Death or Myocardial Infarction
NCT00997503 (37) [back to overview]Incremental Rate of Stent Thrombosis (Protocol Definition)
NCT00997503 (37) [back to overview]Rate of All Cause Death
NCT00997503 (37) [back to overview]Rate of All Cause Death
NCT00997503 (37) [back to overview]Rate of Cardiac Death
NCT00997503 (37) [back to overview]Rate of Cardiac Death
NCT00997503 (37) [back to overview]Rate of Cardiac Death or Myocardial Infarction (MI)
NCT00997503 (37) [back to overview]Rate of Cardiac Death or Myocardial Infarction (MI)
NCT00997503 (37) [back to overview]Rate of Cardiac Death: Study Stent Related
NCT00997503 (37) [back to overview]Rate of Cardiac Death: Study Stent Related
NCT00997503 (37) [back to overview]Rate of Major Adverse Cardiac & Cerebrovascular Events (MACCE): Study Stent Related
NCT01014624 (8) [back to overview]Day at Which 50%, 75%, and 90% of Participants Returned to Baseline Platelet Function Based on the Secondary Definition of Return to Baseline Using the Responder Population
NCT01014624 (8) [back to overview]The Time to Return to Baseline Platelet Function as Assessed by P2Y12 Reaction Units (PRU) Using the Accumetrics VerifyNOW P2Y12 Device Based on the Secondary Definition of Return to Baseline
NCT01014624 (8) [back to overview]Day at Which 50%, 75%, and 90% of Participants Returned to Baseline Platelet Function Based on Secondary Definition of Return to Baseline Using the Primary Population
NCT01014624 (8) [back to overview]Day at Which 50%, 75%, and 90% of Participants Returned to Baseline Platelet Function Based on the Primary Definition of Return to Baseline Using the Responder Population
NCT01014624 (8) [back to overview]Percentage of Inhibition of Platelet Aggregation on Washout Day 1
NCT01014624 (8) [back to overview]Day at Which 50%, 75%, and 90% of Participants Returned to Baseline Platelet Function Based on Primary Definition of Return to Baseline Using the Primary Population
NCT01014624 (8) [back to overview]Time to Return to Baseline PRU for the Primary Population Using the Primary Definition of Return to Baseline in Relation to the Inhibition of Platelet Aggregation 24 Hours Following the Last Maintenance Dose
NCT01014624 (8) [back to overview]The Time to Return to Baseline Platelet Function as Assessed by P2Y12 Reaction Units (PRU) Using the Accumetrics VerifyNOW P2Y12 Device Based on the Primary Definition of Return to Baseline
NCT01015287 (11) [back to overview]Percentage of Participants With All-cause Death, Myocardial Infarction (MI), Stroke, or All Coronary Artery Bypass Graft (CABG) and Non-CABG Thrombolysis in Myocardial Infarction (TIMI) Major Bleeding Through 30 Days From First Loading Dose (LD)
NCT01015287 (11) [back to overview]Percentage of Participants With Incidence of All Coronary Artery Bypass Graft (CABG) or Non-CABG Thrombolysis In Myocardial Infarction (TIMI) Major Bleeding
NCT01015287 (11) [back to overview]Percentage of Participants With Incidence of Cardiovascular (CV) Death or Myocardial Infarction (MI) Through 30 Days From First Loading Dose (LD)
NCT01015287 (11) [back to overview]Percentage of Participants With Incidence of Cardiovascular (CV) Death Through 30 Days From First Loading Dose (LD)
NCT01015287 (11) [back to overview]Percentage of Participants With Incidence of Cardiovascular (CV) Death, Myocardial Infarction (MI), or Stroke Through 30 Days From First Loading Dose (LD)
NCT01015287 (11) [back to overview]Percentage of Participants With Incidence of Definite or Probable Stent Thrombosis (ST) According to the Academic Research Consortium (ARC) Criteria Through 30 Days From First Loading Dose (LD)
NCT01015287 (11) [back to overview]The Percentage of Participants With Occurrence of Cardiovascular (CV) Death, Myocardial Infarction (MI), Stroke, Urgent Revascularization (UR), or Glycoprotein (GP) IIb/IIIa Inhibitor Bailout
NCT01015287 (11) [back to overview]Summary of All-Cause Death
NCT01015287 (11) [back to overview]Percentage of Participants With All-Cause Death, Myocardial Infarction (MI), Stroke, or All Coronary Artery Bypass Graft (CABG) and Non-CABG Thrombolysis in Myocardial Infarction (TIMI) Major Bleeding
NCT01015287 (11) [back to overview]Percentage of Participants With Incidence of Cardiovascular (CV) Death, Myocardial Infarction (MI), or Urgent Revascularization (UR) Through 30 Days From First Loading Dose (LD)
NCT01015287 (11) [back to overview]Change in Standardized Troponin From Baseline to Percutaneous Coronary Intervention (PCI)
NCT01103440 (2) [back to overview]Number of Participants With Major Adverse Cardiac Event (MACE)
NCT01103440 (2) [back to overview]Number of Participants With Elevation of Cardiac Enzyme
NCT01107899 (8) [back to overview]Platelet Function 24 Hours Post Loading Dose
NCT01107899 (8) [back to overview]Effect of Initial Inhibition of Platelet Aggregation on the Day to Return to Baseline Platelet Function: VN-PRU
NCT01107899 (8) [back to overview]Extent of Initial Inhibition of Platelet Aggregation on the Return of Baseline Platelet Function: Light Transmission Aggregometry (LTA)
NCT01107899 (8) [back to overview]Extent of Initial Inhibition of Platelet Aggregation to the Return of Baseline Platelet Function: Multiplate® ADP Test and ADP Test High Sensitivity (HS)
NCT01107899 (8) [back to overview]Platelet Function by LTA at 5 and 20 μM ADP
NCT01107899 (8) [back to overview]Platelet Function by Multiplate® ADP Test and ADP Test HS
NCT01107899 (8) [back to overview]Percentage of Participants Returning to Baseline Platelet Function
NCT01107899 (8) [back to overview]Percentage of Poor Pharmacodynamic Responders by Platelet Aggregation at 24 Hours Post-LD
NCT01107912 (5) [back to overview]Active Metabolite Blood Levels to Drug Exposure as Measured by Pharmacokinetics (PK) Through 4 Hours After Dosing
NCT01107912 (5) [back to overview]Change From Baseline in Maximum Platelet Aggregation (MPA) as Measured by Light Transmission Aggregometry (LTA) From Baseline at Day 12 of Therapy
NCT01107912 (5) [back to overview]Change in Maximum Platelet Aggregation (MPA) to 20 Micromoles (μM) Adenosine Diphosphate (ADP) as Measured by Light Transmission Aggregometry (LTA) From Baseline to 12 Days of Therapy in the First Treatment Period
NCT01107912 (5) [back to overview]Change in VerifyNow P2Y12 Reaction Units (PRU) From Baseline to 12 Days of Therapy
NCT01107912 (5) [back to overview]Change in Vasodilator-associated Stimulated Phosphoprotein (VASP) From Baseline to 12 Days of Therapy
NCT01107925 (5) [back to overview]Change From Baseline in VerifyNow® P2Y12 Reaction Units (PRU) at Day 12 of Therapy
NCT01107925 (5) [back to overview]Change From Baseline in Vasodilator-Associated Stimulated Phosphoprotein (VASP) at Day 12 of Therapy
NCT01107925 (5) [back to overview]Change From Baseline in Maximum Platelet Aggregation (MPA) to 20 Micromolar (µM) Adenosine Diphosphate (ADP) at Day 12 (Period 1)
NCT01107925 (5) [back to overview]Pharmacokinetic (PK) Analysis of the Concentration-Time Curve (AUC)
NCT01107925 (5) [back to overview]Change From Baseline in Maximum Platelet Aggregation (MPA) as Measured by Light Transmission Aggregometry (LTA) at Day 12 of Therapy
NCT01115738 (9) [back to overview]Adenosine Diphosphate (ADP)-Induced P2Y12 Receptor-Mediated Platelet Aggregation 6 Hours After Prasugrel Loading Dose (LD)
NCT01115738 (9) [back to overview]Mean Change From Baseline to 72 Hours in Laboratory Measurements - Hematocrit
NCT01115738 (9) [back to overview]Mean Change From Baseline to 72 Hours in Laboratory Measurements - Hemoglobin
NCT01115738 (9) [back to overview]P2Y12 Reaction Units (PRU) at 6 Hours Post-Prasugrel Loading Dose (LD) by Cytochrome P450 2C19 (CYP2C19)-Predicted Functional Groups - Extensive Metabolizers (EM) and Reduced Metabolizers (RM)
NCT01115738 (9) [back to overview]Adenosine Diphosphate (ADP)-Induced P2Y12 Receptor-Mediated Platelet Aggregation at Baseline, 2, 24 and 72 Hours After Prasugrel Loading Dose (LD)
NCT01115738 (9) [back to overview]Number of Participants With Treatment Emergent Adverse Events (TEAEs)
NCT01115738 (9) [back to overview]Percentage of Inhibition of Platelet Aggregation
NCT01115738 (9) [back to overview]Percentage of Poor Responders
NCT01115738 (9) [back to overview]P2Y12 Reaction Units (PRU) of Clopidogrel Treated Participants at Baseline by Cytochrome P450 2C19 (CYP2C19)-Predicted Functional Groups - CYP2C19 Extensive Metabolizers (EM) and Reduced Metabolizers (RM)
NCT01167023 (7) [back to overview]Intensity of Pain Related to Sickle Cell Disease (SCD) During the Treatment Duration
NCT01167023 (7) [back to overview]P2Y12 Reaction Units (PRU) as Measured by Accumetrics VerifyNow® P2Y12 (VN P2Y12) at 30 Days
NCT01167023 (7) [back to overview]Percentage of Days With Pain Related to Sickle Cell Disease (SCD) During the Treatment Duration
NCT01167023 (7) [back to overview]Percentage of Participants With Hemorrhagic Events Requiring Medical Intervention During the Treatment Duration
NCT01167023 (7) [back to overview]Percentage of Participants With Hemorrhagic Treatment-Emergent Adverse Events (TEAEs) During the Treatment Duration
NCT01167023 (7) [back to overview]Percentage of Participants With Pain Events Related to Sickle Cell Disease (SCD) Requiring Medical Attention During the Treatment Duration
NCT01167023 (7) [back to overview]Platelet Reactivity Index (PRI) Measured by Vasodilator-Associated Stimulated Phosphoprotein (VASP) at 30 Days
NCT01178099 (15) [back to overview]Inhibition of Platelet Aggregation (IPA) to 5 Micromolar (µM) Adenosine Diphosphate (ADP) at Day 12
NCT01178099 (15) [back to overview]P2Y12 Reaction Units (PRU)-Derived VerifyNow (VN) Percent Inhibition at Day 12
NCT01178099 (15) [back to overview]Area Under the Plasma Concentration-Time Curve (AUC) From Time of Dosing Through the Sampling Time of the Last Quantifiable Concentration [AUC(0-tlast)] for Prasugrel's Active Metabolite, R-138727
NCT01178099 (15) [back to overview]Area Under the Plasma Concentration-Time Curve (AUC) From Time of Dosing Through the Sampling Time of the Last Quantifiable Concentration [AUC(0-tlast)] of Prasugrel's Inactive Metabolites, R-95913, R-106583, and R-119251
NCT01178099 (15) [back to overview]Change From Baseline in the Area Under the Aggregation Curve at Day 12
NCT01178099 (15) [back to overview]Change From Baseline in the Maximum Platelet Aggregation (MPA) to 20 Micromolar (µM) Adenosine Diphosphate (ADP) at Day 12
NCT01178099 (15) [back to overview]Change From Baseline in the Maximum Platelet Aggregation (MPA) to 5 Micromolar (µM) Adenosine Diphosphate (ADP) at Day 12
NCT01178099 (15) [back to overview]Change From Baseline in the P2Y12 Reaction Units (PRU) Device Reported P2Y12 Percent Inhibition at Day 12
NCT01178099 (15) [back to overview]Change From Baseline in the Percent Aggregation to 20 µM Adenosine Diphosphate (ADP) at Day 12
NCT01178099 (15) [back to overview]Change From Baseline in the Platelet Reactivity Index (PRI) of Prasugrel at Day 12
NCT01178099 (15) [back to overview]Change From Baseline in the Residual Platelet Aggregation (RPA) to 20 Micromolar (µM) Adenosine Diphosphate (ADP) at Day 12
NCT01178099 (15) [back to overview]Maximum Concentration (Cmax) of Prasugrel's Active Metabolite, R-138727
NCT01178099 (15) [back to overview]Maximum Concentration (Cmax) of Prasugrel's Inactive Metabolites, R-95913, R-106583, and R-119251
NCT01178099 (15) [back to overview]Change From Baseline in the Residual Platelet Aggregation (RPA) to 5 Micromolar (µM) Adenosine Diphosphate (ADP) at Day 12
NCT01178099 (15) [back to overview]Inhibition of Platelet Aggregation (IPA) to 20 Micromolar (µM) Adenosine Diphosphate (ADP) at Day 12
NCT01201772 (1) [back to overview]PRI Levels at 4 Hours
NCT01260584 (7) [back to overview]Responder Rate by Treatment and Smoking Status Based on Platelet Reactivity Index (PRI) <= 50%
NCT01260584 (7) [back to overview]Assessment of P2Y12 Reaction Units (PRU) by Treatment and Smoking Status
NCT01260584 (7) [back to overview]Assessment of Vasodilator Stimulated Phosphoprotein (VASP) by Treatment and Smoking Status
NCT01260584 (7) [back to overview]Characterization of the Pharmacokinetics (PK) Area Under Curve (AUC)(0-Last) of the Active Metabolite of Prasugrel and the Active Metabolite of Clopidogrel in Smokers and Non-smokers
NCT01260584 (7) [back to overview]Characterization of the Pharmacokinetics (PK) Cmax of the Active Metabolite of Prasugrel and the Active Metabolite of Clopidogrel in Smokers and Non-smokers
NCT01260584 (7) [back to overview]Inhibition of Platelet Aggregation (IPA) in Prasugrel-treated and Clopidogrel-treated Smokers and Non-smokers Following 9 Days of Maintenance Therapy.
NCT01260584 (7) [back to overview]Responder Rate by Treatment and Smoking Status Based on P2Y12 Reaction Units (PRU) <= 235
NCT01430091 (3) [back to overview]Pharmacokinetics: Time of Maximum Concentration (Tmax) of Prasugrel's Active Metabolite (PRAS-AM)
NCT01430091 (3) [back to overview]Pharmacokinetics: Maximum Concentration (Cmax) of Prasugrel's Active Metabolite (PRAS-AM)
NCT01430091 (3) [back to overview]Pharmacokinetics: Area Under the Concentration-Time Curve From Time Zero to the Last Measureable Concentration (AUC[0-tlast]) of Prasugrel's Active Metabolite (PRAS-AM)
NCT01452152 (5) [back to overview]Occurrence of Adverse Events
NCT01452152 (5) [back to overview]Occurrence of Bleeding Events
NCT01452152 (5) [back to overview]Occurrence of Post-randomization Cardiovascular Events
NCT01452152 (5) [back to overview]Post-treatment Platelet Aggregation
NCT01452152 (5) [back to overview]Composite of All-cause Death, Myocardial Infarction (MI), Stroke and Repeat Revascularization
NCT01476696 (4) [back to overview]Pharmacokinetics: Area Under the Concentration-Time Curve (AUC) of Prasugrel Active Metabolite (Pras-AM)
NCT01476696 (4) [back to overview]Number of Participants With Hemorrhagic Events Requiring Medical Intervention
NCT01476696 (4) [back to overview]Number of Participants With Pain
NCT01476696 (4) [back to overview]Percentage of Platelet Inhibition as Measured by VerifyNow™P2Y12 (VN)
NCT01515345 (3) [back to overview]Any Bleeding Event
NCT01515345 (3) [back to overview]Definite Stent Thrombosis
NCT01515345 (3) [back to overview]Probable Stent Thrombosis
NCT01560780 (7) [back to overview]Total Target Saphenous Vein Graft Atheroma Volume, as Assessed by Intravascular Ultrasonography
NCT01560780 (7) [back to overview]Saphenous Vein Graft Lipid Core Burden Index, as Assessed at Near-infrared Intracoronary Spectroscopy
NCT01560780 (7) [back to overview]Prevalence of Intragraft Thrombus at 12-month Follow-up Optical Coherence Tomography Imaging
NCT01560780 (7) [back to overview]Number of Patients With Severe Bleeding Using the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO) Criteria
NCT01560780 (7) [back to overview]Number of Patients With Angiographic Saphenous Vein Graft Failure
NCT01560780 (7) [back to overview]Normalized Total Target Saphenous Vein Graft Atheroma Volume, as Assessed by Intravascular Ultrasonography
NCT01560780 (7) [back to overview]Major Adverse Cardiac Events, Defined as the Composite of Death, Acute Coronary Syndrome, or Coronary Revascularization) During Follow-up
NCT01587651 (6) [back to overview]Percentage of Subjects With High On-treatment Platelet Reactivity
NCT01587651 (6) [back to overview]Platelet Reactivity Index
NCT01587651 (6) [back to overview]P2Y12 Reaction Units
NCT01587651 (6) [back to overview]P2Y12 Reaction Units
NCT01587651 (6) [back to overview]PRU Percent Inhibition (Device-reported)
NCT01587651 (6) [back to overview]PRU Percent Inhibition (Calculated)
NCT01589978 (21) [back to overview]Rate of Target Vessel Revascularization (TVR) Events Related to the PROMUS Element Stent
NCT01589978 (21) [back to overview]Target Vessel Failure (TVF) Rate
NCT01589978 (21) [back to overview]Target Vessel Failure (TVF) Rate in PLATINUM-like Medically Treated Diabetic Patients
NCT01589978 (21) [back to overview]Target Vessel Revascularization (TVR) Rate
NCT01589978 (21) [back to overview]Major Adverse Cardiac Event Rate (MACE)
NCT01589978 (21) [back to overview]All Death or Myocardial Infarction Rate
NCT01589978 (21) [back to overview]All Death Rate
NCT01589978 (21) [back to overview]ARC ST Rate in PLATINUM-like Population.
NCT01589978 (21) [back to overview]Cardiac Death or Myocardial Infarction (MI) Rate
NCT01589978 (21) [back to overview]Cardiac Death or Myocardial Infarction Rate in PLATINUM-like Patients
NCT01589978 (21) [back to overview]Cardiac Death Rate
NCT01589978 (21) [back to overview]Definite + Probable Stent Thrombosis (ST) Rate Based on Academic Research Consortium (ARC) Definition in All Patients
NCT01589978 (21) [back to overview]Definite + Probable Stent Thrombosis (ST) Rate Based on Academic Research Consortium (ARC) Definition in PLATINUM-like Patients
NCT01589978 (21) [back to overview]Myocardial Infarction (MI) Rate
NCT01589978 (21) [back to overview]Non-cardiac Death Rate
NCT01589978 (21) [back to overview]Rate of Cardiac Death Events Related to the PROMUS Element Stent
NCT01589978 (21) [back to overview]Rate of Cardiac Death or Myocardial Infarction Events Related to the PROMUS Element Stent
NCT01589978 (21) [back to overview]Rate of Longitudinal Stent Deformation
NCT01589978 (21) [back to overview]Rate of Major Adverse Cardiac Events Related to the PROMUS Element Stent
NCT01589978 (21) [back to overview]Rate of Myocardial Infarction (MI) Events Related to the PROMUS Element Stent
NCT01589978 (21) [back to overview]Rate of Target Vessel Failure (TVF) Related to the PROMUS Element Stent
NCT01591317 (8) [back to overview]Pharmacokinetics (PK): Maximum Concentration (Cmax) for Prasugrel's Active Metabolite R-138727 During Maintenance Dose
NCT01591317 (8) [back to overview]Pharmacokinetics (PK): Time to Maximum Concentration (Tmax) of Prasugrel's Active Metabolite R-138727 During Loading Dose
NCT01591317 (8) [back to overview]Pharmacokinetics (PK): Time to Maximum Concentration (Tmax) of Prasugrel's Active Metabolite R-138727 During Maintenance Dose
NCT01591317 (8) [back to overview]Percent Inhibition of Verify Now (VN)-P2Y12 Reaction Units (PRU)
NCT01591317 (8) [back to overview]Pharmacodynamics: Adenosine Diphosphate (ADP)-Induced P2Y12 Receptor-mediated Platelet Aggregation
NCT01591317 (8) [back to overview]Pharmacokinetics (PK): Maximum Concentration (Cmax) for Prasugrel's Active Metabolite R-138727 During Loading Dose
NCT01591317 (8) [back to overview]Pharmacokinetics (PK): Area Under the Concentration Curve (AUC) of Prasugrel's Active Metabolite R-138727 During Maintenance Dose
NCT01591317 (8) [back to overview]Pharmacokinetics (PK): Area Under the Concentration Curve (AUC) of Prasugrel's Active Metabolite R-138727 During Loading Dose
NCT01597375 (7) [back to overview]Change From Baseline in Asthma Control Questionnaire-7 (ACQ-7) Score After Aspirin Desensitization and High Dose Aspirin Treatment at 8 Weeks
NCT01597375 (7) [back to overview]Difference in PD2 (Provocative Dose of Aspirin That Elicits an Increase in Nasal Symptom Score of 2 During an Aspirin Challenge) on Prasugrel Versus Placebo
NCT01597375 (7) [back to overview]Change From Baseline in Fractional Exhaled Nitric Oxide (FeNO) Measurement After Aspirin Desensitization and High Dose Aspirin Treatment at 8 Weeks
NCT01597375 (7) [back to overview]Change in Total Nasal Symptom Score(TNSS)From Baseline to Peak During Aspirin Challenge on Placebo Versus Prasugrel.
NCT01597375 (7) [back to overview]Change in Urinary LTE4 During Aspirin Challenge on Placebo Versus Prasugrel
NCT01597375 (7) [back to overview]Difference in Participant's Provocative Dose of Aspirin When Pretreated With Prasugrel Versus Placebo
NCT01597375 (7) [back to overview]Change From Baseline in Prostaglandin Metabolites (PGD-M) Measurement After Aspirin Desensitization and High Dose Aspirin Treatment at 8 Weeks
NCT01612884 (2) [back to overview]Thrombelastography (TEG) MA
NCT01612884 (2) [back to overview]Number of Participants With Ischemic Events
NCT01648790 (4) [back to overview]Pharmacokinetics: Maximum Concentration (Cmax) of Prasugrel Test and Reference Formulation
NCT01648790 (4) [back to overview]Pharmacokinetics: Maximum Concentration (Cmax) of Prasugrel Test Formulation in Fasted and Fed State
NCT01648790 (4) [back to overview]Pharmacokinetics: Area Under the Concentration Curve (AUC) of Prasugrel Reference and Test Formulation
NCT01648790 (4) [back to overview]Pharmacokinetics: Area Under the Concentration Curve (AUC) of Prasugrel Test Formulation in Fasted and Fed State
NCT01765400 (3) [back to overview]The Change in Platelet Aggregation Measured by the Accumetrics (VerifyNow P2Y12) Assay Between Baseline and Each Antiplatelet Medication
NCT01765400 (3) [back to overview]The Change in Light Transmission Aggregometry (LTA)Between Baseline and Each Antiplatelet Medication
NCT01765400 (3) [back to overview]The Change in Platelet Activation Assay (VASP)Between Baseline and Each Antiplatelet Medication
NCT01789814 (1) [back to overview]Change From Baseline in ADP-mediated Platelet Aggregation, APP, SFFLRN, AYPGKF.
NCT01794000 (12) [back to overview]Number of Red Blood Cell (RBC) Transfusions Due to Sickle Cell Disease (SCD) Per Participant Per Year (Rate of RBC Transfusions)
NCT01794000 (12) [back to overview]Number of Days Hospitalized for VOC
NCT01794000 (12) [back to overview]Number of Hospitalizations for VOC Per Participant Per Year (Rate of Hospitalizations)
NCT01794000 (12) [back to overview]Number of Painful Crisis Events Per Participant Per Year (Rate of Painful Crisis)
NCT01794000 (12) [back to overview]Number of Acute Chest Syndrome Per Participant Per Year (Rate of Acute Chest Syndrome)
NCT01794000 (12) [back to overview]Monthly Rate of Days With Pain
NCT01794000 (12) [back to overview]Number of Vaso-Occlusive Crisis (VOC) Events Per Participant Per Year (Rate of VOC)
NCT01794000 (12) [back to overview]Monthly Mean in Faces Pain Scale-Revised Score
NCT01794000 (12) [back to overview]Quarterly Rate of School Absence Due to Sickle Cell Pain
NCT01794000 (12) [back to overview]Time From Randomization to First and Second VOC
NCT01794000 (12) [back to overview]Monthly Rate of Days of Analgesic Use
NCT01794000 (12) [back to overview]Percentage of Participants With Hemorrhagic Events Requiring Medical Intervention
NCT01830543 (9) [back to overview]Percentage of Participants With Bleeding Requiring Medical Attention (BRMA)
NCT01830543 (9) [back to overview]Percentage of Participants With Clinically Significant Bleeding
NCT01830543 (9) [back to overview]Percentage of Participants With Cardiovascular Death
NCT01830543 (9) [back to overview]Percentage of Participants With Composite of Adverse Cardiovascular Events (Cardiovascular Death, Myocardial Infarction (MI) and Stroke)
NCT01830543 (9) [back to overview]Percentage of Participants With Myocardial Infarction
NCT01830543 (9) [back to overview]Percentage of Participants With Stent Thrombosis
NCT01830543 (9) [back to overview]Percentage of Participants With Stroke
NCT01830543 (9) [back to overview]Percentage of Participants With Thrombolysis in Myocardial Infarction (TIMI) Major Bleeding
NCT01830543 (9) [back to overview]Percentage of Participants With Thrombolysis in Myocardial Infarction (TIMI) Minor Bleeding
NCT01852019 (5) [back to overview]Bleeding Events in Accordance With the GUSTO Scale
NCT01852019 (5) [back to overview]Extent of Preservation of Inhibitory Effect of Cangrelor Treatment After Prasugrel, Compared to Treatment With Cangrelor Alone
NCT01852019 (5) [back to overview]Extent of Preservation of Inhibitory Effect of Cangrelor Treatment After Prasugrel, Compared to Treatment With Cangrelor Alone
NCT01852019 (5) [back to overview]Extent of Preservation of Inhibitory Effect After Transition From Cangrelor to Prasugrel Compared With Effect Observed With Prasugrel Alone (Reference Timepoint)
NCT01852019 (5) [back to overview]Extent of Preservation of Inhibitory Effect After Transition From Cangrelor to Prasugrel Compared With Effect Observed With Prasugrel Alone (Reference Timepoint)
NCT01852175 (3) [back to overview]Platelet Reactivity Measured by Vasodilator-stimulated Phosphoprotein (VASP)
NCT01852175 (3) [back to overview]Platelet Reactivity Measured by Vasodilator-stimulated Phosphoprotein (VASP)
NCT01852175 (3) [back to overview]Platelet Reactivity by Vasodilator-stimulated Phosphoprotein (VASP)
NCT01852214 (4) [back to overview]Platelet Reactivity Index
NCT01852214 (4) [back to overview]Platelet Reactivity Index
NCT01852214 (4) [back to overview]P2Y12 Reaction Units
NCT01852214 (4) [back to overview]P2Y12 Reaction Units
NCT01979445 (5) [back to overview]Extent Of Preservation Of Platelet Inhibitory Effect Of Cangrelor Treatment After Prasugrel Or Clopidogrel Compared To Treatment With Cangrelor Alone
NCT01979445 (5) [back to overview]Extent of Preservation of Platelet Inhibitory Effect of Cangrelor Treatment After Prasugrel or Clopidogrel Compared to Treatment With Cangrelor Alone Determined By VerifyNow P2Y12 Assay
NCT01979445 (5) [back to overview]Bleeding Events In Accordance With GUSTO Scale
NCT01979445 (5) [back to overview]Extent of Preservation Of Platelet Inhibitory Effect After Transition From Cangrelor To Prasugrel Or Clopidogrel Compared With Effect Observed With Prasugrel Or Clopidogrel Alone
NCT01979445 (5) [back to overview]Extent of Preservation Of Platelet Inhibitory Effect After Transition From Cangrelor to Prasugrel Or Clopidogrel Compared With Effect Observed With Prasugrel Or Clopidogrel Alone Determined By VerifyNow P2Y12 Assay
NCT02016170 (2) [back to overview]Platelet Reactivity Measured as P2Y12 Reaction Units (PRU) Determined by Verify Now-P2Y12 Assay
NCT02016170 (2) [back to overview]Platelet Reactivity Index (PRI) Measured by Whole Blood Vasodilator-stimulated Phosphoprotein (VASP).
NCT02065479 (1) [back to overview]Platelet Reactivity
NCT02075125 (7) [back to overview]Bleeding Event
NCT02075125 (7) [back to overview]Pre-procedure Platelet Reactivity Index (PRI)
NCT02075125 (7) [back to overview]Number of Participants With High Platelet Reactivity
NCT02075125 (7) [back to overview]Number of Participants With Low Platelet Reactivity
NCT02075125 (7) [back to overview]Adverse Drug Reaction
NCT02075125 (7) [back to overview]Major Adverse Cardiac and Cerebrovascular Events
NCT02075125 (7) [back to overview]Pre-procedure P2Y12 Reaction Units (PRU)
NCT02212028 (2) [back to overview]P2Y12 Reaction Units (PRU)
NCT02212028 (2) [back to overview]Platelet Reactivity Index (PRI)
NCT02376283 (3) [back to overview]Pharmacokinetic Quantification of Plasma Concentration of Clopidogrel and Prasugrel Active Metabolite and Ticagrelor Parent Compound and Active Metabolite Assessed Using Liquid Chromatography in Tandem With Mass Spectrometry (LC-MS/MS) Expressed as ng/ml
NCT02376283 (3) [back to overview]Pharmacodynamic Assessment of Degree of Platelet Inhibition as Determined by Verify Now Point of Care Assay and Expressed as P2Y12 Reaction Units (PRU)
NCT02376283 (3) [back to overview]Pharmacodynamic Assessment of Degree of Platelet Inhibition as Determined by VASP (Vasodilator Stimulated Phosphoprotein Phosphorylation) Flow Cytometry and Expressed as %PRI (Platelet Reactivity Index)
NCT02545933 (1) [back to overview]Maximal Platelet Aggregation
NCT02866175 (7) [back to overview]Number of Participants With Bleeding Academic Research Consortium (BARC) Type 1, 2, 3, and 5 Bleeding According to the BARC Definitions Following Edoxaban-based Regimen Compared With Vitamin K Antagonist (VKA)-Based Regimen
NCT02866175 (7) [back to overview]Number of Participants With Adjudicated Major, Minor, and Minimal Bleeding by Thrombolysis in Myocardial Infarction (TIMI) Definition Following Edoxaban-based Regimen Compared With Vitamin K Antagonist (VKA)-Based Regimen
NCT02866175 (7) [back to overview]Number of Participants With Adjudicated Major, Clinically Relevant Non-major and Minor Bleeding (All Events) Defined by International Society on Thrombosis and Haemostasis Following Edoxaban-based Regimen Compared With Vitamin K Antagonist-Based Regimen
NCT02866175 (7) [back to overview]Number of Participants With Treatment-emergent Adverse Events (TEAEs) Following Edoxaban-based Regimen Compared With Vitamin K Antagonist (VKA)-Based Regimen
NCT02866175 (7) [back to overview]Number of Participants With Study Drug-related Treatment-emergent Adverse Events (TEAEs) Experienced by 2 or More Participants Following Edoxaban-based Regimen Compared With Vitamin K Antagonist (VKA)-Based Regimen
NCT02866175 (7) [back to overview]Number of Participants With Main Efficacy Endpoints For the Overall Study Period Following Edoxaban-based Regimen Compared With Vitamin K Antagonist (VKA)-Based Regimen
NCT02866175 (7) [back to overview]Number of Participants With Adjudicated Major or Clinically Relevant Non-major Bleeding As First Event Defined by International Society on Thrombosis and Haemostasis Following Edoxaban-based Regimen Compared With Vitamin K Antagonist (VKA)-Based Regimen
NCT03489863 (1) [back to overview]P2Y12 Reaction Unit (PRU)
NCT03672097 (6) [back to overview]Mean Change From Baseline to Week 4 in P2Y12 Reaction Units During Period 1
NCT03672097 (6) [back to overview]Mean Percentage Change From Baseline to Week 4 in Platelet Inhibition During Period 1
NCT03672097 (6) [back to overview]Number of Participants With High On-Treatment Platelet Reactivity (HTPR) During Period 1
NCT03672097 (6) [back to overview]Number of Participants With Thrombolysis In Myocardial Infarction (TIMI) Major Bleeding Events During Period 2
NCT03672097 (6) [back to overview]Number of Participants With Adverse Events of Special Interest During Period 1
NCT03672097 (6) [back to overview]Number of Participants With Adverse Events of Special Interest During Period 2
NCT04006288 (1) [back to overview]Maximal Platelet Aggregation (MPA%) by Light Transmittance Aggregometry (LTA)

Number of Participants With Major Adverse Cardiovascular Events (MACE)

Number of participants with any of the following: death, nonfatal myocardial infarction, stroke, total or subtotal occlusion of the target vessel, urgent target vessel revascularization, recurrent ischemia requiring hospitalization. (NCT00059215)
Timeframe: randomization though 30 days after percutaneous coronary intervention (PCI)

Interventionparticipants (Number)
Prasugrel (CS-747) 40-mg LD/7.5-mg MD15
Prasugrel (CS-747) 60-mg LD/10-mg MD15
Prasugrel (CS-747) 60-mg LD/15-mg MD17
Clopidogrel24
Prasugrel (CS-747) Combined47

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Number of Participants With Non-CABG TIMI Major or Minor Bleeding Plus MACE

"Number of participants with non-coronary artery bypass graft (non-CABG) Thrombolysis In Myocardial Infarction (TIMI) Major or Minor bleeding or MACE.~Major bleed was defined as an intracranial hemorrhage OR a clinically overt hemorrhage with a >5 g/dL decrease in hemoglobin.~Minor bleed was defined as a clinically overt hemorrhage with a hemoglobin decrease >=3 g/dL and <= 5 g/dL.~MACE is any of the following:death, nonfatal myocardial infarction, stroke, total or subtotal occlusion of the target vessel, urgent target vessel revascularization, recurrent ischemia requiring hospitalization" (NCT00059215)
Timeframe: randomization though 30 days after percutaneous coronary intervention (PCI)

Interventionparticipants (Number)
Prasugrel (CS-747) 40-mg LD/7.5-mg MD17
Prasugrel (CS-747) 60-mg LD/10-mg MD19
Prasugrel (CS-747) 60-mg LD/15-mg MD20
Clopidogrel27
Prasugrel (CS-747) Combined56

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Number of Participants With Non-coronary Artery Bypass Graft (Non-CABG) Thrombolysis in Myocardial Infarction (TIMI) Major or Minor Bleeding Events

"Number of participants with non-coronary artery bypass graft (non-CABG) Thrombolysis In Myocardial Infarction (TIMI) Major or Minor bleeding.~A major bleed was defined as an intracranial hemorrhage OR a clinically overt hemorrhage with a >5 g/dL decrease in hemoglobin.~A minor bleed was defined as a clinically overt hemorrhage with a hemoglobin decrease >=3 g/dL and <= 5 g/dL." (NCT00059215)
Timeframe: randomization though 30 days after percutaneous coronary intervention (PCI)

Interventionparticipants (Number)
Prasugrel (CS-747) 40-mg LD/7.5-mg MD3
Prasugrel (CS-747) 60-mg LD/10-mg MD4
Prasugrel (CS-747) 60-mg LD/15-mg MD4
Clopidogrel3
Prasugrel (CS-747) Combined11

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Number of Participants With Non-Coronary Artery Bypass Graft (Non-CABG) Thrombolysis in Myocardial Infarction (TIMI) Major Bleeding

"Number of participants with non-coronary artery bypass graft (non-CABG) Thrombolysis In Myocardial Infarction (TIMI) Major or Minor bleeding.~A major bleed was defined as an intracranial hemorrhage OR a clinically overt hemorrhage with a >5 g/dL decrease in hemoglobin." (NCT00059215)
Timeframe: randomization though 30 days after percutaneous coronary intervention (PCI)

Interventionparticipants (Number)
Prasugrel (CS-747) 40-mg LD/7.5-mg MD1
Prasugrel (CS-747) 60-mg LD/10-mg MD1
Prasugrel (CS-747) 60-mg LD/15-mg MD1
Clopidogrel2
Prasugrel (CS-747) Combined3

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Number of Subjects Reaching the Composite Endpoint of All-Cause Death, Nonfatal Myocardial Infarction (MI), or Nonfatal Stroke

The endpoint in this measure is a combination of all-cause death, nonfatal MI, or nonfatal stroke. Results are reported for the All ACS population. (NCT00097591)
Timeframe: Randomization up to 15 months

InterventionParticipants (Number)
Prasugrel692
Clopidogrel822

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Number of Subjects Reaching the Composite Endpoint of Cardiovascular (CV) Death, Nonfatal Myocardial Infarction (MI), Nonfatal Stroke, or Rehospitalization for Cardiac Ischemic Events

The endpoint in this measure is a combination of CV death, nonfatal MI, nonfatal stroke, or rehospitalization for cardiac ischemic events. Results are reported for the All ACS population. (NCT00097591)
Timeframe: Randomization up to 15 months

InterventionParticipants (Number)
Prasugrel797
Clopidogrel938

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Number of Subjects Reaching the Composite Endpoint of Cardiovascular (CV) Death, Nonfatal Myocardial Infarction (MI), or Nonfatal Stroke

The endpoint in this measure is a combination of CV death, nonfatal MI, or nonfatal stroke. Results are reported for the All ACS population for the 30 and 90 day periods. (NCT00097591)
Timeframe: Randomization to 30 days; randomization to 90 days

,
InterventionParticipants (Number)
All ACS (Through 30 days)All ACS (Through 90 days)
Clopidogrel502573
Prasugrel389462

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Number of Subjects Reaching the Composite Endpoint of Cardiovascular (CV) Death, Nonfatal Myocardial Infarction (MI), or Nonfatal Stroke

The endpoint in this measure is a combination of CV death, nonfatal MI, or nonfatal stroke. The data is presented by the study population, which is represented as follows: 1) subjects who presented with unstable angina and non-ST-segment elevation myocardial infarction (UA/NSTEMI), 2) subjects who presented with ST segment elevation myocardial infarction (STEMI), and 3) all subjects with acute coronary syndromes (ACS) (i.e. all subjects with UA/NSTEMI or STEMI). (NCT00097591)
Timeframe: Randomization up to 15 months

,
InterventionParticipants (Number)
UA/NSTEMI (n=5044, n=5030)STEMI (n=1769, n=1765)All ACS (n=6813, n=6795)
Clopidogrel565216781
Prasugrel469174643

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Number of Subjects Reaching the Composite Endpoint of Cardiovascular (CV) Death, Nonfatal Myocardial Infarction (MI), or Urgent Target Vessel Revascularization (UTVR)

The endpoint in this measure is a combination of CV death, nonfatal MI, or UTVR. Results are reported for the All ACS subject population for the 30 and 90 day periods. (NCT00097591)
Timeframe: Randomization to 30 days; randomization to 90 days

,
InterventionParticipants (Number)
All ACS (Through 30 days)All ACS (Through 90 days)
Clopidogrel504588
Prasugrel399472

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Maximum Platelet Aggregation (MPA) to 20 uM ADP According to Clopidogrel Use at Time of Qualifying Acute Coronary Syndrome (ACS) Event

Data provided are the MPA to 20 micromolar ADP while taking clopidogrel (measurement taken at end of the 14 day open label phase) grouped by subjects who were taking clopidogrel at the time of the qualifying ACS event compared with subjects who were not taking clopidogrel at the time of the qualifying ACS event. (NCT00356135)
Timeframe: End of 14 day open label

Interventionpercent maximum platelet aggregation (%) (Mean)
Clopidogrel Use60.73
No Clopidogrel Use55.53

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Correlation Coefficent of Verify Now™ P2Y12 Assay Values to Maximum Platelet Aggregation (MPA) and Residual Platelet Aggregation (RPA) to 20 uM ADP at 1 Week

Correlation Coefficient comparing the Accumetrics VerifyNow™ P2Y12 device with light transmittance aggregometry (LTA) for monitoring platelet aggregation. (NCT00356135)
Timeframe: 1 week after randomized study drug

,,
Interventioncorrelation coefficient (Number)
MPA (20 uM ADP) at 1 weekRPA (20 uM ADP) at 1 week
Clopidogrel 75/75 mg0.4260.425
Prasugrel 10/10 mg0.5640.640
Prasugrel 60/10 mg0.4390.547

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Maximum Platelet Aggregation (MPA) (to 5 and 20 uM ADP) at 2 Hours, 24 Hours, 1 Week and 2 Weeks

Maximum platelet aggregation (MPA) to 5 and 20 micromolar adenosine diphosphase (ADP) as measured with light transmittance aggregometry (LTA). (NCT00356135)
Timeframe: 2 hours, 24 hours, 1 week, 2 weeks after first dose of randomized study drug

,,
Interventionpercent maximum platelet aggregation (%) (Mean)
2 Hour (20 uM ADP)24 Hour (20 uM ADP)1 Week (20 uM ADP)2 Week (20 uM ADP)2 Hour (5 uM ADP)24 Hour (5 uM ADP)1 Week (5 uM ADP)2 Week (5 uM ADP)
Clopidogrel 75/75 mg48.0753.8053.8052.2537.2540.8841.9441.05
Prasugrel 10/10 mg49.4652.2942.9540.8437.8738.8432.4430.18
Prasugrel 60/10 mg26.6527.3640.6438.6119.9720.9431.4528.64

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Number of Participants With Bleeding Events by Visit According to Thrombolysis in Myocardial Infarction Study Group (TIMI) Criteria

Bleeding events were classified as Major Bleeding, Minor Bleeding, or Insignificant according to TIMI criteria. Major Bleeding: any intracranial hemorrhage OR any clinically overt bleeding (including bleeding evident on imaging studies) associated with a fall in hemoglobin (Hgb) of ≥5 gm/dL from baseline. Minor Bleeding: any clinically overt bleeding (including bleeding evident on imaging studies) associated with a fall in Hgb of ≥3 gm/dL but <5 gm/dL from baseline. Insignificant Bleeding: any bleeding event that does not meet criteria for a Major or Minor Bleed. (NCT00356135)
Timeframe: End of 14 day open label (baseline); 24 Hours, 7 days, 14 days after first dose of randomized drug

,,
InterventionParticipants (Number)
Any Bleeding at Any Time During Randomized PeriodBaseline: Any BleedingBaseline: Insignificant BleedingBaseline: Minor BleedingBaseline: Major BleedingHour 24: Any BleedingHour 24: Insignificant BleedingHour 24: Minor BleedingHour 24: Major BleedingDay 7: Any BleedingDay 7: Insignificant BleedingDay 7: Minor BleedingDay 7: Major BleedingDay 14: Any BleedingDay 14: Insignificant BleedingDay 14: Minor BleedingDay 14: Major Bleeding
Clopidogrel 75/75 mg63300000022004400
Prasugrel 10/10 mg40000000022002200
Prasugrel 60/10 mg61100110033002200

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Residual Platelet Aggregation (RPA) (to 5 and 20 uM ADP) at 2 Hours, 24 Hours, 1 Week and 2 Weeks

Residual platelet aggregation after the addition 5 and 20 micromolar ADP as measured with light transmittance aggregometry (LTA). (NCT00356135)
Timeframe: 2 hours, 24 hours, 1 week, 2 weeks after first dose of randomized study drug

,,
Interventionpercent residual platelet aggregation (Mean)
2 Hour (20 uM ADP)24 Hour (20 uM ADP)1 Week (20 uM ADP)2 Week (20 uM ADP)2 Hour (5 uM ADP)24 Hour (5 uM ADP)1 Week (5 uM ADP)2 Week (5 uM ADP)
Clopidogrel 75/75 mg28.2135.1634.4534.5614.8419.6621.5719.28
Prasugrel 10/10 mg32.0632.9722.9218.8918.8319.1811.1110.03
Prasugrel 60/10 mg5.104.7017.9415.174.174.459.949.43

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Maximum Platelet Aggregation (MPA) to 20 Micromolar (uM) Adenosine Diphosphase (ADP)

Maximum platelet aggregation (MPA) to 20 micromolar adenosine diphosphase (ADP) as measured with light transmittance aggregometry (LTA). (NCT00356135)
Timeframe: 1 week after first dose of randomized study drug

Interventionpercent maximum platelet aggregation (%) (Least Squares Mean)
Prasugrel 10/10 mg41.1
Clopidogrel 75/75 mg55.0
Prasugrel 60/10 mg41.0

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Myonecrosis Measure: Creatine Kinase-Myocardial Bands (CK-MB) 18 to 24 Hours After the Loading Dose

Mean CK-MB at 18-24 hours after loading dose. CK-MB is a biomarker for myonecrosis. (NCT00357968)
Timeframe: 18 to 24 hours after loading dose

InterventionIU/L (Median)
Prasugrel11.64
Clopidogrel11.16

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Number of Participants With Major Adverse Cardiac Events During the Crossover Maintenance Dose Phase

Number of patients who met any of the following endpoints: cardiovascular death, myocardial infarction, stroke, subacute stent thrombosis, or urgent target vessel revascularization (NCT00357968)
Timeframe: 14 days after cross-over

Interventionparticipants (Number)
Clopidogrel1
Prasugrel0

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Number of Hyporesponsive Participants at the End of the First Maintenance Dose Phase

Number of patients with inhibition of platelet aggregation (IPA) with 20 uM adenosine diphosphate (ADP) <20% (NCT00357968)
Timeframe: From loading dose to day 15

Interventionparticipants (Number)
Prasugrel1
Clopidogrel7

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Number of Hyporesponsive Participants at the End of the Crossover Maintenance Dose Phase

Number of patients with inhibition of platelet aggregation (IPA) with 20 uM adenosine diphosphate (ADP) <20% (NCT00357968)
Timeframe: 14 days after cross-over

Interventionparticipants (Number)
Clopidogrel4
Prasugrel1

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Number of Hyporesponsive Participants at 6 Hours After the Loading Dose

Number of patients with inhibition of platelet aggregation (IPA) with 20 uM adenosine diphosphate (ADP) <20% (NCT00357968)
Timeframe: 6 hours after loading dose

Interventionparticipants (Number)
Prasugrel0
Clopidogrel21

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Myonecrosis Measure: Creatine Kinase-Myocardial Bands (CK-MB) at 6 Hours After the Loading Dose

Mean CK-MB at 6 hours after loading dose. CK-MB is a biomarker for myonecrosis (NCT00357968)
Timeframe: 6 hours after loading dose

InterventionIU/L (Mean)
Prasugrel9.16
Clopidogrel8.13

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Myonecrosis Measure: Cardiac Troponin at 6 Hours After the Loading Dose

Mean troponin level at 6 hours after the loading dose. Troponin is a biomarker for myonecrosis. (NCT00357968)
Timeframe: 6 hours after loading dose

Interventionng/ml (Mean)
Prasugrel0.06
Clopidogrel0.05

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Myonecrosis Measure: Cardiac Troponin 18 to 24 Hours After the Loading Dose

Mean troponin level at 18 to 24 hours after the loading dose. Troponin is a biomarker for myonecrosis. (NCT00357968)
Timeframe: 18 to 24 hours after loading dose

Interventionng/ml (Mean)
Prasugrel0.12
Clopidogrel0.13

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Inhibition of Platelet Aggregation to 20 μM Adenosine Diphosphate at 2 Hours After the Loading Dose

IPA was defined as (1 - [maximal platelet aggregation (MPA) at 2 hours after study drug treatment]/[MPA before drug treatment]) x 100. (NCT00357968)
Timeframe: 2 hours after loading dose

Interventionpercent inhibition (Mean)
Prasugrel64.54
Clopidogrel20.32

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Inhibition of Platelet Aggregation to 20 μM Adenosine Diphosphate After 14 Days of Maintenance Dose Treatment

"Measures IPA during maintenance dosing before and after cross-over for each therapy.~IPA was defined as (1 - [maximal platelet aggregation(MPA) at 14 days after study drug treatment]/[MPA before drug treatment]) x 100." (NCT00357968)
Timeframe: after 14 days of maintenance dosing

Interventionpercent inhibition (Mean)
Prasugrel61.34
Clopidogrel46.06

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Inhibition of Platelet Aggregation (IPA) to 20 Micromolar (μM) Adenosine Diphosphate (ADP) at 6 Hours After the Loading Dose

IPA was defined as (1 - [maximal platelet aggregation(MPA) at 6 hours after study drug treatment]/[MPA before drug treatment]) x 100. (NCT00357968)
Timeframe: 6 hours after loading dose

Interventionpercent inhibition (Mean)
Prasugrel74.81
Clopidogrel31.77

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Platelet Reactivity Index Percent (PRI%) Measured by Vasodilator-stimulated Phosphoprotein (VASP) at 6 Hours After the Loading Dose

VASP phosphorylation in response to prostaglandin E1 (PGE1) with and without ADP was determined by whole-blood flow cytometry and was expressed as a platelet reactivity index (PRI). PRI was defined as [(MFI(with PGE1) - MFI (with PGE1 and ADP))/MFI(with PGE1) x 100] where MFI is mean fluorescence index. A lower PRI indicates greater antiplatelet effect. (NCT00357968)
Timeframe: 6 hours after loading dose

Interventionpercent (%) platelet reactivity index (Mean)
Prasugrel7.4
Clopidogrel68.4

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Platelet Reactivity Index Percent (PRI%) Measured by Vasodilator-stimulated Phosphoprotein (VASP) at 2 Hours After the Loading Dose

VASP phosphorylation in response to prostaglandin E1 (PGE1) with and without ADP was determined by whole-blood flow cytometry and was expressed as a platelet reactivity index (PRI). PRI was defined as [(MFI(with PGE1) - MFI (with PGE1 and ADP))/MFI(with PGE1) x 100] where MFI is mean fluorescence index. A lower PRI indicates greater antiplatelet effect. (NCT00357968)
Timeframe: 2 hours after loading dose

Interventionpercent (%) platelet reactivity index (Mean)
Prasugrel21.5
Clopidogrel75.0

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Platelet Reactivity Index Percent (PRI%) Measured by Vasodilator-stimulated Phosphoprotein (VASP) After 14 Days of Maintenance Dose Treatment

VASP phosphorylation in response to prostaglandin E1 (PGE1) with and without ADP was determined by whole-blood flow cytometry and was expressed as a platelet reactivity index (PRI). PRI was defined as [(MFI(with PGE1) - MFI (with PGE1 and ADP))/MFI(with PGE1) x 100] where MFI is mean fluorescence index. A lower PRI indicates greater antiplatelet effect. (NCT00357968)
Timeframe: after 14 days of maintenance dosing

Interventionpercent (%) platelet reactivity index (Mean)
Prasugrel23.4
Clopidogrel43.8

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Platelet Reactivity Index Percent (PRI%) Measured by Vasodilator-stimulated Phosphoprotein (VASP) 18 to 24 Hours After the Loading Dose

VASP phosphorylation in response to prostaglandin E1 (PGE1) with and without ADP was determined by whole-blood flow cytometry and was expressed as a platelet reactivity index (PRI). PRI was defined as [(MFI(with PGE1) - MFI (with PGE1 and ADP))/MFI(with PGE1) x 100] where MFI is mean flourescence index. A lower PRI indicates greater antiplatelet effect. (NCT00357968)
Timeframe: 18 to 24 hours after loading dose

Interventionpercent (%) platelet reactivity index (Mean)
Prasugrel10.3
Clopidogrel64.3

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Number of Participants With Non-Coronary Artery Bypass Graft (CABG) Thrombolysis in Myocardial Infarction (TIMI) Major or Minor Bleeding During the First Maintenance Dose Phase

"Non-CABG-related TIMI major bleeding was any intracranial hemorrhage OR any clinically overt bleeding associated with a fall in hemoglobin >=5 gm/dL.~Non-CABG-related TIMI minor bleeding was any clinically overt bleeding associated with a fall in hemoglobin >=3 gm/dL but <5 gm/dL." (NCT00357968)
Timeframe: after 14 days of treatment (before cross-over)

Interventionparticipants (Number)
Prasugrel2
Clopidogrel0

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Number of Participants With Non-Coronary Artery Bypass Graft (CABG) Thrombolysis in Myocardial Infarction (TIMI) Major or Minor Bleeding During the Crossover Maintenance Dose Phase

"Non-CABG-related TIMI major bleeding was any intracranial hemorrhage OR any clinically overt bleeding associated with a fall in hemoglobin >=5 gm/dL.~Non-CABG-related TIMI minor bleeding was any clinically overt bleeding associated with a fall in hemoglobin >=3 gm/dL but <5 gm/dL." (NCT00357968)
Timeframe: 14 days after cross-over

Interventionparticipants (Number)
Clopidogrel0
Prasugrel0

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Number of Participants With Major Adverse Cardiac Events (MACE) During the First Maintenance Dose Phase

Number of patients who met any of the following endpoints: cardiovascular death, myocardial infarction, stroke, subacute stent thrombosis, or urgent target vessel revascularization (NCT00357968)
Timeframe: after 14 days of treatment (before cross-over)

Interventionparticipants (Number)
Prasugrel2
Clopidogrel1

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Poor Responder of MPA to 20 μM ADP Following Maintenance Dose (MD)

Poor responder is defined as MPA to 20 μM ADP >75th percentile of the value at 6-18 hours post-clopidogrel LD. (NCT00385944)
Timeframe: 14 days after maintenance dose (MD)

,
InterventionParticipants (Number)
ResponderPoor Responder
Clopidogrel3512
Prasugrel481

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MPA to 20 μM ADP at 14 Days After the First Maintenance Dose (MD)

Maximum platelet aggregation to 20 μM ADP was assessed by LTA. (NCT00385944)
Timeframe: 14 days after the first maintenance dose (MD)

InterventionPercentage aggregation (Mean)
Prasugrel/Clopidogrel28.9
Clopidogrel/Prasugrel38.2

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Inhibition of Residual Platelet Aggregation (IRPA) to 20 μM ADP

"IRPA is calculated as a percent decrease of RPA from baseline using the following formula:~([RPA at baseline - RPA at time of postbaseline] / RPA at baseline) x 100%" (NCT00385944)
Timeframe: 14 days after maintenance dose (MD)

InterventionPercentage inhibition (Mean)
Prasugrel87.1
Clopidogrel75.9

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MPA to 20 μM ADP at 14 Days After the Second Maintenance Dose (MD)

Maximum platelet aggregation to 20 μM ADP was assessed by LTA. (NCT00385944)
Timeframe: 14 days after the second maintenance dose (MD)

InterventionPercentage aggregation (Mean)
Prasugrel/Clopidogrel42.5
Clopidogrel/Prasugrel25

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Change in MPA to 20 μM ADP From 6-18 Hrs Post Loading Dose (LD) to 14 Days After the First Maintenance Dose (MD)

Maximum platelet aggregation to 20 μM ADP was assessed by LTA. (NCT00385944)
Timeframe: 6-18 hrs post loading dose (LD) to 14 days after the first maintenance dose (MD)

InterventionPercentage aggregation (Mean)
Prasugrel/Clopidgrel-9
Clopidogrel/Prasugrel-0.6

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Change in MPA to 20 μM ADP From Baseline to 6-18 Hrs Post Loading Dose (LD)

Maximum platelet aggregation to 20 μM ADP was assessed by LTA. (NCT00385944)
Timeframe: Baseline to 6-18 hrs post loading dose (LD)

InterventionPercentage aggregation (Mean)
Clopidogrel 900 mg-35.5

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Correlation of MPA to 20 μM ADP and PRU

Pearson-correlation estimated between MPA to 20 μM ADP and Accumetrics VerifyNowTM P2Y12 PRU (NCT00385944)
Timeframe: Baseline through 29 days of treatment

InterventionCorrelation coefficient (Number)
Intent-to-treat Population0.8

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Inhibition of Residual Platelet Aggregation (IRPA) to 5 μM ADP

"IRPA is calculated as a percent decrease of RPA from baseline using the following formula:~([RPA at baseline - RPA at time of postbaseline] / RPA at baseline) x 100%" (NCT00385944)
Timeframe: 14 days after maintenance dose (MD)

InterventionPercentage inhibition (Mean)
Prasugrel95.6
Clopidogrel91.4

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Inhibition Platelet Aggregation (IPA) to 20 μM ADP

"IPA is calculated as a percent decrease of MPA from baseline using the following formula:~([MPA at baseline - MPA at time of postbaseline] / MPA at baseline) x 100%" (NCT00385944)
Timeframe: 14 days after maintenance dose (MD)

InterventionPercentage inhibition (Mean)
Prasugrel64.2
Clopidogrel48.5

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Inhibition Platelet Aggregation (IPA) to 5 μM ADP

"IPA is calculated as a percent decrease of MPA from baseline using the following formula:~([MPA at baseline - MPA at time of postbaseline] / MPA at baseline) x 100%" (NCT00385944)
Timeframe: 14 days after maintenance dose (MD)

InterventionPercentage inhibition (Mean)
Prasugrel72.4
Clopidogrel58.8

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Maximum Platelet Aggregation (MPA) to 20 Micromolar (μM) Adenosine Diphosphate (ADP)

Maximum platelet aggregation (MPA) to 20 μM adenosine diphosphate (ADP) was assessed by light transmission aggregometry (LTA). (NCT00385944)
Timeframe: 14 days after maintenance dose (MD)

InterventionPercentage aggregation (Mean)
Prasugrel27.1
Clopidogrel40.3

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Mean Residual Platelet Aggregation (RPA) to 20 µM ADP

Residual platelet aggregation is the percentage (%) aggregation value as measured by LTA at 6 minutes after the addition of ADP. (NCT00385944)
Timeframe: 14 days after maintenance dose (MD)

InterventionPercentage aggregation (Mean)
Prasugrel9.4
Clopidogrel21.6

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Mean Residual Platelet Aggregation (RPA) to 5 µM ADP

Residual platelet aggregation is the percentage (%) aggregation value as measured by LTA at 6 minutes after the addition of ADP. (NCT00385944)
Timeframe: 14 days after maintenance dose (MD)

InterventionPercentage aggregation (Mean)
Prasugrel2.7
Clopidogrel7.1

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MPA to 5 μM ADP

Maximum platelet aggregation to 5 μM ADP was assessed by LTA. (NCT00385944)
Timeframe: 14 days after maintenance dose (MD)

InterventionPercentage aggregation (Mean)
Prasugrel16.9
Clopidogrel25.0

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P2Y12 Reaction Units (PRU)

P2Y12 Reaction Units (PRU) assessed by Accumetrics Verify NowTM P2Y12. PRU represents the rate and extent of adenosine (ADP)-stimulated platelet aggregation. Lower values indicate greater P2Y12 platelet inhibition. (NCT00385944)
Timeframe: 14 days after maintenance dose (MD)

InterventionPRU (Mean)
Prasugrel44
Clopidogrel98.7

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Platelet Reactivity Index (PRI)

"Platelet Reactivity Index percentage was assessed by Vasodilator-stimulated phosphoprotein (VASP). PRI percent (%) was calculated using the median fluorescence intensity (MFI) of samples included with prostaglandin E1 (PGE1) and ADP, according to the following formula:~PRI%=[(MFI(PGE1)-MFI(PGE1 + ADP)/MFI(PGE1)]x100~Lower PRI% values indicate greater P2Y12 receptor blockade." (NCT00385944)
Timeframe: 14 days after maintenance dose (MD)

InterventionPercentage PRI (Mean)
Prasugrel22.1
Clopidogrel39.4

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Number of Participants With Bleeding Events According to Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO)

Bleeding events will be classified according to the GUSTO definitions as follows: Severe or Life-Threatening Bleeding: any ICH OR any bleeding event resulting in substantial hemodynamic compromise requiring treatment. Moderate Bleeding: any bleeding event resulting in the need for transfusion. Minor bleeding: any other bleeding event that does not require transfusion or cause hemodynamic compromise. (NCT00385944)
Timeframe: 14 days after maintenance dose (MD)

,
InterventionParticipants (Number)
Severe or life-threateningModerateMinor
Clopidogrel002
Prasugrel003

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Number of Participants With Bleeding Events According to Thrombolysis in Myocardial Infarction Study Group (TIMI) Criteria

Bleeding events will be classified as Major Bleeding, Minor Bleeding, or Insignificant Bleeding according to the TIMI criteria. Major bleeding: any intracranial hemorrhage (ICH) OR any clinically overt bleeding (including bleeding evident on imaging studies) associated with a fall in hemoglobin (Hgb) of ≥5 gm/dL from baseline. Minor Bleeding: any clinically overt bleeding associated with a fall in Hgb of ≥3 grams/deciliter (gm/dL) but <5 gm/dL from baseline. Insignificant bleeding: any bleeding event that does not meet criteria for a Major or Minor bleed. (NCT00385944)
Timeframe: 14 days after maintenance dose (MD)

,
InterventionParticipants (Number)
MajorMinorInsignificant
Clopidogrel011
Prasugrel003

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Inhibition of Platelet Aggregation at 1- and 24-Hours After Loading Dose (LD) and 24-Hours After Last Maintenance Dose (LMD) Assessed by Accumetrics VerifyNow™ P2Y12 Assay

Inhibition of platelet aggregation 1- and 24-hours after loading dose and 24-hours after last maintenance dose was administered was assessed using Accumetrics VerifyNow™ P2Y12 assay. Percentage inhibition, as reported by VerifyNow™ P2Y12, was calculated from PRU (rate and extent of ADP-stimulated platelet aggregation) and BASE (estimate of baseline platelet reactivity independent of P2Y12 receptor inhibition [reference values]: rate and extent of Thrombin Receptor-Activated Peptide-stimulated platelet aggregation) values as follows: Percentage (%) inhibition = (1-PRU/BASE) x 100. (NCT00642174)
Timeframe: 1 hour and 24 hours after the loading dose (LD) and 24 hours after the last maintenance dose (LMD)

,
Interventionpercent inhibition (Least Squares Mean)
1 Hour After Loading Dose24 Hours After Loading Dose24 Hours After Last Maintenance Dose
Clopidogrel13.429.344.2
Prasugrel49.987.161.8

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Inhibition of Platelet Function as Measured by Thromboelastography (TEG)-Platelet Mapping Maximum Amplitude - Adenosine Diphosphate

Thromboelastography (TEG) platelet mapping (MP) maximum amplitude (MA) - Adenosine Diphosphate (ADP) millimeters (mm) at each time point. The TEG-MP MA measures strength of clot formation in whole blood. MA-ADP is the maximal amplitude resulting from fibrin and platelets not blocked by ADP-receptor inhibiting drugs. Fibrin strands in blood sample link a rotating sample cup with a stationary pin suspended by a torsion wire. The degree of platelet contribution to the MA through platelet-fibrin bonding directly influences the magnitude of pin movement and ultimately the amplitude of the tracing. (NCT00642174)
Timeframe: Baseline, 1 Hour, 4 Hours, and 24 Hours after loading dose, and 24 Hours after last maintenance dose

,
Interventionmillimeters (mm) (Least Squares Mean)
Baseline1 Hour After Loading Dose4 Hours After Loading Dose24 Hours After Loading Dose24 Hours After Last Maintenance Dose
Clopidogrel58.154.848.149.246.8
Prasugrel56.838.524.229.344.2

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Maximum Platelet Aggregation (MPA) as Assessed by Light Transmittance Aggregometry (LTA)

Mean platelet aggregation (MPA) to 5 and 20 µM adenosine diphosphate (ADP) was assessed by light transmittance aggregometry (LTA). Platelet aggregation was monitored for a total of 7 minutes after addition of ADP. Maximum platelet aggregation was the maximal aggregation value achieved during the 7-minute observation period following addition of agonists. (NCT00642174)
Timeframe: Baseline, 1 Hour, 4 Hours, and 24 Hours after loading dose, and 24 Hours after last maintenance dose

,
Interventionpercent platelet aggregation (Least Squares Mean)
Baseline (5 μM ADP)1 Hour After Loading Dose (5 μM ADP)4 Hours After Loading Dose (5 μM ADP)24 Hours After Loading Dose (5 μM ADP)24 Hours After Last Maintenance Dose (5 μM ADP)Baseline (20 μM ADP)1 Hour After Loading Dose (20 μM ADP)4 Hours After Loading Dose (20 μM ADP)24 Hours After Loading Dose (20 μM ADP)24 Hours After Last Maintenance Dose (20 μM ADP)
Clopidogrel65.756.744.645.638.376.969.857.558.450.7
Prasugrel64.933.718.022.329.677.144.722.427.438.3

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Platelet Reactivity Index (PRI)

Data from the Vasodilator-associated stimulated phosphoprotein assay were reported as the platelet reactivity index (PRI) which was calculated from corrected mean fluorescence intensity (cMFI) following incubation of platelets with either prostaglandin E1 (PGE1) alone or PGE1 plus ADP: Platelet Reactivity Index (%) = [1-(cMFI PGEI+ADP/cMFI PGEI)] x 100. Lower PRI values indicate greater platelet P2Y12 inhibition. (NCT00642174)
Timeframe: Baseline, 1 Hour, 4 Hours, and 24 Hours after loading dose, and 24 Hours after last maintenance dose

,
Interventionpercent inhibition (Least Squares Mean)
Baseline1 Hour After Loading Dose4 Hours After Loading Dose24 Hours After Loading Dose24 Hours After Last Maintenance Dose
Clopidogrel80.676.267.558.542.3
Prasugrel83.540.014.515.727.4

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Inhibition of Platelet Aggregation (IPA) 4 Hours After Loading Dose Assessed by Accumetrics VerifyNow™ P2Y12 Assay

The inhibition of platelet aggregation 4 hours after the loading dose was administered was assessed using the Accumetrics VerifyNow™ P2Y12 assay. Percentage inhibition, as reported by VerifyNow™ P2Y12, was calculated from P2Y12 Reaction Unit (PRU) (rate and extent of adenosine diphosphate [ADP]-stimulated platelet aggregation) and BASE (estimate of baseline platelet reactivity independent of P2Y12 receptor inhibition [reference values]: rate and extent of Thrombin Receptor-Activated Peptide-stimulated platelet aggregation) values as follows: Percentage (%) inhibition = (1-PRU/BASE) x 100. (NCT00642174)
Timeframe: 4 hours after loading dose

,
Interventionpercent inhibition (Least Squares Mean)
Baseline4 Hours After Loading Dose
Clopidogrel9.327.7
Prasugrel9.489.3

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Biomarker Measurements of Inflammation/Hemodynamic Stress: Brain Natriuretic Peptide (BNP)

Brain natriuretic peptide (BNP) is secreted by the ventricles of the heart in response to hemodynamic stress and is a biomarker associated with increased CV risk. Results are presented as geometric least squares means (Geometric LS means). Geometric LS means were adjusted for treatment + baseline value + clopidogrel status at randomization. (NCT00699998)
Timeframe: Day 30 and 6 Months

,,,
Interventionpicograms per milliliter (pg/mL) (Geometric Mean)
Day 306 Months (n=725, 125, 701, 174)
Clopidogrel: <75 Years of Age319.345250.982
Clopidogrel: 75 Years of Age or Older951.359722.750
Prasugrel: <75 Years of Age313.494253.434
Prasugrel: 75 Years of Age or Older1082.396770.132

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Percentage of Participants With a Composite Endpoint of CV Death, MI, Stroke, or Re-hospitalization for Recurrent Unstable Angina (UA)

The percentage of participants is the total number of participants experiencing a CV death, nonfatal MI, nonfatal stroke or re-hospitalization for a recurrent UA divided by number of participants in the treatment arm. Endpoints events were adjudicated by the Clinical Endpoint Committee. (NCT00699998)
Timeframe: Randomization through end of study (30-month visit)

Interventionpercentage of participants with an event (Number)
Prasugrel: <75 Years of Age12.13
Prasugrel: 75 Years of Age or Older26.27
Clopidogrel: <75 Years of Age12.83
Clopidogrel: 75 Years of Age or Older25.67

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Percentage of Participants With a Composite Endpoint of CV Death and MI

The percentage of participants is the total number of participants experiencing a CV death or nonfatal MI divided by number of participants in the treatment arm. Endpoint events were adjudicated by the Clinical Endpoint Committee. (NCT00699998)
Timeframe: Randomization through end of study (30-month visit)

Interventionpercentage of participants with an event (Number)
Prasugrel: <75 Years of Age9.61
Prasugrel: 75 Years of Age or Older22.53
Clopidogrel: <75 Years of Age10.21
Clopidogrel: 75 Years of Age or Older22.69

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Percentage of Participants With a Composite Endpoint of Cardiovascular (CV) Death, Myocardial Infarction (MI), or Stroke

The percentage of participants is the total number of participants experiencing a CV death, nonfatal MI, or nonfatal stroke divided by number of participants in the treatment arm multiplied by 100. Endpoint events were adjudicated by the Clinical Endpoint Committee. (NCT00699998)
Timeframe: Randomization through end of study (30-month visit)

Interventionpercentage of participants with an event (Number)
Prasugrel: <75 Years of Age10.06
Prasugrel: 75 Years of Age or Older24.64
Clopidogrel: <75 Years of Age10.96
Clopidogrel: 75 Years of Age or Older24.13

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Summary of All Deaths

All deaths, regardless of possible relatedness, with the exception of 1 event, were adjudicated by the Clinical Endpoint Committee (CEC) and are reported in this table. The 1 event which was not adjudicated was a result of the revocation of consent by the participant prior to their death. Deaths possibly related to study drug in the opinion of the investigator are also contained in the Serious Adverse Event (SAE) module. (NCT00699998)
Timeframe: Randomization through end of study (30-month visit)

,,,
Interventionparticipants (Number)
Congestive Heart FailureCardiogenic ShockCardiac RuptureMyocardial InfarctionDysrhythmiaStent ThrombosisDirectly Related to Revascularization-CABG or PCIIntracranial HemorrhageNon-Hemorrhagic StrokeSudden death due to cardiovascular eventPulmonary EmbolismStroke, unknown typeOther Cardiovascular EventCardiovascular event, unknown typeAccidentalTraumaHemorrhage, not intracranialInfectionMalignancySuicideOther Non-Cardiovascular eventCause unknown (nonadjudicated event)
Clopidogrel: <75 Years of Age13100246014470200451001614080
Clopidogrel: 75 Years of Age or Older2390213011343101451141711060
Prasugrel: <75 Years of Age1080165012475006401211414180
Prasugrel: 75 Years of Age or Older214124201143911141031217041

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Percentage of Participants With a Composite Endpoint of All-cause Death, MI, or Stroke

The percentage of participants is the total number of participants experiencing an all-cause death, nonfatal MI, or nonfatal stroke divided by number of participants in the treatment arm. Endpoint events were adjudicated by the Clinical Endpoint Committee. (NCT00699998)
Timeframe: Randomization through end of study (30-month visit)

Interventionpercentage of participants with an event (Number)
Prasugrel: <75 Years of Age10.61
Prasugrel: 75 Years of Age or Older27.04
Clopidogrel: <75 Years of Age11.12
Clopidogrel: 75 Years of Age or Older26.83

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Platelet Aggregation Measures

Platelet aggregation was measured by as measured by Accumetrics Verify Now™ P2Y12. Results were reported in P2Y12 Reaction Units (PRU). PRU represents the rate and extent of adenosine (ADP)-stimulated platelet aggregation. Lower values indicate greater P2Y12 platelet inhibition and lower platelet activity and aggregation. ANCOVA Model was used and values were corrected for treatment + baseline value + clopidogrel status at randomization. (NCT00699998)
Timeframe: Day 30 and 12 Months

,,,
InterventionP2Y12 Reaction Units (PRU) (Least Squares Mean)
Day 30Month 12 (n=386, 76, 400, 103)
Clopidogrel: <75 Years of Age193.489199.003
Clopidogrel: 75 Years of Age or Older200.285181.360
Prasugrel: <75 Years of Age93.28094.529
Prasugrel: 75 Years of Age or Older151.872135.096

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Economic and Quality of Life Outcomes

Seattle Angina Questionnaire (SAQ) is a validated, disease-specific questionnaire containing 11 questions (Q) yielding 5 summary scales related to angina: physical limitations, angina stability, angina frequency, treatment satisfaction and disease perception. In this study only angina frequency and the physical limitations scales were assessed. Anginal Frequency was assessed using Q3 and Q4 which consists of a Likert scale ranging from 1 to 6 (higher values equals better quality of life) to assess how often a patient is having symptoms now. Physical limitations was assessed using Q1 which contains 9 items each assessed via Likert scale ranging from 1 to 6 (higher values equals better quality of life) to assess how much a participant's condition is hampering their ability to do what they want to do. Scale scores are transformed to a 0-100 by subtracting the lowest possible score, dividing by the range of the scale, and multiplying by 100. Higher values equal better quality of life. (NCT00699998)
Timeframe: Baseline and follow-up (24 months)

,
Interventionunits on a scale (Mean)
Baseline, physical limitationsBaseline, angina frequency24 Months, physical limitations (n=420, 412)24 Months, angina frequency (n=420, 412)
Clopidogrel67.073.174.589.5
Prasugrel67.873.675.189.7

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Biomarker Measurements of Inflammation/Hemodynamic Stress: C-Reactive Protein (CRP)

C-Reactive Protein (CRP) is a biomarker associated with inflammation and increased CV risk. Results are presented as geometric least squares means (Geometric LS means). Geometric LS means were adjusted for treatment + baseline value + clopidogrel status at randomization. (NCT00699998)
Timeframe: Day 30 and Month 6

,,,
Interventionmilligrams per liter (mg/L) (Geometric Mean)
Day 306 Months (n=755, 143, 745, 178)
Clopidogrel: <75 Years of Age2.2872.149
Clopidogrel: 75 Years of Age or Older2.2261.543
Prasugrel: <75 Years of Age2.3302.272
Prasugrel: 75 Years of Age or Older2.4411.593

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Risk of All-cause Death in Primary Cohort and Low Weight/Elderly Cohort

Risk was defined as the number of participants with events of all-cause death. (NCT00830960)
Timeframe: Randomization through end of study (90 days)

InterventionParticipants (Number)
Prasugrel 60/10 Primary5
Prasugrel 30/7.5 Primary4
Prasugrel 30/5 Primary3
Clopidogrel 300/75 Primary2
Prasugrel 30/5 Low Weight/Elderly7
Clopidogrel 300/75 Low Weight/Elderly1

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Adenosine Diphosphate (ADP)-Induced P2Y12 Receptor-mediated Platelet Aggregation (P2Y12 Reaction Units; PRU) Using the Accumetrics VerifyNow (VN) P2Y12 Assay at 4 Hours Post-Loading Dose (LD) in Primary Cohort (≥60 kg and <75 Years)

"ADP-induced PRU represents the rate and extent of ADP-stimulated platelet aggregation and serves as a biomarker of clinical efficacy, with lower values indicating greater P2Y12 platelet inhibition.~Observed PRU values are presented with statistical comparisons of difference in least squares mean (LS mean) PRU values between prasugrel and clopidogrel.~Efficacy analyses are analyzed and presented separately for the LD and maintenance dose (MD) phase." (NCT00830960)
Timeframe: At 4 hours following LD administration

InterventionPRU (Mean)
Prasugrel 60-mg LD Primary88.5
Prasugrel 30-mg LD Primary124.2
Clopidogrel 300-mg LD Primary261.8

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Adenosine Diphosphate (ADP)-Induced P2Y12 Reaction Units (PRU) Using the Accumetrics VerifyNow (VN) P2Y12 Assay at 30 Days During Maintenance Dose (MD) Administration in Primary Cohort

"Efficacy analyses are analyzed and presented separately for the loading dose (LD) and MD phase. This primary outcome analysis compares PRU for the 3 prasugrel MDs (10 mg, 7.5 mg, and 5 mg) with the clopidogrel 75-mg MD at 30 days post-MD in the primary cohort (participants who weighed ≥60 kg and were <75 years).~ADP-induced PRU serves as a biomarker of clinical efficacy, with lower values indicating greater P2Y12 platelet inhibition.~Observed PRU values are presented with statistical comparisons of LS mean difference between prasugrel and clopidogrel." (NCT00830960)
Timeframe: At 30 days during MD therapy

InterventionPRU (Mean)
Prasugrel 60/10 Primary71.6
Prasugrel 30/7.5 Primary99.3
Prasugrel 30/5 Primary150.8
Clopidogrel 300/75 Primary206.5

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Percent Inhibition of Adenosine Diphosphate (ADP)-Induced P2Y12 Reaction Units (PRU) During the Maintenance Dose (MD) Phase at 30 Days and 90 Days in Primary Cohort and Low Weight/Elderly Cohort

A higher percentage (percent inhibition least squares mean [LS mean]) represents greater platelet inhibition. (NCT00830960)
Timeframe: 30 days and at 90 days during MD therapy

,,,,,
InterventionPercent inhibition (Number)
30 Days (n=69, n=63, n=68, n=78, n=47, n=48)90 Days (n=60, n=57, n=64, n=72, n=43, n=42)
Clopidogrel 300/75 Low Weight/Elderly3238
Clopidogrel 300/75 Primary2938
Prasugrel 30/5 Low Weight/Elderly6869
Prasugrel 30/5 Primary4548
Prasugrel 30/7.5 Primary6066
Prasugrel 60/10 Primary6773

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Percent Inhibition of Adenosine Diphosphate (ADP)-Induced P2Y12 Reaction Units (PRU) at 30 Minutes, 2 Hours, and 4 Hours Post-Loading Dose (LD) in Primary in Primary Cohort and Low Weight/Elderly Cohort

A higher percentage (percent inhibition least squares mean [LS mean]) represents greater platelet inhibition. (NCT00830960)
Timeframe: 30 minutes, 2 hours, and 4 hours following LD administration

,,,,
InterventionPercent inhibition (Number)
30 minutes (n=40, n=79, n=47, n=32, n=31)2 hours (n=37, n=80, n=48, n=33, n=33)4 hours (n=34, n=79, n=43, n=33, n=33)
Clopidogrel 300-mg LD Low Weight/Elderly027
Clopidogrel 300-mg LD Primary-5-24
Prasugrel 30-mg LD Low Weight/Elderly115163
Prasugrel 30-mg LD Primary43451
Prasugrel 60-mg LD Primary104965

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Summary of Myocardial Infarction (MI), Stroke, Stent Thrombosis and Urgent Target Vessel Revascularization (UTVR) in Primary Cohort and Low Weight/Elderly Cohort

"Nonfatal MI: American College of Cardiology (ACC) definition Nonfatal stroke: rapid onset of new, persistent neurologic deficit lasting >24 hours; classified as either ischemic or hemorrhagic based on imaging data, if available, or uncertain cause if imaging data was not available.~Stent thrombosis: defined as definite, probable, or possible, based on Academic Research Consortium definitions.~UTVR: percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG) for recurrent ischemia. Revascularization must have included the vessel(s) dilated at the initial procedure" (NCT00830960)
Timeframe: Randomization through end of study (90 days)

,,,,,
InterventionParticipants (Number)
Fatal MINonfatal MIFatal StrokeNonfatal StrokeDefinite Stent ThrombosisUTVR
Clopidogrel 300/75 Low Weight/Elderly020001
Clopidogrel 300/75 Primary010011
Prasugrel 30/5 Low Weight/Elderly100211
Prasugrel 30/5 Primary010000
Prasugrel 30/7.5 Primary001111
Prasugrel 60/10 Primary110001

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Adenosine Diphosphate (ADP)-Induced P2Y12 Reaction Units (PRU) Using the Accumetrics VerifyNow (VN) P2Y12 Assay at During Maintenance Dose (MD) Phase at 30 Days and 90 Days in Primary Cohort and Low Weight/Elderly Cohort

"Efficacy analyses analyzed and presented separately for loading dose (LD) and MD phase. Analysis compares PRU for 3 prasugrel MDs (10 mg, 7.5 mg, and 5 mg) with clopidogrel 75-mg MD at 30 days post-MD.~Data for Primary Cohort at 30 days post-LD, already presented in second Primary Outcome Measure, are also presented here.~ADP-induced PRU serves as a biomarker of clinical efficacy, with lower values indicating greater P2Y12 platelet inhibition.~Observed PRU values are presented with statistical comparisons of least squares (LS) mean difference between prasugrel and clopidogrel." (NCT00830960)
Timeframe: At 30 Days and 90 days during MD therapy

,,,,,
InterventionPRU (Mean)
30 days (n=69, n=63, n=69, n=78, n=47, n=48)90 Days (n=60, n=57, n=64, n=72, n=43, n=42)
Clopidogrel 300/75 Low Weight/Elderly237.5219.6
Clopidogrel 300/75 Primary206.5188.3
Prasugrel 30/5 Low Weight/Elderly134.2128.5
Prasugrel 30/5 Primary150.8138.5
Prasugrel 30/7.5 Primary99.389.4
Prasugrel 60/10 Primary71.664.8

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Adenosine Diphosphate (ADP)-Induced P2Y12 Reaction Units (PRU) Using the Accumetrics VerifyNow (VN) P2Y12 Assay at 30 Minutes, 2 and 4 Hours Post-Loading Dose (LD) in Primary (≥60 kg and <75 Years) and Low Weight/Elderly (<60 kg or ≥75 Years) Cohorts.

"Efficacy analyses analyzed and presented separately for LD and maintenance dose (MD) phase. Analysis compares PRU for prasugrel LDs (30 mg and 60 mg) with clopidogrel 300-mg LD at 30 minutes post-LD.~Data for Primary Cohort at 4 hours post-LD, already presented in first Primary Outcome Measure, are also presented here.~ADP-induced PRU serves as biomarker of clinical efficacy, with lower values indicating greater P2Y12 platelet inhibition.~Observed PRU values presented with statistical comparisons of least-squares mean (LS mean) difference between prasugrel and clopidogrel." (NCT00830960)
Timeframe: At 30 minutes, 2 hours, and 4 hours following LD administration

,,,,
InterventionPRU (Mean)
30 min (n=40, n=79, n=48, n=33, n=34)2 hours (n=37, n=80, n=49, n=33, n=33)4 hours (n=35, n=79, n=44, n=33, n=33)
Clopidogrel 300-mg LD Low Weight/Elderly379.5339.0337.8
Clopidogrel 300-mg LD Primary312.1289.5261.8
Prasugrel 30-mg LD Low Weight/Elderly311.2171.8127.3
Prasugrel 30-mg LD Primary280.4178.8124.2
Prasugrel 60-mg LD Primary250.5116.988.5

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Number of Participants With Stent Thrombosis (ST)

Academic Research Consortium (ARC) criteria was used to define ST. Definite ST is angiographic or pathologic confirmation of partial or total thrombotic occlusion within the peri-stent region, and at least one of the following additional criteria: acute ischemic symptoms; ischemic electrocardiogram changes; elevated cardiac biomarkers. Probable ST is any unexplained death within 30 days of stent implantation; any MI, which is related to documented acute ischemia in the territory of the implanted stent without angiographic confirmation of ST and in the absence of any other obvious cause. (NCT00910299)
Timeframe: Baseline through 6 months

Interventionparticipants (Number)
Prasugrel0
Clopidogrel0

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Number of Participants With Composite Endpoint of Cardiovascular Death or Myocardial Infarction (MI)

The endpoint in this measure is a combination of cardiovascular death or MI. (NCT00910299)
Timeframe: Baseline through 6 months

Interventionparticipants (Number)
Prasugrel0
Clopidogrel1

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Number of Participants With Composite Endpoint of All-Cause Death or Myocardial Infarction (MI)

The endpoint in this measure is a combination of all-cause death or MI. (NCT00910299)
Timeframe: Baseline through 6 months

Interventionparticipants (Number)
Prasugrel0
Clopidogrel2

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Phase I: the Rate of Target Lesion Failure (TLF)

Target lesion failure (TLF) is defined as clinically-driven target lesion revascularization, target vessel myocardial infarction, or cardiac death that could not be clearly attributed to a vessel other than the target vessel at 12 months. (NCT00954707)
Timeframe: 12 months

Interventionparticipants (Number)
CYPHER® Stent149

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Rate of Academic Research Consortium (ARC) Defined Stent Thrombosis (ST)

ARC defined ST classifies ST by type - definite, probable, possible; by timing - acute, sub-acute, late, very late. Definite includes angiographic or pathologic confirmation; probable includes Any unexplained death within the first 30 days or Any MI (related to documented acute ischemia and without another obvious cause) in the territory of the stent; Possible includes Any unexplained death > 30 days. Acute includes those ≤ 24 hours post procedure; sub-acute includes those > 24 hours to ≤ 30 days post procedure; and late includes those > 30 days to ≤ 1 year post procedure; and very late includes those > 1 year post procedure. (NCT00954707)
Timeframe: 12 Months

Interventionparticipants (Number)
CYPHER® Stent26

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Rate of Cardiac Death

Include all deaths due to cardiac causes. (NCT00954707)
Timeframe: 12 Months

Interventionparticipants (Number)
CYPHER® Stent18

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Rate of Clinically-driven Target Lesion Revascularization (TVR)

"Defined as any clinically-driven repeat percutaneous intervention of the target lesion or bypass surgery of the target vessel. Clinically-driven revascularizations are those in which the subject has a positive functional study, ischemic ECG changes at rest in a distribution consistent with the target vessel, or ischemic symptoms, and an in-lesion diameter stenosis ≥50% by QCA." (NCT00954707)
Timeframe: 12 Months

Interventionparticipants (Number)
CYPHER® Stent98

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Rate of Non-cardiac Death

Include all deaths due to non-cardiac causes. (NCT00954707)
Timeframe: 12 Months

Interventionparticipants (Number)
CYPHER® Stent16

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Rate of Procedure Success

Procedure success is defined as the achievement of a final diameter stenosis of < 50% (by QCA) using any percutaneous method, without the occurrence of death, Myocardial infarction (MI), or repeat coronary revascularization of the target lesion during the hospital stay. (NCT00954707)
Timeframe: From post- procedure to hospital discharge, up to 39 days

Interventionparticipants (Number)
CYPHER® Stent2444

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Rate of Protocol Defined Major Bleeding Complications

Defined by the Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO) classification, including severe and moderate bleeding combined. (NCT00954707)
Timeframe: 12 Months

Interventionparticipants (Number)
CYPHER® Stent71

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Rate of Protocol Defined Stent Thrombosis (ST)

Protocol defined ST includes early and late ST. Early thrombosis is defined as composite thirty-day ischemic endpoint including death, Q-wave myocardial infarction, or subabrupt closure requiring revascularization. Late thrombosis is defined as myocardial infarction occurring > 30 days after the index procedure and attributable to the target vessel with angiographic documentation (site reported or by qualitative coronary angiography) of thrombus or total occlusion at the target site and freedom from an interim revascularization of the target vessel. (NCT00954707)
Timeframe: 12 Months

Interventionparticipants (Number)
CYPHER® Stent21

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Rate of Target Vessel Failure (TVF)

Defined as target vessel revascularization, recurrent infarction, or cardiac death that could not be clearly attributed to a vessel other than the target vessel. (NCT00954707)
Timeframe: 12 Months

Interventionparticipants (Number)
CYPHER® Stent184

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Rate of Clinically Driven Target Vessel Revascularization (TVR)

Defined as any clinically driven repeat percutaneous intervention of the target vessel or bypass surgery of the target vessel. Clinically-driven revascularizations are those in which the subject has a positive functional study, ischemic ECG changes at rest in a distribution consistent with the target vessel, or ischemic symptoms, and an in-lesion diameter stenosis ≥50% by QCA. (NCT00954707)
Timeframe: 12 months

Interventionparticipants (Number)
CYPHER® Stent124

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Rate of Lesion Success

Lesion success is defined as the attainment of < 50% residual stenosis (by Quantitative coronary angiography (QCA)) using any percutaneous method. (NCT00954707)
Timeframe: From post- procedure to hospital discharge, up to 39 days

InterventionLesions (Number)
CYPHER® Stent3264

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Rate of Major Adverse Cardiac Events (MACE)

MACE includes Death, myocardial infarction, emergent bypass surgery, or target lesion revascularization at 12 months (NCT00954707)
Timeframe: 12 Months

Interventionparticipants (Number)
CYPHER® Stent172

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Rate of Device Success

A study device success is defined as achievement of a final residual diameter stenosis of < 50% (by QCA), using the assigned device only. If QCA is not available, the visual estimate of diameter stenosis is used. (NCT00954707)
Timeframe: From post- procedure to hospital discharge, up to 39 days

InterventionDevices (Number)
CYPHER® Stent3205

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GUSTO Severe or Moderate Bleeding - Randomized BMS ITT

Bleeding was assessed according to the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries (GUSTO) criteria. (NCT00977938)
Timeframe: 18 months (12-30 months post-index procedure)

Interventionpercentage of patients (Number)
BMS 30-month DAPT2.03
BMS 12-month DAPT0.90

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Definite or Probable Stent Thrombosis (ST) - Randomized DES ITT

The coprimary efficacy endpoints were the cumulative incidence of MACCE and the cumulative incidence of definite or probable ST within randomized DES ITT patients between 12 and 30 months post procedure. ST was assessed according to the Academic Research Consortium (ARC) definitions. (NCT00977938)
Timeframe: 18 months (12-30 months post-index procedure)

Interventionpercentage of patients (KM estimate) (Number)
DES 30-month DAPT0.40
DES 12-month DAPT1.35

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Definite or Probable Stent Thrombosis (ST) - Randomized DES ITT

ST was assessed according to the Academic Research Consortium (ARC) definitions. (NCT00977938)
Timeframe: 21 months (12-33 months post-index procedure)

Interventionpercentage of patients (KM estimate) (Number)
DES 30-month DAPT0.69
DES 12-month DAPT1.45

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Definite or Probable Stent Thrombosis (ST) - Randomized BMS ITT

ST was assessed according to the Academic Research Consortium (ARC) definitions. (NCT00977938)
Timeframe: 21 months (12-33 months post-index procedure)

Interventionpercentage of patients (KM estimate) (Number)
BMS 30-month DAPT0.50
BMS 12-month DAPT1.11

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Definite or Probable Stent Thrombosis (ST) - Propensity Matched DES vs. BMS

Secondary powered endpoint (NCT00977938)
Timeframe: 33 months (0-33 months post-index procedure)

Interventionpercentage of patients (Number)
Propensity-matched DES1.70
Propensity-matched BMS2.61

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MACCE (Death, Myocardial Infarction or Stroke) - Randomized DES ITT

The coprimary efficacy endpoints were the cumulative incidence of MACCE and the cumulative incidence of ARC definite or probable stent thrombosis within randomized DES ITT patients between 12 and 30 months post procedure. (NCT00977938)
Timeframe: 18 months (12-30 months post-index procedure)

Interventionpercentage of patients (KM estimate) (Number)
DES 30-month DAPT4.34
DES 12-month DAPT5.92

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MACCE (Death, Myocardial Infarction or Stroke) - Randomized DES ITT

(NCT00977938)
Timeframe: 21 months (12-33 months post-index procedure)

Interventionpercentage of patients (KM estimate) (Number)
DES 30-month DAPT5.62
DES 12-month DAPT6.49

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MACCE (Death, Myocardial Infarction or Stroke) - Randomized BMS ITT

(NCT00977938)
Timeframe: 21 months (12-33 months post-index procedure)

Interventionpercentage of patients (KM estimate) (Number)
BMS 30-month DAPT4.68
BMS 12-month DAPT5.48

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MACCE (Death, Myocardial Infarction or Stroke) - Randomized BMS ITT

(NCT00977938)
Timeframe: 18 months (12-30 months post-index procedure)

Interventionpercentage of patients (KM estimate) (Number)
BMS 30-month DAPT4.04
BMS 12-month DAPT4.69

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MACCE (Death, Myocardial Infarction or Stroke) - Propensity Matched DES vs. BMS

Secondary powered endpoint (NCT00977938)
Timeframe: 33 months (0-33 months post-index procedure)

Interventionpercentage of patients (Number)
Propensity-matched DES11.37
Propensity-matched BMS13.24

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GUSTO Severe or Moderate Bleeding - Randomized DES ITT

The primary safety endpoint was moderate or severe bleeding within randomized DES ITT patients between 12 and 30 months post procedure. Bleeding was assessed according to the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries (GUSTO) criteria. (NCT00977938)
Timeframe: 18 months (12-30 months post-index procedure)

Interventionpercentage of patients (Number)
DES 30-month DAPT2.53
DES 12-month DAPT1.57

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GUSTO Severe or Moderate Bleeding - Randomized DES ITT

Bleeding was assessed according to the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries (GUSTO) criteria. (NCT00977938)
Timeframe: 21 months (12-33 months post-index procedure)

Interventionpercentage of patients (Number)
DES 30-month DAPT2.74
DES 12-month DAPT1.88

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GUSTO Severe or Moderate Bleeding - Randomized BMS ITT

Bleeding was assessed according to the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries (GUSTO) criteria. (NCT00977938)
Timeframe: 21 months (12-33 months post-index procedure)

Interventionpercentage of patients (Number)
BMS 30-month DAPT2.09
BMS 12-month DAPT1.05

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Definite or Probable Stent Thrombosis (ST) - Randomized BMS ITT

ST was assessed according to the Academic Research Consortium (ARC) definitions. (NCT00977938)
Timeframe: 18 months (12-30 months post-index procedure)

Interventionpercentage of patients (KM estimate) (Number)
BMS 30-month DAPT0.50
BMS 12-month DAPT1.11

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Rate of Major Adverse Cardiac and Cerebrovascular Events (MACCE)

"MACCE defined as the composite of cardiac death, myocardial infarction, target vessel revascularization and stroke.~Binary rate" (NCT00997503)
Timeframe: 12 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population7.8

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Rate of Major Adverse Cardiac and Cerebrovascular Events (MACCE)

"MACCE defined as the composite of cardiac death, myocardial infarction, target vessel revascularization and stroke.~Binary rate" (NCT00997503)
Timeframe: 6 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population4.7

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Rate of Major Adverse Cardiac Events (MACE)

"MACE defined as the composite of cardiac death, myocardial infarction and target vessel revascularization.~Binary rate" (NCT00997503)
Timeframe: 12 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population7.3

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Rate of Major Adverse Cardiac Events (MACE)

"MACE defined as the composite of cardiac death, myocardial infarction and target vessel revascularization.~Binary rate" (NCT00997503)
Timeframe: 6 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population4.3

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Rate of Major Bleeding

"Major Bleeding defined as the composite of severe or moderate bleeding complication (based upon GUSTO classification).~Binary rate" (NCT00997503)
Timeframe: 12 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population3.6

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Rate of Major Bleeding

"Major Bleeding defined as the composite of severe or moderate bleeding complication (based upon GUSTO classification).~Binary rate" (NCT00997503)
Timeframe: 6 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population2.3

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Rate of Myocardial Infarction (MI)

-Binary rate (NCT00997503)
Timeframe: 12 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population1.4

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Rate of Myocardial Infarction (MI)

-Binary rate (NCT00997503)
Timeframe: 6 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population1.0

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Rate of Stent Thrombosis (ARC Definite + Probable)

"ARC - Academic Research Consortium~Binary Rate" (NCT00997503)
Timeframe: 12 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population0.8

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Rate of Stent Thrombosis (ARC Definite + Probable)

"ARC - Academic Research Consortium~Binary rate" (NCT00997503)
Timeframe: 6 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population0.6

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Rate of Stent Thrombosis (Protocol Definition)

"-Binary rate~The occurrence of any of the following:~Clinical presentation of acute coronary syndrome with angiographic evidence of stent thrombosis:~Angiographic documentation of acute complete occlusion (TIMI flow 0 or 1) of a previously successfully treated artery (TIMI flow 2 to 3 immediately after stent placement and diameter stenosis less than or equal to 30%) and/or Angiographic documentation of a flow limiting thrombus within or adjacent to a previously successfully treated lesion~Acute MI in the distribution of the treated vessel.~Death within the first 30 days post index procedure (without other obvious cause) is considered a surrogate for stent thrombosis when angiography is not available." (NCT00997503)
Timeframe: 12 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population0.9

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Rate of Stent Thrombosis (Protocol Definition)

"-Binary rate~The occurrence of any of the following:~Clinical presentation of acute coronary syndrome with angiographic evidence of stent thrombosis:~Angiographic documentation of acute complete occlusion (TIMI flow 0 or 1) of a previously successfully treated artery (TIMI flow 2 to 3 immediately after stent placement and diameter stenosis less than or equal to 30%) and/or Angiographic documentation of a flow limiting thrombus within or adjacent to a previously successfully treated lesion~Acute MI in the distribution of the treated vessel.~Death within the first 30 days post index procedure (without other obvious cause) is considered a surrogate for stent thrombosis when angiography is not available." (NCT00997503)
Timeframe: 6 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population0.6

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Rate of Stroke

-Binary Rate (NCT00997503)
Timeframe: 12 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population0.5

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Rate of Stroke

-Binary Rate (NCT00997503)
Timeframe: 6 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population0.4

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Rate of Target Vessel Failure (TVF)

"Target vessel failure is defined as any revascularization of the target vessel, MI (Q- and non-Q wave) related to the target vessel, or death related to the target vessel.~Binary rate" (NCT00997503)
Timeframe: 12 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population6.4

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Rate of Target Vessel Failure (TVF)

"Target vessel failure is defined as any revascularization of the target vessel, MI (Q- and non-Q wave) related to the target vessel, or death related to the target vessel.~Binary Rate" (NCT00997503)
Timeframe: 6 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population3.9

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Rate of Target Vessel Reintervention (TVR)

-Binary rate (NCT00997503)
Timeframe: 12 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population5.8

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Rate of Target Vessel Reintervention (TVR)

-Binary rate (NCT00997503)
Timeframe: 6 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population3.3

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Target Vessel Failure (TVF) for the Medically-Treated Diabetic Population

Target vessel failure (TVF) for TAXUS Libertē Post-Approval Study medically-treated diabetic population. For pooled data from the TAXUS Liberté population, please see the citations (NCT00997503)
Timeframe: 12 months

Interventionpercentage of participants (Number)
Medically Treated Diabetic Population6.1

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Cardiac Death or Myocardial Infarction

Cardiac death or myocardial infarction in the TAXUS Liberte Post-Approval Study enrolled population. For pooled data from the TAXUS Liberté and TAXUS Express patient populations, please see the citations. (NCT00997503)
Timeframe: 12 months

Interventionpercentage of participants (Number)
TAXUS Libertē Post-Approval Study Enrolled Population2.1

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Incremental Rate of Stent Thrombosis (Protocol Definition)

"Stent Thrombosis (protocol definition):~The occurrence of any of the following:~Clinical presentation of acute coronary syndrome with angiographic evidence of stent thrombosis:~Angiographic documentation of acute complete occlusion (TIMI flow 0 or 1) of a previously successfully treated artery (TIMI flow 2 to 3 immediately after stent placement and diameter stenosis less than or equal to 30%) and/or Angiographic documentation of a flow limiting thrombus within or adjacent to a previously successfully treated lesion~Acute MI in the distribution of the treated vessel.~Death within the first 30 days post index procedure (without other obvious cause) is considered a surrogate for stent thrombosis when angiography is not available." (NCT00997503)
Timeframe: 1-2 years

Interventionpercentage of participants (Number)
TAXUS Libertē: Overall Enrolled Population1.3

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Rate of All Cause Death

-Binary rate (NCT00997503)
Timeframe: 12 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population1.4

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Rate of All Cause Death

-Binary rate (NCT00997503)
Timeframe: 6 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population0.7

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Rate of Cardiac Death

-Binary rate (NCT00997503)
Timeframe: 12 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population0.9

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Rate of Cardiac Death

-Binary rate (NCT00997503)
Timeframe: 6 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population0.4

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Rate of Cardiac Death or Myocardial Infarction (MI)

- Binary Rate (NCT00997503)
Timeframe: 12 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population2.1

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Rate of Cardiac Death or Myocardial Infarction (MI)

- Binary Rate (NCT00997503)
Timeframe: 6 months

Interventionpercentage of participants (Number)
TAXUS Liberté: Overall Enrolled Population1.4

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Day at Which 50%, 75%, and 90% of Participants Returned to Baseline Platelet Function Based on the Secondary Definition of Return to Baseline Using the Responder Population

On the first day of the Washout Period (Visit 3), the blood draw for platelet function testing was obtained 24 hour (+/- 6 hours) after the last dose of study medication. Following Visit 3, platelet function testing was performed during each visit of the Washout Period until the participant met the following exit criteria: (Baseline PRU-PRU) less than or equal to 60 units and (Baseline PRU-PRU)/(Baseline PRU) less than or equal to (<=) 20%. (NCT01014624)
Timeframe: up to 12 days after the last dose

,
Interventiondays (Number)
Washout day 50% returned to baseline PRUWashout day 75% returned to baseline PRUWashout day 90% returned to baseline PRU
Clopidogrel567
Prasugrel679

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The Time to Return to Baseline Platelet Function as Assessed by P2Y12 Reaction Units (PRU) Using the Accumetrics VerifyNOW P2Y12 Device Based on the Secondary Definition of Return to Baseline

On the first day of the Washout Period (visit 3), the blood draw for platelet function testing was obtained 24 hours (+/- 6 hours) after the last dose of study medication. Following Visit 3, platelet function testing was performed during each visit of the Washout Period until the participant met the following exit criteria: (Baseline PRU-PRU) less than or equal to 60 units and (Baseline PRU-PRU)/(Baseline PRU) less than or equal to 20%. (NCT01014624)
Timeframe: up to 12 days after last dose

,
Interventioncumulative percentage of participants (Number)
returned to baseline PRU by washout day 1returned to baseline PRU by washout day 3returned to baseline PRU by washout day 5returned to baseline PRU by washout day 6returned to baseline PRU by washout day 7returned to baseline PRU by washout day 9
Clopidogrel30.853.980.888.596.2100.0
Prasugrel0.00.037.055.677.8100.0

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Day at Which 50%, 75%, and 90% of Participants Returned to Baseline Platelet Function Based on Secondary Definition of Return to Baseline Using the Primary Population

On the first day of the Washout Period (Visit 3), the blood draw for platelet function testing was obtained 24 hours (+/-6 hours) after the last dose of study medication. Following Visit 3, platelet function testing was performed during each visit of the Washout Period until the participant met the following exit criteria: (Baseline PRU-PRU) less than or equal to 60 units and (Baseline PRU-PRU)/Baseline PRU less than or equal to 20%. (NCT01014624)
Timeframe: up to 12 days after last dose

,
Interventiondays (Number)
Washout day 50% returned to baseline PRUWashout day 75% returned to baseline PRUWashout day 90% returned to baseline PRU
Clopidogrel357
Prasugrel679

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Day at Which 50%, 75%, and 90% of Participants Returned to Baseline Platelet Function Based on the Primary Definition of Return to Baseline Using the Responder Population

On the first day of the Washout Period (Visit 3), the blood draw for platelet function testing was obtained 24 hours (+/-6 hours) after the last dose of study medication. Following Visit 3, platelet function testing was performed during each visit of the Washout Period until the participant met the following exit criteria: (Baseline PRU-PRU) less than or equal to 60 units and (Baseline PRU-PRU)/Baseline PRU less than or equal to 20%. (NCT01014624)
Timeframe: up to 12 days after last dose

,
Interventiondays (Number)
Washout day 50% returned to baseline PRUWashout day 75% returned to baseline PRUWashout day 90% returned to baseline PRU
Clopidogrel556
Prasugrel679

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Percentage of Inhibition of Platelet Aggregation on Washout Day 1

Inhibition of platelet aggregation was assessed by Accumetrics VerifyNow® P2Y12 reaction units (PRU). On the first day of the Washout Period (Visit 3), the blood draw for platelet function testing was obtained 24 hour (+/- 6 hours) after the last dose of study medication. Following Visit 3, platelet function testing was performed during each visit of the Washout Period until the participant met the following exit criteria: (Baseline PRU-PRU) less than or equal to 60 units and (Baseline PRU-PRU)/(Baseline PRU) less than or equal to 20%. (NCT01014624)
Timeframe: Washout Day 1

Interventionpercentage (Mean)
Prasugrel72.3
Clopidogrel35.4

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Day at Which 50%, 75%, and 90% of Participants Returned to Baseline Platelet Function Based on Primary Definition of Return to Baseline Using the Primary Population

On the first day of the Washout Period (Visit 3), the blood draw for platelet function testing was obtained 24 hours (+/-6 hours) after the last dose of study medication. Following Visit 3, platelet function testing was performed during each visit of the Washout Period until the participants met the following exit criteria: (Baseline PRU-PRU) less than or equal to 60 units and (Baseline PRU-PRU)/Baseline PRU less than or equal to 20%. (NCT01014624)
Timeframe: up to 12 days after last dose

,
Interventiondays (Number)
Washout day 50% returned to baseline PRUWashout day 75% returned to baseline PRUWashout day 90% returned to baseline PRU
Clopidogrel356
Prasugrel679

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Time to Return to Baseline PRU for the Primary Population Using the Primary Definition of Return to Baseline in Relation to the Inhibition of Platelet Aggregation 24 Hours Following the Last Maintenance Dose

Time to return to baseline PRU (<= 60 units of baseline) dependent upon baseline PRU and platelet % inhibition on Washout Period Day 1 but independent of treatment. The following regression model was derived for predicting number of days to return to baseline PRU where PI(1) represents platelet percentage inhibition on Washout Day 1. Number days to return to baseline PRU derived from: Number days to return to baseline PRU=-3.350+0.079*PI(1)+0.014*baseline PRU. The predicted number of days to return to baseline based on device-derived platelet percentage inhibition is reported for each treatment group. (NCT01014624)
Timeframe: up to 12 days after the last dose

Interventiondays (Number)
Prasugrel6.2
Clopidogrel3.7

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The Time to Return to Baseline Platelet Function as Assessed by P2Y12 Reaction Units (PRU) Using the Accumetrics VerifyNOW P2Y12 Device Based on the Primary Definition of Return to Baseline

On the first day of the Washout Period (Visit 3), the blood draw for platelet function testing was obtained 24 hours (+/- 6 hours) after the last dose of study medication. Following Visit 3, platelet function testing was performed during each visit of the Washout Period until the participant met the following exit criteria: (Baseline PRU-PRU) less than or equal to 60 units and (Baseline PRU-PRU)/(Baseline PRU) less than or equal to 20%. The results are expressed as cumulative percentage of participants. (NCT01014624)
Timeframe: up to 12 days after last dose

,
Interventioncumulative percentage of participants (Number)
return to baseline PRU by washout day 1return to baseline PRU by washout day 3return to baseline PRU by washout day 5return to baseline PRU by washout day 6return to baseline PRU by washout day 7return to baseline PRU by washout day 9
Clopidogrel30.853.984.696.296.2100.0
Prasugrel03.637.062.977.8100.0

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Percentage of Participants With All-cause Death, Myocardial Infarction (MI), Stroke, or All Coronary Artery Bypass Graft (CABG) and Non-CABG Thrombolysis in Myocardial Infarction (TIMI) Major Bleeding Through 30 Days From First Loading Dose (LD)

The percentage of participants is the total number of participants experiencing an all-cause death, MI, stroke or CABG and non-CABG TIMI major bleeding divided by number of participants in the treatment arm multiplied by 100. Endpoint events were adjudicated by the Clinical Endpoint Committee. (NCT01015287)
Timeframe: First LD through 30 days after first LD

Interventionpercentage of participants (Number)
Non Pre-treatment8.52
Pre-treatment9.47

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Percentage of Participants With Incidence of All Coronary Artery Bypass Graft (CABG) or Non-CABG Thrombolysis In Myocardial Infarction (TIMI) Major Bleeding

The percentage of participants is the total number of participants experiencing a CABG or non-CABG TIMI major bleeding divided by number of participants in the treatment arm multiplied by 100. Endpoint events were adjudicated by the Clinical Endpoint Committee. (NCT01015287)
Timeframe: First loading dose (LD) through 7 days after first LD

Interventionpercentage of participants (Number)
Non Pre-treatment1.35
Pre-treatment2.55

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Percentage of Participants With Incidence of Cardiovascular (CV) Death or Myocardial Infarction (MI) Through 30 Days From First Loading Dose (LD)

The percentage of participants is the total number of participants experiencing a CV death or MI divided by number of participants in the treatment arm multiplied by 100. Endpoint events were adjudicated by the Clinical Endpoint Committee. (NCT01015287)
Timeframe: First LD through 30 days after first LD

Interventionpercentage of participants (Number)
Non Pre-treatment6.51
Pre-treatment6.63

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Percentage of Participants With Incidence of Cardiovascular (CV) Death Through 30 Days From First Loading Dose (LD)

The percentage of participants is the total number of participants experiencing a CV death divided by number of participants in the treatment arm multiplied by 100. Endpoint events were adjudicated by the Clinical Endpoint Committee. (NCT01015287)
Timeframe: First LD through 30 days after first LD

Interventionpercentage of participants (Number)
Non Pre-treatment1.10
Pre-treatment0.69

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Percentage of Participants With Incidence of Cardiovascular (CV) Death, Myocardial Infarction (MI), or Stroke Through 30 Days From First Loading Dose (LD)

The percentage of participants is the total number of participants experiencing a CV death, MI, or stroke divided by number of participants in the treatment arm multiplied by 100. Endpoint events were adjudicated by the Clinical Endpoint Committee. (NCT01015287)
Timeframe: First LD through 30 days after first LD

Interventionpercentage of participants (Number)
Non Pre-treatment7.21
Pre-treatment7.07

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Percentage of Participants With Incidence of Definite or Probable Stent Thrombosis (ST) According to the Academic Research Consortium (ARC) Criteria Through 30 Days From First Loading Dose (LD)

ARC criteria were used to define ST. Definite ST is angiographic or pathologic confirmation of partial or total thrombotic occlusion within the peri-stent region, and at least one of the following additional criteria: acute ischemic symptoms; ischemic electrocardiogram changes; elevated cardiac biomarkers. Probable ST is any unexplained death within 30 days of stent implantation; any MI, which is related to documented acute ischemia in the territory of the implanted stent without angiographic confirmation of ST and in the absence of any other obvious cause. The percentage of participants is the total number of participants experiencing a definite or probable stent thrombosis divided by number of participants in the treatment arm multiplied by 100. Endpoint events were adjudicated by the Clinical Endpoint Committee. (NCT01015287)
Timeframe: First LD through 30 days after first LD

Interventionpercentage of participants (Number)
Non Pre-treatment0.25
Pre-treatment0.10

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The Percentage of Participants With Occurrence of Cardiovascular (CV) Death, Myocardial Infarction (MI), Stroke, Urgent Revascularization (UR), or Glycoprotein (GP) IIb/IIIa Inhibitor Bailout

The percentage of participants is the total number of participants experiencing a CV death, MI, stroke, UR or GPIIb/IIIa Inhibitor bailout divided by number of participants in the treatment arm multiplied by 100. Endpoint events were adjudicated by the Clinical Endpoint Committee. (NCT01015287)
Timeframe: First loading dose (LD) through 7 days after first LD

Interventionpercentage of participants (Number)
Non Pre-treatment9.77
Pre-treatment9.97

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Summary of All-Cause Death

All deaths, regardless of possible relatedness, were adjudicated by the Clinical Endpoint Committee (CEC) and are reported in this table. (NCT01015287)
Timeframe: Randomization through 30 days

,
Interventionparticipants (Number)
Congestive Heart FailureCardiogenic ShockDuring or Immediately Following a CABG ProcedureDuring or Immediately Following a PCI ProcedureMyocardial InfarctionDysrhythmiaSudden Cardiac DeathIntracranial HemorrhageStroke, non-hemorrhagicOther CardiovascularNon-Cardiac Hemorrhage, Not IntracranialInfectionCancer
Non Pre-treatment1552204102010
Pre-treatment0511111112101

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Percentage of Participants With All-Cause Death, Myocardial Infarction (MI), Stroke, or All Coronary Artery Bypass Graft (CABG) and Non-CABG Thrombolysis in Myocardial Infarction (TIMI) Major Bleeding

The percentage of participants is the total number of participants experiencing an all-cause death, MI, stroke or CABG and non-CABG TIMI major bleeding divided by number of participants in the treatment arm multiplied by 100. Endpoint events were adjudicated by the Clinical Endpoint Committee. (NCT01015287)
Timeframe: First loading dose (LD) through 7 days after first LD

Interventionpercentage of participants (Number)
Non Pre-treatment7.57
Pre-treatment8.64

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Percentage of Participants With Incidence of Cardiovascular (CV) Death, Myocardial Infarction (MI), or Urgent Revascularization (UR) Through 30 Days From First Loading Dose (LD)

The percentage of participants is the total number of participants experiencing a CV death, MI, or UR divided by number of participants in the treatment arm multiplied by 100. Endpoint events were adjudicated by the Clinical Endpoint Committee. (NCT01015287)
Timeframe: First LD through 30 days after first LD

Interventionpercentage of participants (Number)
Non Pre-treatment7.31
Pre-treatment7.71

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Change in Standardized Troponin From Baseline to Percutaneous Coronary Intervention (PCI)

Standardized troponin is defined as the ratio of the assayed troponin value divided by the upper limit of normal (ULN). Least Squares (LS) means were obtained from an Analysis of Covariance (ANCOVA) model with treatment as a fixed effect and baseline standardized troponin as a covariate. (NCT01015287)
Timeframe: Baseline, before PCI (not greater than 48 hours after randomization)

Interventionratio of assayed troponin/ULN (Least Squares Mean)
Non Pre-treatment-11.24
Pre-treatment2.82

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Number of Participants With Major Adverse Cardiac Event (MACE)

Number of participants with MACE which is any event of Death, MI, Stent Thrombosis, Urgent Revascularization, Bleeding. Major adverse cardiac events (MACE), defined as the composite of death, MI (CK-MB > 3 times normal), urgent revascularization and definite or probable stent thrombosis (ST) within 30 days. Stent thrombosis was defined according to the new academic research consortium definitions; 2) bleeding complications within 30 days. Major bleeding was defined as intracranial or intraocular bleeding or a drop in hemoglobin > 5 g/dL. Minor bleeding was defined as hemorrhage at the access site requiring intervention, hematoma with a diameter of at least 5 cm, a reduction in hemoglobin levels of at least 4 g/dL without an overt bleeding source or at least 3 g/dL with such a source, reoperation for bleeding or transfusion of a blood product. (NCT01103440)
Timeframe: 30 days

InterventionParticipants (Count of Participants)
Conventional Strategy5
Aggressive Strategy1

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Number of Participants With Elevation of Cardiac Enzyme

Number of participants with peri-procedural biomarker elevation defined as any elevation above baseline of CK-MB or Tn-I within 24 hours after completion of the procedure. (NCT01103440)
Timeframe: 24 hours

InterventionParticipants (Count of Participants)
Conventional Strategy4
Aggressive Strategy2

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Platelet Function 24 Hours Post Loading Dose

PRU was assessed by Accumetrics Verify Now™ P2Y12. PRU represents the rate and extent of ADP-stimulated platelet aggregation. (NCT01107899)
Timeframe: 24 hours post-loading dose

InterventionP2Y12 Reaction Units (PRU) (Mean)
Clopidogrel 600 mg193.0
Prasugrel 60 mg32.5
Prasugrel 30 mg70.0

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Effect of Initial Inhibition of Platelet Aggregation on the Day to Return to Baseline Platelet Function: VN-PRU

To show effect of initial inhibition of platelet aggregation as measured by Accumetrics Verify Now™ P2Y12 on the day to return to baseline platelet function, a regression model was fitted with day to return as outcome variable and initial inhibition as fixed effect. Results are reported as the predicted day to return to baseline platelet function by derived VN-PRU percent (%) inhibition at 24 hours post LD. The derived VN-PRU % inhibition is calculated as a percent decrease of PRU from baseline using the following formula: ([PRU at baseline - PRU at 24 hours post LD]/PRU at baseline) x 100%. (NCT01107899)
Timeframe: Up through 11 days

Interventiondays (Number)
20% Initial Inhibition40% Initial Inhibition60% Initial Inhibition80% Initial Inhibition
All Treatments3.24.66.07.4

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Extent of Initial Inhibition of Platelet Aggregation on the Return of Baseline Platelet Function: Light Transmission Aggregometry (LTA)

Initial inhibition of platelet aggregation was measured by LTA at 5 and 20 μM ADP. Maximum platelet aggregation (MPA) is reported by day. (NCT01107899)
Timeframe: Up through 11 days

,,
Interventionpercent platelet aggregation (Mean)
Baseline (20 μM ADP) (n=5, n=10, n=6)Day 1 (20 μM ADP) (n=5, n=10, n=6)Day 3 (20 μM ADP) (n=5, n=10, n=6)Day 5 (20 μM ADP) (n=5, n=10, n=4)Day 7 (20 μM ADP) (n=5, n=10, n=5)Day 9 (20 μM ADP) (n=5, n=10, n=5)Day 11 (20 μM ADP) (n=5, n=10, n=5)Baseline (5 μM ADP) (n=5, n=10, n=6)Day 1 (5 μM ADP) (n=5, n=10, n=6)Day 3 (5 μM ADP) (n=5, n=10, n=6)Day 5 (5 μM ADP) (n=5, n=10, n=4)Day 7 (5 μM ADP) (n=5, n=10, n=5)Day 9 (5 μM ADP) (n=5, n=10, n=5)Day 11 (5 μM ADP) (n=5, n=10, n=5)
Clopidogrel 600 mg68.0052.6056.0070.4071.0062.4072.0064.4039.4050.2064.2060.4058.4061.80
Prasugrel 30 mg76.3331.6746.3358.2573.2068.6063.8070.6725.5048.6753.2565.4060.0056.00
Prasugrel 60 mg72.7027.3042.5047.0058.3062.0065.2062.6022.0032.8039.5052.4056.0058.90

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Extent of Initial Inhibition of Platelet Aggregation to the Return of Baseline Platelet Function: Multiplate® ADP Test and ADP Test High Sensitivity (HS)

Return of baseline platelet function was assessed by Multiplate® ADP test and ADP test High Sensitivity (HS). Multiplate analyzer was used to assess platelet aggregation based on impedance aggregometry in whole blood. The agonist ADP was added to stirred whole blood after dilution (1:2 with 0.9% NaCl solution) in a final concentration of 6.4 µM (ADP Test) or in final concentration of 6.4 µM ADP plus 9.4 nM Prostaglandin E1 (PGE1) (ADPtest HS). Platelet aggregation was continuously recorded for 5 minutes and quantified as area under the aggregation curve (AUC=AU*min) of aggregation units (AU). (NCT01107899)
Timeframe: Up through 11 days

,,
InterventionAggregation Units * minutes (Mean)
Baseline (ADP) (n=5, n=10, n=6)Day 1 (ADP) (n=5, n=10, n=6)Day 3 (ADP) (n=5, n=10, n=6)Day 5 (ADP) (n=5, n=10, n=4)Day 7 (ADP) (n=5, n=10, n=5)Day 9 (ADP) (n=5, n=10, n=5)Day 11 (ADP) (n=5, n=10, n=5)Baseline (ADP HS) (n=5, n=10, n=6)Day 1 (ADP HS) (n=5, n=10, n=6)Day 3 (ADP HS) (n=5, n=10, n=6)Day 5 (ADP HS) (n=5, n=10, n=4)Day 7 (ADP HS) (n=5, n=10, n=5)Day 9 (ADP HS) (n=5, n=10, n=5)Day 11 (ADP HS) (n=5, n=10, n=5)
Clopidogrel 600 mg536.60248.80347.60428.40478.80529.40555.00361.00166.80257.60256.80263.60388.20373.20
Prasugrel 30 mg459.33118.17134.67296.00295.40484.40564.00344.0070.1790.50145.00170.60343.60404.00
Prasugrel 60 mg601.6090.00140.90231.30316.20549.00500.20411.7034.5079.30114.10189.50344.60365.40

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Platelet Function by LTA at 5 and 20 μM ADP

MPA to 5 and 20 μM ADP were assessed by LTA. (NCT01107899)
Timeframe: 24 hours post-loading dose

,,
Interventionpercent aggregation (Mean)
Maximum Aggregation (20 µM ADP)Maximum Aggregation (5 µM ADP)
Clopidogrel 600 mg52.6039.40
Prasugrel 30 mg31.6725.50
Prasugrel 60 mg27.3022.00

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Platelet Function by Multiplate® ADP Test and ADP Test HS

The Multiplate analyzer was used to assess platelet aggregation based on impedance aggregometry in whole blood. After adding 6.4 µM ADP (ADP test) or 6.4 µM ADP plus 9.4 nM PGE1 (ADP test HS), area under the aggregation curve (AUC) were calculated. (NCT01107899)
Timeframe: 24 hours post-loading dose

,,
Interventionaggregation units*minute (Mean)
ADP Test AUCADP Test HS AUC
Clopidogrel 600 mg248.80166.80
Prasugrel 30 mg118.1770.17
Prasugrel 60 mg90.0034.50

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Percentage of Participants Returning to Baseline Platelet Function

Participants were classified as having platelet function return to baseline after loading dose (LD) on the first day that P2Y12 Reaction Units (PRU) was no more than 60 PRU below baseline and remained in this range. PRU was assessed by Accumetrics Verify Now™ P2Y12. PRU represents the rate and extent of adenosine diphosphate (ADP)-stimulated platelet aggregation. (NCT01107899)
Timeframe: Days 3, 5, 7, 9, and 11

,,
Interventionpercentage of participants (Number)
Day 3Day 5Day 7Day 9Day 11
Clopidogrel 600 mg60.080.0100.0100.0100.0
Prasugrel 30 mg00100.0100.0100.0
Prasugrel 60 mg010.060.0100.0100.0

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Percentage of Poor Pharmacodynamic Responders by Platelet Aggregation at 24 Hours Post-LD

Platelet aggregation was assessed by Accumetrics Verify Now™ P2Y12, and poor responders were those with PRU greater than or equal to 230. (NCT01107899)
Timeframe: 24 hours post-loading dose

Interventionpercentage of participants (Number)
Clopidogrel 600 mg40.0
Prasugrel 60 mg0
Prasugrel 30 mg0

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Active Metabolite Blood Levels to Drug Exposure as Measured by Pharmacokinetics (PK) Through 4 Hours After Dosing

A descriptive pharmacokinetic-pharmacodynamic (PK-PD) analysis comparing prasugrel and clopidogrel active metabolite exposures to MPA in response to 20 µM ADP (by LTA) was conducted as originally intended; however, the graphic output from that analysis is not possible here. Therefore, the PK portion is presented here as AUC and the PD portion is presented in Secondary Outcome Measure #5. AUC was calculated through the last scheduled sampling time of 4 hours [AUC (0-4)] or through the sampling time of the last quantifiable concentration prior to 4 hours. AUC values were denoted AUC(0-tlast) in both instances. (NCT01107912)
Timeframe: Baseline up to 4 hours post-dose

Interventionnanogram*hour/milliliter (ng*hr/mL) (Geometric Mean)
5 mg Prasugrel (Elderly)18.9
10 mg Prasugrel (Elderly)41.2
75 mg Clopidogrel (Elderly)13.0
5 mg Prasugrel (Non-Elderly)16.1
10 mg Prasugrel (Non-Elderly)36.7
75 mg Clopidogrel (Non-Elderly)11.8

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Change From Baseline in Maximum Platelet Aggregation (MPA) as Measured by Light Transmission Aggregometry (LTA) From Baseline at Day 12 of Therapy

Maximum Platelet Aggregation (MPA) to 20 μM ADP was assessed by light transmission aggregometry (LTA), an assay that measures platelet aggregation by determining the amount of light transmitted through a cuvette containing the platelet-rich plasma stimulated with a platelet activator, such as ADP, relative to platelet-poor plasma (100% light transmittance). A lower MPA reflects stronger platelet inhibition, whereas a higher MPA reflects weaker inhibition. (NCT01107912)
Timeframe: Baseline, Day 12

,,,,,
Interventionpercentage of aggregation (Mean)
BaselineDay 12 (n=71, 70, 70, 78, 79, 79)
10 mg Prasugrel (Elderly)78.7545.54
10 mg Prasugrel (Non-Elderly)76.6145.83
5 mg Prasugrel (Elderly)79.1057.05
5 mg Prasugrel (Non-Elderly)76.6156.83
75 mg Clopidogrel (Elderly)79.1163.08
75 mg Clopidogrel (Non-Elderly)76.6159.09

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Change in Maximum Platelet Aggregation (MPA) to 20 Micromoles (μM) Adenosine Diphosphate (ADP) as Measured by Light Transmission Aggregometry (LTA) From Baseline to 12 Days of Therapy in the First Treatment Period

Maximum Platelet Aggregation (MPA) to 20 μM ADP was assessed by light transmission aggregometry (LTA), an assay that measures platelet aggregation by determining the amount of light transmitted through a cuvette containing the platelet-rich plasma stimulated with a platelet activator, such as ADP, relative to platelet-poor plasma (100% light transmittance). Lower MPA values reflect stronger platelet inhibition, whereas higher MPA values reflect weaker inhibition. (NCT01107912)
Timeframe: Baseline, 12 days

,
Interventionpercentage of aggregation (Median)
BaselinePeriod 1 (12 days) (n=71, 79)
10 mg Prasugrel (Non-Elderly)75.0046.00
5 mg Prasugrel (Elderly)78.0058.00

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Change in VerifyNow P2Y12 Reaction Units (PRU) From Baseline to 12 Days of Therapy

The Accumetrics VerifyNow® P2Y12 assay measures platelet aggregation in whole blood and is reported in P2Y12 reaction units (PRU). PRU report the extent of P2Y12 receptor-mediated platelet aggregation calculated as a function of the rate and extent of platelet aggregation in the presence of adenosine phosphate ADP. A lower PRU reflects stronger inhibition of P2Y12, whereas a higher PRU reflects weaker inhibition of P2Y12. (NCT01107912)
Timeframe: Baseline, Day 12

,,,,,
InterventionP2Y12 reaction units (PRU) (Mean)
BaselineDay 12 (n=71, 67, 69, 77, 79, 79)
10 mg Prasugrel (Elderly)314.1184.13
10 mg Prasugrel (Non-Elderly)291.6285.46
5 mg Prasugrel (Elderly)315.63175.52
5 mg Prasugrel (Non-Elderly)291.81177.01
75 mg Clopidogrel (Elderly)314.14212.33
75 mg Clopidogrel (Non-Elderly)291.62181.22

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Change in Vasodilator-associated Stimulated Phosphoprotein (VASP) From Baseline to 12 Days of Therapy

Vasodilator-associated stimulated phosphoprotein (VASP) phosphorylation levels, expressed as the platelet reactivity index (PRI), reflect the degree of thienopyridine-mediated P2Y12 receptor inhibition. A lower PRI reflects stronger inhibition of P2Y12, whereas a higher PRI reflects weaker inhibition of P2Y12. (NCT01107912)
Timeframe: Baseline, Day 12

,,,,,
Interventionpercentage platelet reactive index (PRI) (Mean)
Baseline (n=68, 66, 67, 71, 72, 72)Day 12 (n=67, 65, 67, 73, 74, 73)
10 mg Prasugrel (Elderly)85.6622.66
10 mg Prasugrel (Non-Elderly)86.1827.74
5 mg Prasugrel (Elderly)85.6244.30
5 mg Prasugrel (Non-Elderly)86.1054.72
75 mg Clopidogrel (Elderly)85.6054.95
75 mg Clopidogrel (Non-Elderly)86.1854.53

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Change From Baseline in VerifyNow® P2Y12 Reaction Units (PRU) at Day 12 of Therapy

The Accumetrics VerifyNow® P2Y12 assay measures platelet aggregation in whole blood and is reported in PRU. PRU indicates the extent of P2Y12 receptor-mediated platelet aggregation calculated as a function of rate and extent of platelet aggregation in an adenosine phosphate (ADP)-containing channel of the device. A lower PRU reflects stronger inhibition of platelet aggregation, whereas a higher PRU reflects weaker inhibition of platelet aggregation. (NCT01107925)
Timeframe: Baseline, Day 12

,,,,,
InterventionP2Y12 reaction units (PRU) (Mean)
BaselineDay 12 (n=32,31,32,35,34,34)
10 mg Prasugrel (HBW)311.0102.1
10 mg Prasugrel (LBW)315.355.9
5 mg Prasugrel (HBW)312.8193.9
5 mg Prasugrel (LBW)317.9129.5
75 mg Clopidogrel (HBW)312.8207.0
75 mg Clopidogrel (LBW)315.3151.7

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Change From Baseline in Vasodilator-Associated Stimulated Phosphoprotein (VASP) at Day 12 of Therapy

VASP phosphorylation levels, expressed as the platelet reactivity index (PRI), reflect the degree of thienopyridine-mediated P2Y12 receptor inhibition and were used to compare prasugrel versus clopidogrel, in low body weight (LBW) participants compared to higher body weight (HBW) participants. PRI was calculated by VASP. The PRI indicates the level of P2Y12 receptor inhibition. A lower PRI reflects stronger inhibition of P2Y12 receptor thus stronger platelet inhibition, whereas a higher PRI reflects weaker inhibition of P2Y12 receptor and weaker platelet inhibition. (NCT01107925)
Timeframe: Baseline, Day 12

,,,,,
Interventionpercentage PRI (Mean)
BaselineDay 12 (n=32,31,30,32,36,34)
10 mg Prasugrel (HBW)86.7627.79
10 mg Prasugrel (LBW)86.4415.09
5 mg Prasugrel (HBW)86.7756.87
5 mg Prasugrel (LBW)86.5733.54
75 mg Clopidogrel (HBW)86.7756.35
75 mg Clopidogrel (LBW)86.4439.01

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Change From Baseline in Maximum Platelet Aggregation (MPA) to 20 Micromolar (µM) Adenosine Diphosphate (ADP) at Day 12 (Period 1)

MPA to 20 micromolar (μM) ADP was assessed by light transmission aggregometry (LTA), an assay that measures platelet aggregation by determining the amount of light transmitted through a cuvette containing platelet-rich plasma stimulated with a platelet activator, such as ADP, relative to platelet-poor plasma (100% light transmittance). A lower MPA reflects stronger platelet inhibition, whereas a higher MPA reflects weaker inhibition. (NCT01107925)
Timeframe: Baseline, Day 12

,
Interventionpercent aggregation (Median)
BaselineDay 12 (n=32, 37)
Prasugrel 10 mg (HBW)76.4047.00
Prasugrel 5 mg (LBW)75.0047.00

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Pharmacokinetic (PK) Analysis of the Concentration-Time Curve (AUC)

A pharmacokinetic-pharmacodynamic (PK-PD) analysis comparing MPA (LTA) and AUC was conducted as originally intended, however the graphic output is not possible here. Therefore, the PK portion is presented here as AUC and the PD portion is presented in Secondary Outcome Measure #5. AUC was calculated through the last scheduled sampling time of 4 hours [AUC (0-4)] or through the sampling time of the last quantifiable concentration prior to 4 hours. AUC values were denoted AUC(0-tlast) in both instances. (NCT01107925)
Timeframe: baseline (pre-dose) up to 4 hours post-dose

Interventionnanogram•hour/milliliter (ng•hr/mL) (Geometric Mean)
Prasugrel 5 mg (LBW)28.9
Prasugrel 10 mg (LBW)59.3
Clopidogrel 75 mg (LBW)18.4
Prasugrel 5 mg (HBW)19.4
Prasugrel 10 mg (HBW)46.7
Clopidogrel 75 mg (HBW)12.7

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Change From Baseline in Maximum Platelet Aggregation (MPA) as Measured by Light Transmission Aggregometry (LTA) at Day 12 of Therapy

MPA to 20 micromolar (μM) adenosine diphosphate (ADP) was assessed by LTA, an assay that measures platelet aggregation by determining the amount of light transmitted through a cuvette containing platelet-rich plasma stimulated with a platelet activator, such as ADP, relative to platelet-poor plasma (100% light transmittance). A lower MPA reflects stronger platelet inhibition, whereas a higher MPA reflects weaker inhibition. (NCT01107925)
Timeframe: Baseline , Day 12

,,,,,
Interventionpercent aggregation (Mean)
BaselineDay 12 ( n= 32,32,31,35,37,35)
10 mg Prasugrel (HBW)77.9347.92
10 mg Prasugrel (LBW)76.2038.11
5 mg Prasugrel (HBW)77.6361.90
5 mg Prasugrel (LBW)76.2748.10
75 mg Clopidogrel (HBW)77.6365.28
75 mg Clopidogrel (LBW)76.2051.41

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Adenosine Diphosphate (ADP)-Induced P2Y12 Receptor-Mediated Platelet Aggregation 6 Hours After Prasugrel Loading Dose (LD)

ADP-induced P2Y12 receptor mediated platelet aggregation serves as a biomarker of platelet function. It is measured in P2Y12 Reaction Units (PRU) with lower PRU reflecting stronger inhibition of P2Y12 and reduced platelet aggregation. Least Squares (LS) Mean values were controlled for treatment, visit, treatment and visit interaction, and country. (NCT01115738)
Timeframe: 6 hours after prasugrel loading dose

InterventionPRU (Least Squares Mean)
Placebo and 60-mg Prasugrel57.86
600-mg Clopidogrel and 60-mg Prasugrel35.61
600-mg Clopidogrel and 30-mg Prasugrel53.92

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Mean Change From Baseline to 72 Hours in Laboratory Measurements - Hematocrit

(NCT01115738)
Timeframe: Baseline, 72 hours

Interventionproportion of 1.0 (Mean)
Placebo and 60-mg Prasugrel0.0
600-mg Clopidogrel and 60-mg Prasugrel0.0
600-mg Clopidogrel and 30-mg Prasugrel0.0

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Mean Change From Baseline to 72 Hours in Laboratory Measurements - Hemoglobin

(NCT01115738)
Timeframe: Baseline, 72 hours

Interventiongram per deciliter (g/dL) (Mean)
Placebo and 60-mg Prasugrel-0.9
600-mg Clopidogrel and 60-mg Prasugrel-0.6
600-mg Clopidogrel and 30-mg Prasugrel-0.6

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P2Y12 Reaction Units (PRU) at 6 Hours Post-Prasugrel Loading Dose (LD) by Cytochrome P450 2C19 (CYP2C19)-Predicted Functional Groups - Extensive Metabolizers (EM) and Reduced Metabolizers (RM)

CYP2C19 is a drug metabolizing enzyme. CYP2C19 Extensive metabolizers (EM) are individuals with two fully active / normal function CYP2C19 alleles (*1/*1, *1/*17). CYP2C19 Reduced metabolizers (RM) are individuals with at least one reduced-function CYP2C19 allele (*2/*2, *1/*2). Least Squares (LS) Mean values were controlled for CYP2C19 genetic group. (NCT01115738)
Timeframe: 6 hours after prasugrel loading dose

InterventionPRU (Least Squares Mean)
Placebo and 60 mg Prasugrel-CYP2C19 EM39.036
Placebo and 60 mg Prasugrel -CYP2C19 RM47.750
600 mg Clopidogrel and 60 mg Prasugrel - CYP2C19 EM20.190
600 mg Clopidogrel and 60 mg Prasugrel - CYP2C19 RM23.625
600 mg Clopidogrel and 30 mg Prasugrel - CYP2C19 EM36.478
600 mg Clopidogrel and 30 mg Prasugrel - CYP2C19 RM24.778

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Adenosine Diphosphate (ADP)-Induced P2Y12 Receptor-Mediated Platelet Aggregation at Baseline, 2, 24 and 72 Hours After Prasugrel Loading Dose (LD)

ADP-induced P2Y12 receptor mediated platelet aggregation serves as a biomarker of platelet function. It is measured in P2Y12 Reaction Units (PRU) with lower PRU reflecting stronger inhibition of P2Y12 and reduced platelet aggregation. Least Squares (LS) Mean values were controlled for treatment, visit, treatment and visit interaction, and country. (NCT01115738)
Timeframe: Baseline and 2 hours and 24 hours and 72 hours after prasugrel loading dose

,,
InterventionPRU (Least Squares Mean)
Baseline2 Hours after Prasugrel LD24 Hours after Prasugrel LD72 Hours after Prasugrel LD
600-mg Clopidogrel and 30-mg Prasugrel229.62117.1051.4360.29
600-mg Clopidogrel and 60-mg Prasugrel248.58113.1034.0548.08
Placebo and 60-mg Prasugrel265.51122.5562.7356.95

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Number of Participants With Treatment Emergent Adverse Events (TEAEs)

TEAE is a worsening or new occurrence of adverse event (AE) during treatment compared to baseline. A summary of serious adverse events (SAE) and other nonserious AE are located in the Reported Adverse Events section. (NCT01115738)
Timeframe: Baseline through 72 hours after prasugrel loading dose

,,
Interventionparticipants (Number)
Serious Adverse EventsNonserious Adverse Events
600-mg Clopidogrel and 30-mg Prasugrel131
600-mg Clopidogrel and 60-mg Prasugrel831
Placebo and 60-mg Prasugrel237

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Percentage of Inhibition of Platelet Aggregation

Adenosine Diphosphate (ADP)-induced P2Y12 receptor mediated platelet aggregation serves as a biomarker of platelet function. It is measured in P2Y12 Reaction Units (PRU) with lower PRU reflecting stronger inhibition of P2Y12 and reduced platelet aggregation. The internal BASE standard is an independent measurement and serves as an estimate of the participant's baseline platelet aggregation independent of P2Y12 receptor inhibition. Percent Inhibition of Platelet Aggregation=(1-[PRU/BASE) x 100%, high numbers represent increased platelet inhibition. Least Squares (LS) Mean values were controlled for treatment, visit, treatment and visit interaction, and country. (NCT01115738)
Timeframe: Baseline and 2 and 6 and 24 and 72 hours after loading dose

,,
Interventionpercentage of inhibition (Least Squares Mean)
Baseline2 Hours after Prasugrel LD6 Hours after Prasugrel LD24 Hours after Prasugrel LD72 Hours after Prasugrel LD
600-mg Clopidogrel and 30-mg Prasugrel14.9454.8978.5578.5678.17
600-mg Clopidogrel and 60-mg Prasugrel13.0258.7586.7787.6483.51
Placebo and 60-mg Prasugrel9.7156.0479.8777.5778.48

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Percentage of Poor Responders

Poor responders are those who had P2Y12 Reaction Units (PRU)≥ 240. (NCT01115738)
Timeframe: Baseline and 2 and 6 and 24 and 72 hours after loading dose

,,
Interventionpercentage of participants (Number)
Baseline2 Hours after Prasugrel LD6 Hours after Prasugrel LD24 Hours after Prasugrel LD72 Hours after Prasugrel LD
600-mg Clopidogrel and 30-mg Prasugrel51.221.44.48.80
600-mg Clopidogrel and 60-mg Prasugrel66.712.85.32.90
Placebo and 60-mg Prasugrel68.123.311.69.50

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P2Y12 Reaction Units (PRU) of Clopidogrel Treated Participants at Baseline by Cytochrome P450 2C19 (CYP2C19)-Predicted Functional Groups - CYP2C19 Extensive Metabolizers (EM) and Reduced Metabolizers (RM)

CYP2C19 is a drug metabolizing enzyme. CYP2C19 Extensive metabolizers (EM) are individuals with two fully active / normal function CYP2C19 alleles (*1/*1, *1/*17). CYP2C19 Reduced metabolizers (RM) are individuals with at least one reduced-function CYP2C19 allele (*2/*2, *1/*2). Least Squares (LS) Mean values were controlled for CYP2C19 genetic group. (NCT01115738)
Timeframe: Baseline

InterventionPRU (Least Squares Mean)
Clopidogrel at Baseline -CYP2C19 EM243.549
Clopidogrel at Baseline - CYP2C19 RM240.100

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P2Y12 Reaction Units (PRU) as Measured by Accumetrics VerifyNow® P2Y12 (VN P2Y12) at 30 Days

PRU represents the rate and extent of adenosine (ADP)-stimulated platelet aggregation. The VN P2Y12 assay is a point-of-care device that measures platelet aggregation with single-use, disposable cartridges. A low PRU reflects stronger inhibition of P2Y12, whereas a high PRU reflects weaker inhibition of P2Y12. The Least Squares Mean values were calculated from a mixed-effects model repeated measures analysis with baseline measurement, stratification variable sickle cell genotype, treatment, time, and time*treatment interaction as fixed effects, and participant as a random effect in the model. (NCT01167023)
Timeframe: 30 days

InterventionP2Y12 Reaction Units (PRU) (Least Squares Mean)
Placebo336.8
5 mg Prasugrel208.5

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Percentage of Participants With Hemorrhagic Events Requiring Medical Intervention During the Treatment Duration

A hemorrhagic event requiring medical intervention. Medical intervention was defined as any medical attention resulting in therapy or further investigation during the 30-day treatment duration. (NCT01167023)
Timeframe: Baseline through 30 days

Interventionpercentage of participants (Number)
Placebo0
5 mg Prasugrel0

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Percentage of Participants With Hemorrhagic Treatment-Emergent Adverse Events (TEAEs) During the Treatment Duration

TEAEs were defined as AEs that occurred or worsened after receiving the study drug. (NCT01167023)
Timeframe: Baseline through 30 days

Interventionpercentage of participants (Number)
Placebo5.3
5 mg Prasugrel19.5

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Platelet Reactivity Index (PRI) Measured by Vasodilator-Associated Stimulated Phosphoprotein (VASP) at 30 Days

PRI was calculated by VASP phosphorylation assay using flow cytometry. The PRI indicates the level of P2Y12 inhibition. A low PRI reflects strong inhibition of P2Y12, whereas a high PRI reflects weak/absent inhibition of P2Y12. The Least Squares (LS) Mean values were calculated from a mixed-effects model repeated measures (MMRM) analysis with baseline measurement, stratification variable sickle cell genotype, treatment, time, and time*treatment interaction as fixed effects, and participant as a random effect in the model. (NCT01167023)
Timeframe: 30 days

Interventionpercentage of PRI (Least Squares Mean)
Placebo74.843
5 mg Prasugrel50.792

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Inhibition of Platelet Aggregation (IPA) to 5 Micromolar (µM) Adenosine Diphosphate (ADP) at Day 12

"IPA is calculated as a percent decrease of maximum platelet aggregation (MPA) from baseline using the following formula:~([MPA at baseline - MPA postbaseline] / MPA at baseline) x 100%" (NCT01178099)
Timeframe: Day 12

Interventionpercent inhibition (Mean)
Prasugrel Healthy Participants61.2
Prasugrel Sickle Cell Disease41.7

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P2Y12 Reaction Units (PRU)-Derived VerifyNow (VN) Percent Inhibition at Day 12

"PRU-derived VN percent inhibition is calculated as a percent decrease of PRU from baseline using the following formula:~([PRU at baseline - PRU at time of post baseline] / PRU at baseline) x 100%" (NCT01178099)
Timeframe: Day 12

Interventionpercent inhibition (Mean)
Prasugrel Healthy Participants65.8
Prasugrel Sickle Cell Disease47.8

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Area Under the Plasma Concentration-Time Curve (AUC) From Time of Dosing Through the Sampling Time of the Last Quantifiable Concentration [AUC(0-tlast)] for Prasugrel's Active Metabolite, R-138727

The AUC of Prasugrel's active metabolite, R-138727, was calculated through the sampling time of the last quantifiable plasma concentration [AUC(0-tlast)]. Geometric Least Squares (LS) Means were obtained. The log-transformed AUC was analyzed with a mixed effect model with dose, population, dose*population interaction as fixed effects, and participant as a random effect. (NCT01178099)
Timeframe: Time of dosing up to 8 hours post-dose on Day 1 and Day 12

,
Interventionnanogram*hour per milliliter (ng*h/mL) (Least Squares Mean)
10 mg SD (overall)7.5 mg MD (N=9, 8)5 mg MD (N=4, 4)
Prasugrel Healthy Participants68.250.439.8
Prasugrel Sickle Cell Disease71.545.236.0

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Area Under the Plasma Concentration-Time Curve (AUC) From Time of Dosing Through the Sampling Time of the Last Quantifiable Concentration [AUC(0-tlast)] of Prasugrel's Inactive Metabolites, R-95913, R-106583, and R-119251

AUC was calculated through the sampling time of the last quantifiable plasma concentration [AUC(0-tlast)]. Geometric Least Squares (LS) Means were obtained. The log-transformed AUC was analyzed with a mixed effect model with dose, population, dose*population interaction as fixed effects, and participant as a random effect. (NCT01178099)
Timeframe: Day 1, Day 12

,
Interventionnanogram*hour per milliliter (ng*h/mL) (Least Squares Mean)
10 mg SD (overall) for R-959137.5 mg MD for R-95913 (N=9, 8)5 mg MD for R-95913 (N=4, 4)10 mg SD (overall) for R-1065837.5 mg MD for R-106583 (N=9, 8)5 mg MD for R-106583 (N=4, 4)10 mg SD (overall) for R-1192517.5 mg MD for R-119251 (N=9, 8)5 mg MD for R-119251 (N=4, 4)
Prasugrel Healthy Participants52.849.433.624821315132.722.220.1
Prasugrel Sickle Cell Disease80.270.947.924117414438.323.816.3

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Change From Baseline in the Area Under the Aggregation Curve at Day 12

AUC to 20 micromolar (μM) adenosine diphosphate (ADP), 6.5μM ADP, Collagen, and thrombin receptor activator for peptide 6 (TRAP-6) were calculated by whole blood multi-electrode aggregometry (MEA) assay. Platelet aggregation was continuously recorded for 5 minutes and quantified as area under the aggregation curve, measured in aggregation units*minutes (AU*min). (NCT01178099)
Timeframe: Baseline, Day 12

,
Interventionaggregation units*minutes (AU*min) (Mean)
AU*min to 6.5 µM ADP at Baseline (Day 1)AU*min to 6.5 µM ADP, Day 12 Change (N=13, 11)AU*min to 20 µM ADP at Baseline (Day 1)AU*min to 20 µM ADP, Day 12 Change (N=13, 11)AU*min to Collagen at Baseline (Day 1)AU*min to Collagen, Day 12 Change (N=13, 11)AU*min to TRAP-6 at Baseline (Day 1)AU*min to TRAP-6, Day 12 Change (N=13, 11)
Prasugrel Healthy Participants76.5-49.53885.0-54.07785.5-7.692120.2-7.846
Prasugrel Sickle Cell Disease106.4-63.182108.1-66.182102.3-3.000131.5-2.818

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Change From Baseline in the Maximum Platelet Aggregation (MPA) to 20 Micromolar (µM) Adenosine Diphosphate (ADP) at Day 12

MPA to 20 μM ADP was assessed by light transmission aggregometry (LTA), an assay that measures platelet aggregation by determining the amount of light transmitted through a cuvette containing the platelet-rich plasma stimulated with a platelet activator, such as ADP, relative to platelet-poor plasma (100% light transmittance). The LTA results were collected as MPA, for which low values indicate strong platelet inhibition. (NCT01178099)
Timeframe: Baseline, Day 12

,
Interventionpercent aggregation (Mean)
Baseline (Day 1)Change from Baseline at Day 12 (N=12, 9)
Prasugrel Healthy Participants85.0-43.3
Prasugrel Sickle Cell Disease73.4-30.9

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Change From Baseline in the Maximum Platelet Aggregation (MPA) to 5 Micromolar (µM) Adenosine Diphosphate (ADP) at Day 12

MPA to 5 μM ADP was assessed by light transmission aggregometry (LTA), an assay that measures platelet aggregation by determining the amount of light transmitted through a cuvette containing the platelet-rich plasma stimulated with a platelet activator, such as ADP, relative to platelet-poor plasma (100% light transmittance). The LTA results were collected as MPA, for which low values indicate strong platelet inhibition. (NCT01178099)
Timeframe: Baseline, Day 12

,
Interventionpercent aggregation (Mean)
Baseline (Day 1)Change from Baseline at Day 12 (N=12, 7)
Prasugrel Healthy Participants80.4-49.9
Prasugrel Sickle Cell Disease73.1-33.4

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Change From Baseline in the P2Y12 Reaction Units (PRU) Device Reported P2Y12 Percent Inhibition at Day 12

PRU device reported VerifyNow percent inhibition is reported by Accumetrics VerifyNow™ P2Y12 (VN-P2Y12) assay, a point-of-care device that measures platelet aggregation with single-use, disposable cartridges. (NCT01178099)
Timeframe: Baseline, Day 12

,
Interventionpercent inhibition (Mean)
Baseline (Day 1)Change from Baseline at Day 12 (N=11, 10)
Prasugrel Healthy Participants12.060.1
Prasugrel Sickle Cell Disease1.047.9

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Change From Baseline in the Percent Aggregation to 20 µM Adenosine Diphosphate (ADP) at Day 12

Percent aggregation was assessed by Plateletworks® ADP assay, a whole blood-based test of platelet aggregation for the assessment of platelet inhibition. The assay determines the change in single platelet count due to activation and aggregation by ADP and inhibition thereof by antiplatelet agents. (NCT01178099)
Timeframe: Baseline, Day 12

,
Interventionpercent aggregation (Mean)
Baseline (Day 1)Change from Baseline at Day 12 (N=12, 10)
Prasugrel Healthy Participants91.3-53.0
Prasugrel Sickle Cell Disease74.0-46.7

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Change From Baseline in the Platelet Reactivity Index (PRI) of Prasugrel at Day 12

PRI was calculated by vasodilator-associated phosphoprotein (VASP) phosphorylation assay using flow cytometry (FC) and a VASP assay using enzyme-linked immunosorbent assay (ELISA). The PRI indicates the level of P2Y12 inhibition. A low PRI reflects strong inhibition of P2Y12, whereas a high PRI reflects weak/absent inhibition of P2Y12. (NCT01178099)
Timeframe: Baseline, Day 12

,
Interventionpercentage PRI (Mean)
Flow Cytometry at Baseline (Day 1), (N=12, 8)Flow Cytometry, Day 12 Change, (N=12, 8)ELISA at Baseline (Day 1), (N=11, 13)ELISA, Day 12 Change (N=11, 12)
Prasugrel Healthy Participants78.91-49.88394.70-70.436
Prasugrel Sickle Cell Disease59.36-46.00092.03-68.117

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Change From Baseline in the Residual Platelet Aggregation (RPA) to 20 Micromolar (µM) Adenosine Diphosphate (ADP) at Day 12

RPA is the percentage aggregation as measured by light transmission aggregometry (LTA) at 6 minutes after the addition of 20 μM ADP. LTA is an assay that measures platelet aggregation by determining the amount of light transmitted through a cuvette containing the platelet-rich plasma stimulated with a platelet activator, such as ADP, relative to platelet-poor plasma (100% light transmittance). (NCT01178099)
Timeframe: Baseline, Day 12

,
Interventionpercent aggregation (Mean)
Baseline (Day 1)Change from Baseline at Day 12 (N=12, 8)
Prasugrel Healthy Participants84.1-67.0
Prasugrel Sickle Cell Disease72.2-45.5

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Maximum Concentration (Cmax) of Prasugrel's Active Metabolite, R-138727

Cmax was observed from the data and used to calculate Geometric Least Squares (LS) Means. The log-transformed Cmax was analyzed with a mixed effect model with dose, population, dose*population interaction as fixed effects, and participant as a random effect. (NCT01178099)
Timeframe: Day 1, Day 12

,
Interventionnanogram per milliliter (ng/mL) (Least Squares Mean)
10 mg SD (overall)7.5 mg MD (N=9, 8)5 mg MD (N=4, 4)
Prasugrel Healthy Participants67.962.540.9
Prasugrel Sickle Cell Disease64.738.242.0

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Maximum Concentration (Cmax) of Prasugrel's Inactive Metabolites, R-95913, R-106583, and R-119251

Cmax was observed from the data and used to calculate geometric Least Squares (LS) Means. The log-transformed Cmax was analyzed with a mixed effect model with dose, population, dose*population interaction as fixed effects, and participant as a random effect. (NCT01178099)
Timeframe: Day 1, Day 12

,
Interventionnanogram per milliliter (ng/mL) (Least Squares Mean)
10 mg SD (overall) for R-959137.5 mg MD for R-95913 (N=9, 8)5 mg MD for R-95913 (N=4, 4)10 mg SD (overall) for R-1065837.5 mg MD for R-106583 (N=9, 8)5 mg MD for R-106583 (N=4, 4)10 mg SD (overall) for R-1192517.5 mg MD for R-119251 (N=9, 8)5 mg MD for R-119251 (N=4, 4)
Prasugrel Healthy Participants30.233.418.468.556.838.724.915.520.3
Prasugrel Sickle Cell Disease45.436.334.459.838.734.826.515.915.5

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Change From Baseline in the Residual Platelet Aggregation (RPA) to 5 Micromolar (µM) Adenosine Diphosphate (ADP) at Day 12

RPA is the percentage aggregation as measured by LTA at 6 minutes after the addition of 5 μM ADP. LTA is an assay that measures platelet aggregation by determining the amount of light transmitted through a cuvette containing the platelet-rich plasma stimulated with a platelet activator, such as ADP, relative to platelet-poor plasma (100% light transmittance). (NCT01178099)
Timeframe: Baseline, Day 12

,
Interventionpercent aggregation (Mean)
Baseline (Day 1)Change from Baseline at Day 12 (N=12, 7)
Prasugrel Healthy Participants76.9-70.3
Prasugrel Sickle Cell Disease72.2-47.3

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Inhibition of Platelet Aggregation (IPA) to 20 Micromolar (µM) Adenosine Diphosphate (ADP) at Day 12

"IPA is calculated as a percent decrease of maximum platelet aggregation (MPA) from baseline using the following formula:~([MPA at baseline - MPA postbaseline] / MPA at baseline) x 100%" (NCT01178099)
Timeframe: Day 12

Interventionpercent inhibition (Mean)
Prasugrel Healthy Participants52.6
Prasugrel Sickle Cell Disease38.5

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PRI Levels at 4 Hours

(NCT01201772)
Timeframe: 4 hours after treatment

Interventionpercentage of platelet reactivity (Mean)
Prasugrel 10mg28.8
Prasugrel 30mg11
Prasugrel 60mg2.8

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Responder Rate by Treatment and Smoking Status Based on Platelet Reactivity Index (PRI) <= 50%

"Numerous studies have established an association between high on-treatment platelet reactivity with clopidogrel and an increased risk for post-PCI ischemic events. In this study, the percentages of responders and poor responders following treatment with prasugrel and clopidogrel were compared. Poor responders were defined based on an Accumetrics VerifyNow PRU >235 and a VASP PRI >50%, as assessed 24 hours after the 9th maintenance dose." (NCT01260584)
Timeframe: Day 10 for Active Treatment Periods 1 and 2

Intervention% participants with PRI <=50% (Number)
Prasugrel Smokers96.0
Prasugrel Non-Smokers82.7
Clopidogrel Smokers51.1
Clopidogrel Non-Smokers44.4

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Assessment of P2Y12 Reaction Units (PRU) by Treatment and Smoking Status

"Day 10 occurs in each treatment period at which time data collections are made. 12.1.4. Responders and Poor Responders~Numerous studies have established an association between high on-treatment platelet reactivity with clopidogrel and an increased risk for post-PCI ischemic events. In this study, the percentages of responders and poor responders following treatment with prasugrel and clopidogrel were compared. Poor responders were defined based on an Accumetrics VerifyNow PRU >235 and a VASP PRI >50%, as assessed 24 hours after the 9th maintenance dose." (NCT01260584)
Timeframe: Day 10 for Active Treatment Periods 1 and 2

InterventionP2Y12 reaction unit (Least Squares Mean)
Prasugrel Smokers85.1
Prasugrel Non-Smokers106.3
Clopidogrel Smokers178.9
Clopidogrel Non-Smokers215.1

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Assessment of Vasodilator Stimulated Phosphoprotein (VASP) by Treatment and Smoking Status

"Day 10 occurs in each treatment period at which time data collections are made. Numerous studies have established an association between high on-treatment platelet reactivity with clopidogrel and an increased risk for post-PCI ischemic events. In this study, the percentages of responders and poor responders following treatment with prasugrel and clopidogrel were compared. Poor responders were defined based on an Accumetrics VerifyNow PRU >235 and a VASP PRI >50%, as assessed 24 hours after the 9th maintenance dose." (NCT01260584)
Timeframe: Day 10 for Active Treatment Periods 1 and 2

Intervention% vasodilator stimulated phosphoprotein (Least Squares Mean)
Prasugrel Smokers25.4
Prasugrel Non-Smokers31.2
Clopidogrel Smokers48.1
Clopidogrel Non-Smokers55.7

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Characterization of the Pharmacokinetics (PK) Area Under Curve (AUC)(0-Last) of the Active Metabolite of Prasugrel and the Active Metabolite of Clopidogrel in Smokers and Non-smokers

Blood samples for determination of plasma concentrations of the prasugrel active metabolite, clopidogrel active metabolite, and clopidogrel inactive metabolite will be collected following the administration of the 10th (last) maintenance dose of each of the 2 Active Treatment Periods at 0.5, 1, 2, 4, and 6 hours post-dose. (NCT01260584)
Timeframe: After dose on Day 10 of Active Treatment Periods 1 and 2

Interventionhr*ng/mL (Geometric Mean)
Prasugrel Smokers53.7
Prasugrel Non-Smokers48.1
Clopidogrel Smokers19.9
Clopidogrel Non-Smokers16.2

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Characterization of the Pharmacokinetics (PK) Cmax of the Active Metabolite of Prasugrel and the Active Metabolite of Clopidogrel in Smokers and Non-smokers

(NCT01260584)
Timeframe: After dose on Day 10 of Active Treatment Periods 1 and 2

Interventionng/mL (Geometric Mean)
Prasugrel Smokers42.9
Prasugrel Non-Smokers35.9
Clopidogrel Smokers14.1
Clopidogrel Non-Smokers10.8

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Inhibition of Platelet Aggregation (IPA) in Prasugrel-treated and Clopidogrel-treated Smokers and Non-smokers Following 9 Days of Maintenance Therapy.

IPA will be measured by the Accumetrics P2Y12 Assay Device. Response will be assessed in P2Y12 Reaction Units and as Platelet Reactivity Index (vasodilator-stimulated phosphoprotein assay). (NCT01260584)
Timeframe: Baseline to day 10 for Active Treatment Periods 1 and 2

Interventionpercentage of device derived inhibition (Least Squares Mean)
Prasugrel Smokers70.3
Prasugrel Non-Smokers65.6
Clopidogrel Smokers38.6
Clopidogrel Non-Smokers30.9

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Responder Rate by Treatment and Smoking Status Based on P2Y12 Reaction Units (PRU) <= 235

(NCT01260584)
Timeframe: Day 10 for Active Treatment Periods 1 and 2

Intervention% participants with PRU <=235 (Number)
Prasugrel Smokers98.0
Prasugrel Non-Smokers96.2
Clopidogrel Smokers76.6
Clopidogrel Non-Smokers61.1

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Pharmacokinetics: Time of Maximum Concentration (Tmax) of Prasugrel's Active Metabolite (PRAS-AM)

(NCT01430091)
Timeframe: Pre-dose up to 8 hours post-dose after each treatment

Interventionhours (Median)
Clinical Tablet0.50
ODT on Top of Tongue0.50
ODT on Top of Tongue With Juice Chaser0.75
ODT Chewed and Swallowed0.75
ODT Placed Under the Tongue0.50

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Pharmacokinetics: Maximum Concentration (Cmax) of Prasugrel's Active Metabolite (PRAS-AM)

(NCT01430091)
Timeframe: Pre-dose up to 8 hours post-dose after each treatment

Interventionnanogram per milliliter (ng/mL) (Geometric Mean)
Clinical Tablet47.3
ODT on Top of Tongue47.6
ODT on Top of Tongue With Juice Chaser32.3
ODT Chewed and Swallowed38.3
ODT Placed Under the Tongue41.9

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Pharmacokinetics: Area Under the Concentration-Time Curve From Time Zero to the Last Measureable Concentration (AUC[0-tlast]) of Prasugrel's Active Metabolite (PRAS-AM)

(NCT01430091)
Timeframe: Pre-dose up to 8 hours post-dose after each treatment

Interventionnanogram * hour per milliliter (ng*h/mL) (Geometric Mean)
Clinical Tablet43.3
ODT on Top of Tongue42.7
ODT on Top of Tongue With Juice Chaser42.3
ODT Chewed and Swallowed41.0
ODT Placed Under the Tongue42.0

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Occurrence of Adverse Events

The number of subjects reporting any AEs will be tabulated. (NCT01452152)
Timeframe: One year

Interventionparticipants (Number)
Genotype-directed, Clopidogrel1
Standard of Care3

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Occurrence of Bleeding Events

Bleeding events will classified by the Bleeding Academic Research Consortium definition. The number of bleeding events will be tabulated. (NCT01452152)
Timeframe: One year

Interventionevents (Number)
Genotype-directed, Clopidogrel0
Standard of Care0

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Occurrence of Post-randomization Cardiovascular Events

Cardiovascular events include non-fatal myocardial infarction, non-fatal stroke, definite or probable stent thrombosis (ARC definition) and death secondary to any cardiovascular cause. (NCT01452152)
Timeframe: One year

Interventionparticipants (Number)
Genotype-directed, Clopidogrel0
Standard of Care0

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Post-treatment Platelet Aggregation

Platelet aggregation will be performed on a subset of subjects using VerifyNow P2Y12 which measures platelet reactivity due to the effect of a P2Y12. Values less than 180 P2Y12 Reaction Units (PRU) suggest evidence of a P2Y12 inhibitor effect. Platelet aggregation studies are optional and will not be used to modulate antiplatelet therapy. (NCT01452152)
Timeframe: 10 days

Interventionpercentage of inhibition (Mean)
Genotype-directed, Clopidogrel33.7

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Composite of All-cause Death, Myocardial Infarction (MI), Stroke and Repeat Revascularization

(NCT01452152)
Timeframe: One year

Interventionparticipants (Number)
Genotype-directed, Clopidogrel0
Standard of Care0

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Pharmacokinetics: Area Under the Concentration-Time Curve (AUC) of Prasugrel Active Metabolite (Pras-AM)

AUC of Pras-AM from time 0 up to the last sampling time of 4 hours postdose [AUC(0-tlast)] is reported by dose administered [0.03, 0.05, 0.07, 0.09, 0.11, 0.13, 0.15, 0.2, 0.25, 0.3, 0.35, 0.4, 0.45, 0.5, 0.55, and 0.6 milligrams per kilogram (mg/kg)] during Part A (single-dose range finding phase) and is reported for doses administered on site (0.06, 0.08, and 0.12 mg/kg) during Part B (once-daily repeated dosing phase) of the study. Four participants received the same dose at multiple visits where pharmacokinetic samples were collected. (NCT01476696)
Timeframe: Parts A and B: 0.5, 1, 1.5, 2, 4 hours postdose

Interventionnanograms*hour per milliliter (ng*hr/mL) (Geometric Mean)
Part A: 0.03 mg/kg (n=2)Part A: 0.05 mg/kg (n=2)Part A: 0.07 mg/kg (n=2)Part A: 0.09 mg/kg (n=2)Part A: 0.11 mg/kg (n=1)Part A: 0.13 mg/kg (n=2)Part A: 0.15 mg/kg (n=2)Part A: 0.2 mg/kg (n=2)Part A: 0.25 mg/kg (n=3)Part A: 0.3 mg/kg (n=6)Part A: 0.35 mg/kg (n=11)Part A: 0.4 mg/kg (n=14)Part A: 0.45 mg/kg (n=8)Part A: 0.5 mg/kg (n=7)Part A: 0.55 mg/kg (n=1)Part A: 0.6 mg/kg (n=3)Part B: 0.06 mg/kg (n=7)Part B: 0.08 mg/kg (n=17)Part B: 0.12 mg/kg (n=8)
Entire Study Population8.6814.520.831.322.250.335.243.760.787.911110813618687.029916.327.138.5

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Number of Participants With Hemorrhagic Events Requiring Medical Intervention

Hemorrhagic events were determined by the study investigator. Medical intervention was defined as any medical attention resulting in therapy or further investigation, as determined by a trained medical professional. (NCT01476696)
Timeframe: Part B: Baseline up to Day 36

Interventionparticipants (Number)
Part B: Prasugrel Once-Daily Dose0

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Number of Participants With Pain

"The number of participants who answered yes to the first question in the Sickle Cell Disease Pain (SCD) Questionnaire is reported. Question 1: In the past 2 weeks, did you experience any sickle cell pain?" (NCT01476696)
Timeframe: Part B: Baseline and Day14 ± 4 days postdose in each dosing period

Interventionparticipants (Number)
Part B: Baseline6
Part B: Prasugrel Once-Daily Dose (0.06 mg/kg)4
Part B: Prasugrel Once-Daily Dose (0.08 mg/kg)1
Part B: Prasugrel Once-Daily Dose (0.12 mg/kg)2

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Percentage of Platelet Inhibition as Measured by VerifyNow™P2Y12 (VN)

Accumetrics VN assay: A point-of-care device that measures platelet aggregation. Percentage of platelet inhibition is reported by dose administered [0.03, 0.05, 0.07, 0.09, 0.11, 0.13, 0.15, 0.2, 0.25, 0.3, 0.35, 0.4, 0.45, 0.5, 0.55, and 0.6 milligrams per kilogram (mg/kg)] during Part A (single-dose range finding phase) and also during the once-daily repeated dosing phase in Part B, at steady state, 14 ± 4 days after each new dose (0.06, 0.08, and 0.12 mg/kg) is administered. One participant received the same dose at multiple visits (Part A) and one participant received the same daily dose during both dosing periods in Part B. (NCT01476696)
Timeframe: Part A: 4 hours postdose and Part B: at steady state (14 ± 4 days after the start of each new dosage)

Interventionpercentage of platelet inhibition (Mean)
Part A: 0.03 mg/kg (n=2)Part A: 0.05 mg/kg (n=2)Part A: 0.07 mg/kg (n=2)Part A: 0.08 mg/kg (n=18)Part A: 0.09 mg/kg (n=2)Part A: 0.11 mg/kg (n=1)Part A: 0.13 mg/kg (n=2)Part A: 0.15 mg/kg (n=2)Part A: 0.2 mg/kg (n=2)Part A: 0.25 mg/kg (n=3)Part A: 0.3 mg/kg (n=6)Part A: 0.35 mg/kg (n=11)Part A: 0.4 mg/kg (n=14)Part A: 0.45 mg/kg (n=8)Part A: 0.5 mg/kg (n=7)Part A: 0.55 mg/kg (n=1)Part A: 0.6 mg/kg (n=3)Part B: 0.06 mg/kg (n=8)Part B: 0.08 mg/kg (n=18)Part B: 0.12 mg/kg (n=8)
Entire Study Population2.00.00.07.72.50.09.54.00.018.042.338.039.135.355.931.070.338.637.848.1

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Any Bleeding Event

"Bleeding classified by the TIMI hemorrhage classification scheme:~Minor: any clinically overt sign of hemorrhage (including imaging) that is associated with a hemoglobin drop of 3 to < 5 g/dL~Major: (1) if it is intracranial, or (2) clinically significant overt signs of hemorrhage associated with a drop inhemoglobin of > 5 g/dL" (NCT01515345)
Timeframe: 30days

Interventionparticipants (Number)
Standard Therapy17
Individualized Therapy9

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Definite Stent Thrombosis

"The angiographic or pathological confirmation of stent thrombosis is called definite stent thrombosis" (NCT01515345)
Timeframe: 30 days

Interventionparticipants (Number)
Standard Therapy1
Individualized Therapy0

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Probable Stent Thrombosis

"Probable stent thrombosis is considered to have occurred in case of~any unexplained death within the first 30 days.~any MI that is related to documented acute ischemia in the territory of the implanted stent without angiographic confirmation of stent thrombosis and in the absence of any other obvious cause, irrespective of the time after the index procedure" (NCT01515345)
Timeframe: 30days

Interventionparticipants (Number)
Standard Therapy2
Individualized Therapy0

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Total Target Saphenous Vein Graft Atheroma Volume, as Assessed by Intravascular Ultrasonography

Total target saphenous vein graft atheroma volume (mm3) as assessed by Intravascular ultrasound imaging in imaged saphenous vein grafts. (NCT01560780)
Timeframe: 12 months

Interventionmm3 (Mean)
Arm 1: Prasugrel349
Arm 2: Placebo358

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Saphenous Vein Graft Lipid Core Burden Index, as Assessed at Near-infrared Intracoronary Spectroscopy

Lipid core burden as measured by Lipid Core Burden Index on near infrared intracoronary spectroscopy imaging of saphenous vein graft. Lipid Core Burden Index is defined as the fraction of pixels within the scanned region with a probability >0.60 that a lipid core plaque is present (calculated by an algorithm developed to identify the NIRS signals associated with the molecular structure of lipids), multiplied by 1000 using EchoPlaque software (INDEC Medical Systems; Los Altos, CA) . Thus, the lipid core burden index (LCBI) is a quantitative summary metric of the probability of the presence of lipid within the scanned region, with a range of 0-1000, with higher indices indicating a higher proportion of pixels with a >0.6 probability of lipid being present in the pullback of the catheter along the length of the entire vessel. (NCT01560780)
Timeframe: 12 months

Interventionunits on a scale (Mean)
Arm 1: Prasugrel7.5
Arm 2: Placebo7.4

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Prevalence of Intragraft Thrombus at 12-month Follow-up Optical Coherence Tomography Imaging

Number of patients with intragraft thrombus seen at 12 month follow-up by optical coherence tomography in imaged saphenous vein graft (NCT01560780)
Timeframe: 12 months

InterventionParticipants (Count of Participants)
Arm 1: Prasugrel14
Arm 2: Placebo14

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Number of Patients With Severe Bleeding Using the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO) Criteria

Number of patients with major bleeding defined by the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries criteria. (NCT01560780)
Timeframe: 12 months

InterventionParticipants (Count of Participants)
Arm 1: Prasugrel1
Arm 2: Placebo0

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Number of Patients With Angiographic Saphenous Vein Graft Failure

Number of patients with angiographic saphenous vein graft failure (defined as =75% SVG diameter stenosis in at least one saphenous vein graft) (NCT01560780)
Timeframe: 12 months

InterventionParticipants (Count of Participants)
Arm 1: Prasugrel7
Arm 2: Placebo12

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Normalized Total Target Saphenous Vein Graft Atheroma Volume, as Assessed by Intravascular Ultrasonography

"On IVUS images, atheroma volume was defined as the sum of the cross-sectional areas between the leading edges of the lumen and external elastic membrane. Total Target SVG atheroma volume was calculated as:~∑(EEM area - Lumen area).~Normalized atheroma volume represents the atheroma volume corrected for pullback length, and this parameter was calculated as:~∑(EEM area - Lumen area)/number of frames in pullback" (NCT01560780)
Timeframe: 12 months

Interventionmm3/frame (Mean)
Arm 1: Prasugrel0.093
Arm 2: Placebo0.079

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Major Adverse Cardiac Events, Defined as the Composite of Death, Acute Coronary Syndrome, or Coronary Revascularization) During Follow-up

Number of patients with the composite outcome of death, acute coronary syndrome, or coronary revascularization. (NCT01560780)
Timeframe: 12 months

InterventionParticipants (Count of Participants)
Arm 1: Prasugrel8
Arm 2: Placebo4

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Percentage of Subjects With High On-treatment Platelet Reactivity

"Percentage of subjects with High on-treatment Platelet Reactivity (HPR) defined as a) >= 208 PRU and b) >= 230 PRU by the VerifyNow P2Y12 assay and c) >50% PRI by the VASP assay, 2, 4, 24, and 48 hours and 7 days after first randomized study treatment.~A poor response of the platelets to drug, called High Residual Platelet Reactivity (HRPR), has been incriminated to account for a recurrence of ischemic events" (NCT01587651)
Timeframe: 2, 4, 24, 48 hours, 7 days after first randomized dose

,,,
Interventionpercentage of subjects (Number)
>= 208 PRU 2 hours post dose>= 208 PRU 4 hours post dose>= 208 PRU 24 hours post dose>= 208 PRU 48 hours post dose>= 208 PRU 7 days post dose>= 230 PRU by VerifyNow P2Y12 2 hours post dose>= 230 PRU by VerifyNow P2Y12 4 hours post dose>= 230 PRU by VerifyNow P2Y12 24 hours post dose>= 230 PRU by VerifyNow P2Y12 48 hours post dose>= 230 PRU by VerifyNow P2Y12 7 days post dose>50% PRI by VASP assay 2 hours post dose>50% PRI by VASP assay 4 hours post dose>50% PRI by VASP assay 24 hours post dose>50% PRI by VASP assay 48 hours post dose>50% PRI by VASP assay 7 days post dose
Prasugrel Combined Groups0017.530.21.50014.322.21.53.51.821.34515.5
Prasugrel Loading Dose003.316.13.2003.36.53.23.603.413.823.1
Prasugrel Maintenance Dose0037.543.800024.237.503.43.437.574.29.4
Ticagrelor00003000033.33.312.96.33.4

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Platelet Reactivity Index

"Platelet Reactivity Index (PRI) by the Vasodilator-Stimulated Phosphoprotein(VASP) assay 2, 4, 24, 48 hours and 7 days after first randomized study treatment.~The VASP assay is an indirect, but relatively specific measure of inhibition of P2Y12-induced platelet activation. The assay quantifies the level of phosphorylation of the intracellular protein VASP, which undergoes phosphorylation when platelet P2Y12 receptors are blocked. The level of VASP phosphorylation, expressed as the PRI, represents the percentage inhibition relative to an assay baseline/maximal P2Y12-independent platelet aggregation." (NCT01587651)
Timeframe: 2, 4, 24, 48 hours, 7 days after first randomized dose

,,,
Interventionpercentage PRI (Least Squares Mean)
2 hours post-dose4 hours post-dose24 hours post-dose48 hours post-dose7 days post-dose
Prasugrel Combined Groups18.216.334.348.133.5
Prasugrel Loading Dose15.811.424.238.038.8
Prasugrel Maintenance Dose20.420.943.757.729.1
Ticagrelor13.214.319.118.719.8

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P2Y12 Reaction Units

P2Y12 Reaction Units (PRU) measured by VerifyNow P2Y12 assay VerifyNow P2Y12 assay, developed by Accumetrics, Inc. (San Diego, CA, USA), has been approved by the FDA to assess clopidogrel response using whole blood in a point-of-care testing fashion. Platelet aggregation with this system is defined by PRU, with a higher PRU indicative of greater platelet aggregation, and a lower PRU indicative of inhibition. (NCT01587651)
Timeframe: 7 days after first randomized dose

InterventionPRU (P2Y12 Reaction Units) (Least Squares Mean)
Prasugrel Combined Groups95.0
Ticagrelor49.0

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P2Y12 Reaction Units

P2Y12 Reaction Units (PRU) measured by VerifyNow P2Y12 assay measured at 2, 4, 24, 48 hours after first randomized study treatment (NCT01587651)
Timeframe: 2, 4, 24, 48 hours after first randomized dose

,,,
InterventionPRU (Least Squares Mean)
2 hours4 hours24 hours48 hours
Prasugrel Combined Groups33.741.1126.8159.3
Prasugrel Loading Dose22.124.181.6118.3
Prasugrel Maintenance Dose44.857.0167.8199.0
Ticagrelor28.929.347.638.6

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PRU Percent Inhibition (Device-reported)

"PRU VerifyNow P2Y12 assay device-reported percent inhibition 2, 4, 24, and 48 hours, and 7 days after first randomized study treatment~VerifyNow P2Y12 assay, developed by Accumetrics, Inc. (San Diego, CA, USA), has been approved by the FDA to assess clopidogrel response using whole blood in a point-of-care testing fashion. The percent inhibition reported by VerifyNow device represents the percentage inhibition relative to maximal P2Y12-independent platelet aggregation achieved with the same sample in the presence of the iso-thrombin receptor activating peptide." (NCT01587651)
Timeframe: 2, 4, 24, 48 hours, 7 days after first randomized dose

,,,
Interventionpercent inhibition (Least Squares Mean)
2 hours post-dose4 hours post-dose24 hours post-dose48 hours post-dose7 days post-dose
Prasugrel Combined Groups87.884.954.142.365.5
Prasugrel Loading Dose91.490.269.658.365.6
Prasugrel Maintenance Dose84.379.840.026.865.4
Ticagrelor89.289.681.985.881.0

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PRU Percent Inhibition (Calculated)

"Analysis of Mean Calculated Percent Inhibition by time point~Calculated percent inhibition at time point t is defined as: 100 × (baseline PRU - PRUt)/baseline PRU where baseline PRU is the VerifyNow PRU value at pre-run-in baseline and PRUt is the VerifyNow PRU value at time t." (NCT01587651)
Timeframe: 2, 4, 24, 48 hours, 7 days after first randomized dose

,,,
InterventionPercent Inhibition (Least Squares Mean)
2 hours post-dose4 hours post dose24 hours post dose48 hours post dose7 days psot dose
Prasugrel Combined Groups88.2285.0653.6341.5964.97
Prasugrel Loading Dose92.5591.3671.4057.9864.97
Prasugrel Maintenance Dose84.1579.3538.0126.2064.97
Ticagrelor89.7389.2681.8685.0680.69

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Target Vessel Failure (TVF) Rate

"Target vessel failure (TVF) is defined as any revascularization of the target vessel, myocardial infarction (MI) related to the target vessel, or death related to the target vessel.~For the purposes of this protocol, if it cannot be determined with certainty whether MI or death was related to the target vessel it will be considered TVF." (NCT01589978)
Timeframe: ≤24 hours, 30 days, 180 days, annually through 5 years

Interventionpercentage of patients (Number)
PROMUS Element6.7

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Target Vessel Failure (TVF) Rate in PLATINUM-like Medically Treated Diabetic Patients

Any revascularization of the target vessel, myocardial infarction related to the target vessel, or death related to the target vessel. See individual components for descriptions. Statistical testing will determine if the rate meets the performance goal (12.6%) (NCT01589978)
Timeframe: 12 Months

Interventionpercentage of patients (Number)
PROMUS Element3.26

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Target Vessel Revascularization (TVR) Rate

Target vessel revascularization is defined as any attempted or successfully completed percutaneous or surgical revascularization of a target vessel. (NCT01589978)
Timeframe: ≤24 hours, 30 days, 180 days, annually through 5 years

Interventionpercentage of patients (Number)
PROMUS Element5.6

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Major Adverse Cardiac Event Rate (MACE)

Composite of cardiac death, myocardial infarction, and target vessel revascularization (NCT01589978)
Timeframe: ≤24 hours, 30 days, 180 days, annually through 5 years

Interventionpercentage of patients (Number)
PROMUS Element6.9

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All Death or Myocardial Infarction Rate

See description of individual events. (NCT01589978)
Timeframe: ≤24 hours, 30 days, 180 days, annually through 5 years

Interventionpercentage of patients (Number)
PROMUS Element3.2

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All Death Rate

All death includes cardiac death and non-cardiac death. (NCT01589978)
Timeframe: ≤24 hours, 30 days, 180 days, annually through 5 years

Interventionpercentage of patients (Number)
PROMUS Element2.3

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ARC ST Rate in PLATINUM-like Population.

Using the Academic Research Consortium (ARC) definition, the (definite/probable) stent thrombosis (ST) rate in the PLATINUM-like* population will be analyzed. Statistical testing will be used to determine if the annual increase after the first year in ST rates observed in PLATINUM-like patients meets the performance goal of 1.0% (expected rate of 0.4% + a delta of 0.6%). (NCT01589978)
Timeframe: Annually through 5 years

Interventionpercentage of participants (Number)
PROMUS Element Overall Population0.0023

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Cardiac Death or Myocardial Infarction (MI) Rate

See individual descriptions of events. (NCT01589978)
Timeframe: ≤24 hours, 30 days, 180 days, annually through 5 years

Interventionpercentage of patients (Number)
PROMUS Element2.3

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Cardiac Death or Myocardial Infarction Rate in PLATINUM-like Patients

Cardiac death or myocardial infarction rate at 12 months post implantation in PLATINUM-like patients (no acute myocardial infarction, graft stenting, chronic total occlusion, in-stent restenosis, failed brachytherapy, bifurcation, ostial lesion, severe tortuosity, moderate/severe calcification, 3-vessel stenting, cardiogenic shock, left main disease, or acute/chronic renal dysfunction; lesion length ≤28 mm with reference vessel diameter ≥2.25 mm and <2.5 mm, or lesion length ≤24 mm with diameter ≥2.5 mm and ≤4.25 mm); statistical testing will assess if rate meets the performance goal (3.2%) (NCT01589978)
Timeframe: 12 months

Interventionpercentage of patients (Number)
PROMUS Element1.78

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Cardiac Death Rate

Cardiac death is defined as death due to any of the following: acute myocardial infarction; cardiac perforation/pericardial tamponade; arrhythmia or conduction abnormality; cerebrovascular accident through hospital discharge or cerebrovascular accident suspected of being related to the procedure; death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery; any death in which a cardiac cause cannot be excluded (NCT01589978)
Timeframe: ≤24 hours, 30 days, 180 days, annually through 5 years

Interventionpercentage of patients (Number)
PROMUS Element1.4

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Definite + Probable Stent Thrombosis (ST) Rate Based on Academic Research Consortium (ARC) Definition in All Patients

DEFINITE ST: acute coronary syndrome and angiographic or pathologic evidence of stent thrombosis; PROBABLE ST: unexplained death within 30 days or target-vessel infarction without angiographic information ARC ST is reported as a cumulative value at different time points and within the different separate time points. Time 0 is the time point after the guide catheter has been removed. Acute ST: 0-24 hours after stent implantation; Subacute ST: >24 hours to 30 days post; late ST: >30 days to 1 year post; Very late ST: >1 year post; NOTE: Acute/subacute can be replaced by early ST (0-30 days) (NCT01589978)
Timeframe: ≤24 hours, 30 days, 180 days, annually through 5 years

Interventionpercentage of patients (Number)
PROMUS Element0.7

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Definite + Probable Stent Thrombosis (ST) Rate Based on Academic Research Consortium (ARC) Definition in PLATINUM-like Patients

ARC definite/probable ST rate in PLATINUM-like patients (no acute myocardial infarction, graft stenting, chronic total occlusion, in-stent restenosis, failed brachytherapy, bifurcation, ostial lesion, severe tortuosity, moderate/severe calcification, 3-vessel stenting, cardiogenic shock, left main disease, or acute/chronic renal dysfunction; lesion length ≤28 mm with reference vessel diameter ≥2.25 mm and <2.5 mm, or lesion length ≤24 mm with diameter ≥2.5 mm and ≤4.25 mm); statistical testing will assess if the annual ST rate increase after the first year meets the performance goal (1.0%) (NCT01589978)
Timeframe: 12 months

Interventionpercentage of patients (Number)
PROMUS Element0.3

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Myocardial Infarction (MI) Rate

New Q-waves in ≥2 leads lasting ≥0.04 sec with creatine kinase myoglobin band(CK-MB) or troponin >upper limit of normal(ULN); if no new Q-waves total CK levels >3×ULN (peri-percutaneous coronary intervention [PCI]) or >2×ULN (spontaneous) with elevated CK-MB or troponin >3×ULN (peri-PCI) or >2×ULN (spontaneous) plus ≥one of the following: ECG changes indicating new ischemia (new ST-T changes, left bundle branch block), imaging evidence of new loss of viable myocardium, new regional wall motion abnormality. Similar for MI diagnosis post coronary artery bypass graft with CK-MB or troponin >5×ULN (NCT01589978)
Timeframe: ≤24 hours, 30 days, 180 days, annually through 5 years

Interventionpercentage of patients (Number)
PROMUS Element1.1

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Non-cardiac Death Rate

"Non-cardiac death is defined as death not due to cardiac causes.~Cardiac death is death due to any of the following: acute myocardial infarction; cardiac perforation/pericardial tamponade; arrhythmia or conduction abnormality; cerebrovascular accident through hospital discharge or cerebrovascular accident suspected of being related to the procedure; death due to complication of the procedure, including bleeding, vascular repair, transfusion reaction, or bypass surgery; any death in which a cardiac cause cannot be excluded." (NCT01589978)
Timeframe: ≤24 hours, 30 days, 180 days, annually through 5 years

Interventionpercentage of patients (Number)
PROMUS Element0.9

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Rate of Longitudinal Stent Deformation

Compression/elongation of a stent along its long axis resulting from interaction with an ancillary device (e.g., guide catheter) which catches the stent end or an internal stent strut; can occur with advancement or withdrawal of ancillary device. Under fluoroscopy, longitudinal compression usually results in increased strut density and elongation in decreased strut density ('pseudo-fracture'); both can occur in the same stent. (NCT01589978)
Timeframe: Index Procedure

Interventionstents (Number)
PROMUS Element2

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Pharmacokinetics (PK): Maximum Concentration (Cmax) for Prasugrel's Active Metabolite R-138727 During Maintenance Dose

(NCT01591317)
Timeframe: Day 11 predose to 24 hours post dose

Interventionng/mL (Geometric Mean)
Prasugrel 10 mg92.3
Prasugrel 7.5 mg61.9
Prasugrel 5 mg41.0

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Pharmacokinetics (PK): Time to Maximum Concentration (Tmax) of Prasugrel's Active Metabolite R-138727 During Loading Dose

(NCT01591317)
Timeframe: Day 1 predose up to 24 hours post dose

Interventionhours (Median)
Prasugrel 60 mg0.50
Prasugrel 30 mg0.50

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Pharmacokinetics (PK): Time to Maximum Concentration (Tmax) of Prasugrel's Active Metabolite R-138727 During Maintenance Dose

(NCT01591317)
Timeframe: Day 11 predose to 24 hours post dose

Interventionhours (Median)
Prasugrel 10 mg0.50
Prasugrel 7.5 mg0.50
Prasugrel 5 mg0.38

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Percent Inhibition of Verify Now (VN)-P2Y12 Reaction Units (PRU)

PRU device reported VerifyNow percent inhibition is reported by Accumetrics VerifyNow™ P2Y12 (VN-P2Y12) assay, a point-of-care device that measures platelet aggregation with single-use, disposable cartridges (NCT01591317)
Timeframe: Predose up to 24 hours post dose on Day 12

,,
InterventionPercent inhibition of PRU (Mean)
Day 1, predoseDay 1, 0.5 hoursDay 1, 1 hourDay1, 2 hoursDay 1, 4 hoursDay 1, 24 hoursDay 10, predoseDay 11, predoseDay 11, 24 hours
Prasugrel - 30 mg/5 mg9.9048.886.994.096.892.063.664.867.0
Prasugrel - 30 mg/7.5 mg6.8066.994.297.799.198.387.691.291.0
Prasugrel - 60 mg/10 mg9.9064.995.898.999.297.889.388.592.5

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Pharmacodynamics: Adenosine Diphosphate (ADP)-Induced P2Y12 Receptor-mediated Platelet Aggregation

ADP-induced PRU represents the rate and extent of ADP-stimulated platelet aggregation and serves as a biomarker of clinical efficacy, with lower values indicating greater P2Y12 platelet inhibition (NCT01591317)
Timeframe: Predose up to 24 hours post dose on Day 12

,,
InterventionPRU (Mean)
Day 1, predoseDay 1, 0.5 hoursDay 1, 1 hourDay1, 2 hoursDay 1, 4 hoursDay 1, 24 hoursDay 10, predoseDay 11, predoseDay 11, 24 hours
Prasugrel - 30 mg/5 mg29717246.020.112.126.9121123107
Prasugrel - 30 mg/7.5 mg27310719.07.003.105.1035.126.427.2
Prasugrel - 60 mg/10 mg29011813.53.302.707.1034.839.624.4

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Pharmacokinetics (PK): Maximum Concentration (Cmax) for Prasugrel's Active Metabolite R-138727 During Loading Dose

(NCT01591317)
Timeframe: Day 1 predose up to 24 hours post dose

Interventionnanogram/milliliter (ng/mL) (Geometric Mean)
Prasugrel 60 mg498
Prasugrel 30 mg271

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Pharmacokinetics (PK): Area Under the Concentration Curve (AUC) of Prasugrel's Active Metabolite R-138727 During Maintenance Dose

AUC from time zero to the last quantifiable plasma concentration (tlast) (NCT01591317)
Timeframe: Day 11 predose to 24 hours post dose

Interventionng*h/mL (Geometric Mean)
Prasugrel 10 mg78.1
Prasugrel 7.5 mg58.4
Prasugrel 5 mg38.3

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Pharmacokinetics (PK): Area Under the Concentration Curve (AUC) of Prasugrel's Active Metabolite R-138727 During Loading Dose

AUC from time zero to the last quantifiable plasma concentration (tlast) (NCT01591317)
Timeframe: Day 1 predose up to 24 hours post dose

Interventionnanogram times hour/milliliter (ng*h/mL) (Geometric Mean)
Prasugrel 60 mg600
Prasugrel 30 mg283

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Change From Baseline in Asthma Control Questionnaire-7 (ACQ-7) Score After Aspirin Desensitization and High Dose Aspirin Treatment at 8 Weeks

We will note difference in the Asthma Control Questionnaire-7 (ACQ-7) score [ The ACQ has 7 questions on a 7-point scale (minimum score of 0=no impairment, maximum score of 6= maximum impairment)] obtained before any treatment ( baseline ) and after one day Aspirin desensitization followed by 8 weeks Aspirin treatment ( 650 mg oral aspirin tablet twice daily ) (NCT01597375)
Timeframe: Evaluated at baseline and reported at 8 weeks

Interventionscore on a scale (Mean)
Subjects With AERD Completing 8 Weeks of Aspirin Treatment-0.11

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Difference in PD2 (Provocative Dose of Aspirin That Elicits an Increase in Nasal Symptom Score of 2 During an Aspirin Challenge) on Prasugrel Versus Placebo

"The PD2 is the provocative dose of aspirin that elicits an increase in nasal symptom score of 2 during an aspirin challenge. The PD2 is calculated by:~inverse〖log〗_10 (((2-(PrevTNSS-BaselineTNSS))×(〖log〗_10 ProvocDose-〖log〗_10 PrevDose))/((MaxTNSS-BaselineTNSS)-(PrevTNSS-BaselineTNSS) )+(〖log〗_10 PrevDose))" (NCT01597375)
Timeframe: Difference in PD2 (provocative dose of aspirin that elicits an increase in nasal symptom score of 2 during an aspirin challenge) between Visits 2 and 3 (weeks 8 and 14), calculated at visit 3

Interventionmg (Mean)
Placebo79
Prasugrel139

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Change From Baseline in Fractional Exhaled Nitric Oxide (FeNO) Measurement After Aspirin Desensitization and High Dose Aspirin Treatment at 8 Weeks

We will note difference in the fractional exhaled nitric oxide (FeNO) obtained before any treatment ( baseline ) and after one day Aspirin desensitization followed by 8 weeks Aspirin treatment ( 650 mg oral aspirin tablet twice daily ) (NCT01597375)
Timeframe: Evaluated at baseline and reported at 8 weeks

Interventionparts per billion (Mean)
Subjects With AERD Completing 8 Weeks of Aspirin Treatment15.8

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Change in Total Nasal Symptom Score(TNSS)From Baseline to Peak During Aspirin Challenge on Placebo Versus Prasugrel.

The primary outcome in Part 1 will be the maximum Total Nasal Symptom Score (TNSS) attained for subjects with AERD during the clinical reaction to aspirin challenge. The primary analysis will compare this outcome within each participant after treatment with prasugrel versus placebo. Nasal symptoms including congestion, rhinorrhea, runny nose, itchy nose, sneezing, itchy eyes, teary eyes, itchy ears/throat, and eye redness were assessed on a 0- to 5-point scale (0, none-5, very severe) in response to the provocative dose of aspirin during aspirin challenge/desensitization and summed together to generate the TNSS score (range 0-40). (NCT01597375)
Timeframe: Data obtained at visits 2 and 3 (weeks 8 and 14) and change calculated at visit 3

Interventionunits on scale (Mean)
Placebo7
Prasugrel6.5

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Change in Urinary LTE4 During Aspirin Challenge on Placebo Versus Prasugrel

We will compare the participant's Leukotriene E4 (LTE4) obtained from the aspirin challenge done after pretreatment with prasugrel, the aspirin challenge done after pretreatment with placebo. (NCT01597375)
Timeframe: Change from visits 2 at visit 3 (weeks 8, 14), calculated and reported at visit 3

Interventionpercentage change from baseline (Mean)
Placebo37
Prasugrel19

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Difference in Participant's Provocative Dose of Aspirin When Pretreated With Prasugrel Versus Placebo

We will monitor the dose of aspirin at which the participant shows symptoms (increased discomfort, 15% drop in FEV1) during the aspirin challenge/desensitization. We will compare the provocative aspirin dose obtained from the aspirin challenge occurring after pretreatment with prasugrel to the dose obtained after pretreatment with placebo. (NCT01597375)
Timeframe: Evaluated at visits 2 and 3 (weeks 8 and 14)

Interventionmg (Mean)
Placebo109
Prasugrel164

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Change From Baseline in Prostaglandin Metabolites (PGD-M) Measurement After Aspirin Desensitization and High Dose Aspirin Treatment at 8 Weeks

We will note difference in the Prostaglandin metabolites (PGD-M) measurement obtained before any treatment ( baseline ) and after one day Aspirin desensitization followed by 8 weeks Aspirin treatment ( 650 mg oral aspirin tablet twice daily ) (NCT01597375)
Timeframe: Evaluated at baseline and reported at 8 weeks

Interventionng/mg creatinine (Mean)
Subjects With AERD Completing 8 Weeks of Aspirin Treatment-1.4957

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Thrombelastography (TEG) MA

Persistence of high tensile clot strength measured by TEG 16-24 hours after reloading of either clopidogrel or prasugrel (NCT01612884)
Timeframe: 1 day

Interventionmm (Mean)
Thrombelastography (TEG) Guided66.4
Light Transmittance Aggregometry Guided65.8

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Number of Participants With Ischemic Events

Death, recurrent myocardial infarction, recurrent unstable angina, repeat coronary intervention (NCT01612884)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
Death72248361Death72248362Myocardial Infarction72248361Myocardial Infarction72248362Recurrent coronary intervention72248361Recurrent coronary intervention72248362Unstable Angina72248362Unstable Angina72248361
No EventEvent
Thrombelastography (TEG) Guided0
Thrombelastography (TEG) Guided19
Thrombelastography (TEG) Guided1
Light Transmittance Aggregometry Guided0
Thrombelastography (TEG) Guided18
Light Transmittance Aggregometry Guided18
Thrombelastography (TEG) Guided3
Light Transmittance Aggregometry Guided2
Thrombelastography (TEG) Guided16
Light Transmittance Aggregometry Guided16
Thrombelastography (TEG) Guided2
Thrombelastography (TEG) Guided17

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Pharmacokinetics: Maximum Concentration (Cmax) of Prasugrel Test and Reference Formulation

Cmax= maximum concentration measured from predose through 8 hours postdose. Test formulation is defined as the orally disintegrating tablet containing Magnasweet® (ODT2) and the reference formulation is defined as the orally disintegrating tablet without Magnasweet® (ODT1) specific to the 5 milligrams (mg) prasugrel dosing. Pharmacokinetics will measure prasugrel's (LY640315) active metabolite. (NCT01648790)
Timeframe: Predose through 8 Hours Post Dose

Interventionnanograms per milliliter (ng/mL) (Geometric Mean)
5 mg Prasugrel (ODT1)28.6
5 mg Prasugrel (ODT2)28.1

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Pharmacokinetics: Maximum Concentration (Cmax) of Prasugrel Test Formulation in Fasted and Fed State

Cmax= maximum concentration measured from predose through 8 hours postdose. Test formulation is defined as the orally disintegrating tablet containing Magnasweet® (ODT2) specific to the 5 mg prasugrel dosing in the fasted and fed state. Pharmacokinetics will measure prasugrel's active metabolite. (NCT01648790)
Timeframe: Predose through 8 Hours Post Dose

Interventionnanograms per milliliter (ng/mL) (Geometric Mean)
5 mg Prasugrel (ODT1)28.6
5 mg Prasugrel (ODT2)28.1
5 mg Prasugrel (ODT2)-Suspension31.5
5 mg Prasugrel (ODT2)-Fed7.79
2 mg Prasugrel (ODT2)8.81

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Pharmacokinetics: Area Under the Concentration Curve (AUC) of Prasugrel Reference and Test Formulation

AUC(0-tlast) = area under the concentration versus time curve from time zero to time t, where t is the last time point with a measurable concentration. Test formulation is defined as the orally disintegrating tablet containing Magnasweet® (ODT2) and the reference formulation is defined as the orally disintegrating tablet without Magnasweet® (ODT1) specific to the 5 mg prasugrel dosing. Pharmacokinetics will measure prasugrel's active metabolite. (NCT01648790)
Timeframe: Predose through 8 Hours Post Dose

Interventionnanograms*hour per milliliter (ng*h/mL) (Geometric Mean)
5 mg Prasugrel (ODT1)27.1
5 mg Prasugrel (ODT2)26.8

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Pharmacokinetics: Area Under the Concentration Curve (AUC) of Prasugrel Test Formulation in Fasted and Fed State

AUC(0-tlast) = area under the concentration versus time curve from time zero to time t, where t is the last time point with a measurable concentration. Test formulation is defined as the orally disintegrating tablet containing Magnasweet® (ODT2) specific to the 5 mg prasugrel dosing in the fasted and fed state. Pharmacokinetics will measure prasugrel's active metabolite. (NCT01648790)
Timeframe: Predose through 8 Hours Post Dose

Interventionnanograms*hour per milliliter (ng*h/mL) (Geometric Mean)
5 mg Prasugrel (ODT1)27.1
5 mg Prasugrel (ODT2)26.8
5 mg Prasugrel (ODT2)-Suspension27
5 mg Prasugrel (ODT2)-Fed20.8
2 mg Prasugrel (ODT2)8.97

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The Change in Platelet Aggregation Measured by the Accumetrics (VerifyNow P2Y12) Assay Between Baseline and Each Antiplatelet Medication

(NCT01765400)
Timeframe: Baseline, 2 weeks post clopidogrel, and 2 weeks post prasugrel, Change From Baseline at Week 2 Reported

InterventionPRU (P2Y12 reactivity units) (Mean)
Prasugrel66.4
Clopidogrel156.2

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The Change in Light Transmission Aggregometry (LTA)Between Baseline and Each Antiplatelet Medication

(NCT01765400)
Timeframe: Baseline, 2 weeks post clopidogrel, and 2 weeks post prasugrel

,
Interventionpercentage of platelt inhibition (Mean)
5 umol/L ADP20 umol/L ADP
Clopidogrel4754
Prasugrel3238

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The Change in Platelet Activation Assay (VASP)Between Baseline and Each Antiplatelet Medication

(NCT01765400)
Timeframe: Baseline, 2 weeks post clopidogrel, and 2 weeks post prasugrel

InterventionPRI (platelt reactivity index) (Mean)
Prasugrel25
Clopidogrel49

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Change From Baseline in ADP-mediated Platelet Aggregation, APP, SFFLRN, AYPGKF.

"To document the extent of inhibition of ADP mediated platelet aggregation following the discontinuation of bivalirudin therapy in patients treated with prasugrel as compared to patients treated with clopidogrel.~The percent inhibition of platelet aggregation was measured by light transmission aggregometry of platelet-rich plasma in response to P2Y12 and PAR1 and PAR4 thrombin receptor agonists at baseline and at 1, 2, 4 and 16 h following the cessation of bivalirudin infusion. Platelet response to agonists: 20 mM ADP(P2Y12), 5 mM SFLLRN (PAR1), and 160 mM AYPGKF (PAR4) was performed. The magnitude of inhibition of platelet aggregation for each agonist was calculated as the mean final change from baseline in light transmission aggregometry at each time point." (NCT01789814)
Timeframe: Baseline, 60, 120, 240, 960 mins following termination of bivalirudin infusion

,
Intervention% inhibitn of platelet aggregation (Number)
ADP 20 uM-1 hour %ADP 20 uM-2 hour %ADP 20 uM-4 hour %ADP 20 uM-16 hour %SFFLRN 5 uM-1 hourSFFLRN 5 uM-2 hourSFFLRN 5 uM-4 hourSFFLRN 5 uM-16 hourAYP 160 uM-1 hourAYP 160 uM-2 hourAYP 160 uM-4 hourAYP 160 uM-16 hour
Clopidogrel38538585291715791311
Prasugrel849498986264755839445341

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Number of Red Blood Cell (RBC) Transfusions Due to Sickle Cell Disease (SCD) Per Participant Per Year (Rate of RBC Transfusions)

RBC transfusions that occurred within 7 days of the prior event onset date were not counted as a new episode. Data collected through the primary completion date are presented below. (NCT01794000)
Timeframe: Randomization through 24 Months

InterventionNumber of Events per Participant-Year (Number)
Prasugrel0.497
Placebo0.420

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Number of Days Hospitalized for VOC

The total length of hospitalization in days for VOC was calculated for each participant. Data collected through the primary completion date are presented below. (NCT01794000)
Timeframe: Randomization through 24 Months

InterventionDays (Least Squares Mean)
Prasugrel12.9
Placebo12.0

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Number of Hospitalizations for VOC Per Participant Per Year (Rate of Hospitalizations)

Hospitalization that occurred within 7 days of the prior event onset date were not counted as a new episode. Data collected through the primary completion date are presented below. (NCT01794000)
Timeframe: Randomization through 24 Months

InterventionNumber of Events per Participant-Year (Number)
Prasugrel1.064
Placebo1.126

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Number of Painful Crisis Events Per Participant Per Year (Rate of Painful Crisis)

A painful crisis is defined as an onset of moderate to severe pain that lasts at least 2 hours for which there is no explanation other than vaso-occlusion and which requires therapy with oral or parenteral opioids, ketorolac, or other analgesics prescribed by a health care provider (HCP) in a medical setting such as a hospital, clinic, emergency room visit, or telephone management. The painful crisis that occurred within 7 days from the prior event onset date was not counted as a new episode. Data collected through the primary completion date are presented below. (NCT01794000)
Timeframe: Randomization through 24 Months

InterventionNumber of Events per Participant-Year (Number)
Prasugrel2.239
Placebo2.720

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Number of Acute Chest Syndrome Per Participant Per Year (Rate of Acute Chest Syndrome)

Acute chest syndrome was defined as an acute illness characterized by fever and/or respiratory symptoms, accompanied by a new pulmonary infiltrate on a chest X-ray. Acute chest syndrome that occurred within 7 days of the prior event onset date was not counted as a new episode. Data collected through the primary completion date are presented below. (NCT01794000)
Timeframe: Randomization through 24 Months

InterventionNumber of Events per Participant-Year (Number)
Prasugrel0.112
Placebo0.115

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Monthly Rate of Days With Pain

Monthly rate of days with pain was measured through participant diaries using a modified version of the Faces Pain Scale-Revised (FPS-R). Each day participants selected the face on the scale that reflected their worst pain related to sickle cell disease (SCD) on that day. This pain scale contains six faces corresponding to the pain intensity of 0, 2, 4, 6, 8 or 10, in which 0 denotes no pain and 10 denotes the worst pain possible. Any day the participant selected a face other than face 0 was considered a day with pain. Monthly rate of days with pain was calculated for each participant by summing the number of days reported with any pain divided by the number of non-missing diary entries completed in the month. A month was defined as 4 weeks (28 days).The monthly rate was set to missing if there were more than 14 missing entries for the FPS-R in a specific month. Data collected through the primary completion date are present below. (NCT01794000)
Timeframe: Randomization through 9 Months

InterventionPercentage of Days in a Month (Least Squares Mean)
Prasugrel17.457
Placebo17.699

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Number of Vaso-Occlusive Crisis (VOC) Events Per Participant Per Year (Rate of VOC)

The VOC is a composite endpoint of painful crisis or acute chest syndrome. Events that occurred within 7 days from the prior event onset date were not counted as a new episode. Data collected through the primary completion date reported below. (NCT01794000)
Timeframe: Randomization through 24 Months

InterventionNumber of Events per Participant-Year (Number)
Prasugrel2.295
Placebo2.767

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Monthly Mean in Faces Pain Scale-Revised Score

Each day participants selected the face on the FPS-R scale that reflected their worst pain related to sickle cell disease (SCD) on that day. Monthly mean in FPS-R score was calculated for each participant by summing the FPS-R score divided by the number of non-missing diary entries completed in the month. This pain scale contains six faces corresponding to the pain intensity of 0, 2, 4, 6, 8 or 10, in which 0 denotes no pain and 10 denotes the worst pain possible. A month was defined as 4 weeks (28 days). The monthly mean in FPS-R score was set to missing if there were more than 14 missing entries for the FPS-R in a specific month. Data collected through the primary completion date are presented below. (NCT01794000)
Timeframe: Randomization through 9 Months

InterventionUnits on a Scale (Least Squares Mean)
Prasugrel0.7116
Placebo0.6148

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Quarterly Rate of School Absence Due to Sickle Cell Pain

Quarterly rate of school absence due to sickle cell pain was measured through participant diaries and was calculated for each participant by summing the number of days with school absence due to sickle cell pain divided by the number of school dates in the quarter. A quarter was defined as 12 weeks. The quarterly rate was set to missing if there were more than 6 weeks of missing diary entries during a specific quarter. Data collected through the primary completion date are presented below. (NCT01794000)
Timeframe: Randomization through 9 Months

InterventionPercentage of Days in a Quarter (Least Squares Mean)
Prasugrel11.527
Placebo10.255

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Time From Randomization to First and Second VOC

Data collected through the primary completion date are presented below. (NCT01794000)
Timeframe: Randomization to First VOC and Second VOC respectively (up to 24 Months)

,
InterventionDays (Median)
Time from Randomization to the First VOCTime from Randomization to the Second VOC
Placebo87.0238.0
Prasugrel90.0338.0

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Monthly Rate of Days of Analgesic Use

Monthly rate of days of analgesic use was measured through participant diaries and was calculated for each participant by summing the number of days they reported analgesic use divided by the number of diary entries completed in the month. A month was defined as 4 weeks (28 days). The monthly rate was set to missing if there were more than 14 missing entries for analgesic use in a specific month. Data collected through the primary completion date are presented below. (NCT01794000)
Timeframe: Randomization through 9 Months

InterventionPercentage of Days in a Month (Least Squares Mean)
Prasugrel24.270
Placebo22.757

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Percentage of Participants With Hemorrhagic Events Requiring Medical Intervention

Medical intervention was defined as any medical evaluation resulting in therapy or further investigation, as determined by a trained medical professional. Data collected from the first dose of study medication through 10 days after last dose of study medication during the double blind study period are presented below. (NCT01794000)
Timeframe: First Dose through 24 Months

InterventionPercentage of Participants (Number)
Prasugrel6.5
Placebo4.7

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Percentage of Participants With Bleeding Requiring Medical Attention (BRMA)

A BRMA event is defined as any bleeding event that requires medical treatment, surgical treatment, or laboratory evaluation, and does not meet criteria for a major or minor bleeding event. (NCT01830543)
Timeframe: Up to Month 12 and end of DAPT-Month 1, 6 and 12

,,
Interventionpercentage of participants (Number)
Up to Month 12 (n= 696, 706, 697)End of DAPT-1 Month (n= 0, 108, 113)End of DAPT-6 Month (n= 0, 248, 243)End of DAPT-12 Month (n= 0, 350, 341)
Rivaroxaban 15 mg13.4NANANA
Rivaroxaban 2.5 mg Twice Daily (BID)/15 mg Once Daily(QD)14.416.712.914.9
Vitamin K Antagonist (VKA)19.918.62318.2

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Percentage of Participants With Clinically Significant Bleeding

Clinically significant bleeding is a composite of Thrombolysis in Myocardial Infarction (TIMI) major bleeding, minor bleeding, and bleeding requiring medical attention (BRMA). TIMI major bleeding is defined as any symptomatic intracranial hemorrhage, clinically overt signs of hemorrhage (including imaging) associated with a drop in hemoglobin of greater than or equal to (>=) 5 grams per deciliter (g/dL) (or when the hemoglobin concentration is not available, an absolute drop in hematocrit of >=15 percent (%)). TIMI minor bleeding event is defined as any clinically overt sign of hemorrhage (including imaging) that is associated with a fall in hemoglobin concentration of 3 to less than (<) 5 g/dL (or, when hemoglobin concentration is not available, a fall in hematocrit of 9 percent to <15 percent). A BRMA event is defined as any bleeding event that requires medical treatment, surgical treatment, or laboratory evaluation, and does not meet criteria for a major or minor bleeding event. (NCT01830543)
Timeframe: Up to Month 12

Interventionpercentage of participants (Number)
Rivaroxaban 15 mg15.7
Rivaroxaban 2.5 mg Twice Daily (BID)/15 mg Once Daily(QD)16.6
Vitamin K Antagonist (VKA)24.0

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Percentage of Participants With Cardiovascular Death

The percentage of participants with the first occurrence of cardiovascular death were evaluated. (NCT01830543)
Timeframe: Up to Month 12 and end of DAPT-Month 1, 6 and 12

,,
Interventionpercentage of participants (Number)
Up to Month 12 (n= 694, 704, 695)End of DAPT-1 Month (n= 0, 108, 112)End of DAPT-6 Month (n= 0, 248, 243)End of DAPT-12 Month (n= 0, 348, 340)
Rivaroxaban 15 mg2.2NANANA
Rivaroxaban 2.5 mg Twice Daily (BID)/15 mg Once Daily(QD)21.92.41.7
Vitamin K Antagonist (VKA)1.61.81.61.5

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Percentage of Participants With Composite of Adverse Cardiovascular Events (Cardiovascular Death, Myocardial Infarction (MI) and Stroke)

Percentage of participants who experienced adverse cardiovascular events (cardiovascular death, myocardial Infarction (MI) and stroke) collectively, were assessed. (NCT01830543)
Timeframe: Up to Month 12 and end of DAPT-Month 1, 6 and 12

,,
Interventionpercentage of participants (Number)
Up to Month 12 (n= 694, 704, 695)End of DAPT-1 Month (n= 0, 108, 112)End of DAPT-6 Month (n= 0, 248, 243)End of DAPT-12 Month (n= 0, 348, 340)
Rivaroxaban 15 mg5.9NANANA
Rivaroxaban 2.5 mg Twice Daily (BID)/15 mg Once Daily(QD)5.15.66.54
Vitamin K Antagonist (VKA)5.24.53.76.5

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Percentage of Participants With Myocardial Infarction

The percentage of participants with the first occurrence of Myocardial Infarction were evaluated. (NCT01830543)
Timeframe: Up to Month 12 and end of DAPT-Month 1, 6 and 12

,,
Interventionpercentage of participants (Number)
Up to Month 12 (n= 694, 704, 695)End of DAPT-1 Month (n= 0, 108, 112)End of DAPT-6 Month (n= 0, 248, 243)End of DAPT-12 Month (n= 0, 348, 340)
Rivaroxaban 15 mg2.7NANANA
Rivaroxaban 2.5 mg Twice Daily (BID)/15 mg Once Daily(QD)2.42.82.82
Vitamin K Antagonist (VKA)30.92.54.1

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Percentage of Participants With Stent Thrombosis

The percentage of participants with the first occurrence of stent thrombosis were evaluated. (NCT01830543)
Timeframe: Up to Month 12 and end of DAPT-Month 1, 6 and 12

,,
Interventionpercentage of participants (Number)
Up to Month 12 (n= 694, 704, 695)End of DAPT-1 Month (n= 0, 108, 112)End of DAPT-6 Month (n= 0, 248, 243)End of DAPT-12 Month (n= 0, 348, 340)
Rivaroxaban 15 mg0.7NANANA
Rivaroxaban 2.5 mg Twice Daily (BID)/15 mg Once Daily(QD)0.91.91.60
Vitamin K Antagonist (VKA)0.60.90.40.6

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Percentage of Participants With Stroke

The percentage of participants with the first occurrence of Stroke were evaluated. (NCT01830543)
Timeframe: Up to Month 12 and end of DAPT-Month 1, 6 and 12

,,
Interventionpercentage of participants (Number)
Up to Month 12 (n= 694, 704, 695)End of DAPT-1 Month (n= 0, 108, 112)End of DAPT-6 Month (n= 0, 248, 243)End of DAPT-12 Month (n= 0, 348, 340)
Rivaroxaban 15 mg1.2NANANA
Rivaroxaban 2.5 mg Twice Daily (BID)/15 mg Once Daily(QD)1.41.92.40.6
Vitamin K Antagonist (VKA)12.701.2

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Percentage of Participants With Thrombolysis in Myocardial Infarction (TIMI) Major Bleeding

TIMI major bleeding is defined as any symptomatic intracranial hemorrhage, Clinically overt signs of hemorrhage (including imaging) associated with a drop in hemoglobin of >= 5 g/dL (or when the hemoglobin concentration is not available, an absolute drop in hematocrit of >=15 percent). (NCT01830543)
Timeframe: Up to Month 12 and end of DAPT-Month 1, 6 and 12

,,
Interventionpercentage of participants (Number)
Up to Month 12 (n= 696, 706, 697)End of DAPT-1 Month (n= 0, 108,113)End of DAPT-6 Month (n= 0, 248,243)End of DAPT-12 Month (n= 0, 350,341)
Rivaroxaban 15 mg2.0NANANA
Rivaroxaban 2.5 mg Twice Daily (BID)/15 mg Once Daily(QD)1.70.92.81.1
Vitamin K Antagonist (VKA)2.94.43.71.8

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Percentage of Participants With Thrombolysis in Myocardial Infarction (TIMI) Minor Bleeding

TIMI minor bleeding event is defined as any clinically overt sign of hemorrhage (including imaging) that is associated with a fall in hemoglobin concentration of 3 to <5 g/dL (or, when hemoglobin concentration is not available, a fall in hematocrit of 9 percent to <15 percent). (NCT01830543)
Timeframe: Up to Month 12 and end of DAPT-Month 1, 6 and 12

,,
Interventionpercentage of participants (Number)
Up to Month 12 (n= 696, 706, 697)End of DAPT-1 Month (n= 0, 108, 113)End of DAPT-6 Month (n= 0, 248, 243)End of DAPT-12 Month (n= 0, 350, 341)
Rivaroxaban 15 mg1.0NANANA
Rivaroxaban 2.5 mg Twice Daily (BID)/15 mg Once Daily(QD)1.00.90.41.4
Vitamin K Antagonist (VKA)1.91.82.51.5

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Bleeding Events in Accordance With the GUSTO Scale

Bleeding was assessed by history, physical exam, and complete blood count (CBC) that was performed on study Days 1 and 8. Reports of bleeding were to be evaluated by performance of a CBC. Bleeding was to be reported as recommended and quantified in accordance with the GUSTO criteria [The GUSTO Investigators, 1993]. (NCT01852019)
Timeframe: Day 1 through Day 8

,
Interventionparticipants (Number)
MildModerateLife-threatening/Severe
Day 8 - Prasugrel (10mg) Dosing (5 Doses)000
Day 8 - Prasugrel (10mg) Dosing (6 Doses)100

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Extent of Preservation of Inhibitory Effect of Cangrelor Treatment After Prasugrel, Compared to Treatment With Cangrelor Alone

A reference point for the inhibitory effect of cangrelor alone was chosen for comparison and designated the first draw during the cangrelor infusion (1.0 or 1.5 hours) or within 5 minutes post cangrelor infusion on Day 1. The extent of aggregation was observed during the cangrelor infusion on Day 8, either 24 or 48 hours after discontinuation of prasugrel using light transmittance aggregometry (LTA) and expressed as % aggregation in response to 20 μM adenosine diphosphate (ADP) at 300 seconds (final/terminal aggregation response). (NCT01852019)
Timeframe: Day 8 - at 1.0 and 2.0 hours after initiation of cangrelor infusion

,
Intervention% aggregation (Mean)
1.0 h2.0 h
Day 8 - Prasugrel (10mg) Dosing (5 Doses)1.31.0
Day 8 - Prasugrel (10mg) Dosing (6 Doses)0.50.0

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Extent of Preservation of Inhibitory Effect of Cangrelor Treatment After Prasugrel, Compared to Treatment With Cangrelor Alone

A reference point for the inhibitory effect of cangrelor alone was chosen for comparison and designated the first draw during the cangrelor infusion (1.0 or 1.5 hours) or within 5 minutes post cangrelor infusion on Day 1. The extent of aggregation was observed during the cangrelor infusion on Day 8, either 24 or 48 hours after discontinuation of prasugrel as assessed by platelet reaction units (PRU) from the VerifyNow P2Y12 assay. (NCT01852019)
Timeframe: Day 8 - at 1.0 and 2.0 hours after initiation of cangrelor infusion

,
Interventionplatelet reaction units (PRU) (Mean)
1.0 h - PRU2.0 h - PRU
Day 8 - Prasugrel (10mg) Dosing (5 Doses)8.313
Day 8 - Prasugrel (10mg) Dosing (6 Doses)6.34.7

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Extent of Preservation of Inhibitory Effect After Transition From Cangrelor to Prasugrel Compared With Effect Observed With Prasugrel Alone (Reference Timepoint)

A reference point for the effect of prasugrel alone was chosen for comparison and designated the final draw on study Day 1 (3.5 or 4.0 hours after cangrelor had been discontinued) as the reference for the effect of prasugrel. The extent of aggregation in the presence or absence of the study drugs was examined for each of the endpoints using light transmittance aggregometry (LTA) and expressed as % aggregation in response to 20 micromolar (μM) adenosine diphosphate (ADP) at 300 seconds (final/terminal aggregation response). (NCT01852019)
Timeframe: Day 1 measures taken at timepoints after cangrelor infusion end to end of Day 1 measures.

,,
Intervention% aggregation (Mean)
Prasugrel Reference (6.0h or 5.5 h)2.25 h2.5 h2.75 h3.0 h4.0 h
Day 1 - Cangrelor + Prasugrel (60mg) a 1.0h5.04562695115
Day 1 - Cangrelor + Prasugrel (60mg) at 1.5h2.82542312410
Day 1 - Cangrelor + Prasugrel (60mg) Post Infusion (2.0h)1.0275664581.0

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Extent of Preservation of Inhibitory Effect After Transition From Cangrelor to Prasugrel Compared With Effect Observed With Prasugrel Alone (Reference Timepoint)

A reference point for the effect of prasugrel alone was chosen for comparison and designated the final draw on study Day 1 (3.5 or 4.0 hours after cangrelor had been discontinued) as the reference for the effect of prasugrel. The extent of aggregation in the presence of absence of the study drugs was examined for each of the endpoints as assessed by platelet reaction units (PRU) from the VerifyNow P2Y12 assay. (NCT01852019)
Timeframe: Day 1 measures taken at timepoints after cangrelor infusion end to end of Day 1 measures.

,,
Interventionplatelet reaction units (PRU) (Mean)
Prasugrel Reference (6.0h or 5.5h) - PRU2.25h - PRU2.5h - PRU2.75h - PRU3.0h - PRU4.0h - PRU
Day 1 - Cangrelor + Prasugrel (60mg) a 1.0h74151269285242117
Day 1 - Cangrelor + Prasugrel (60mg) at 1.5h418218113412756
Day 1 - Cangrelor + Prasugrel (60mg) Post Infusion (2.0h)7.79124226723920

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Platelet Reactivity Measured by Vasodilator-stimulated Phosphoprotein (VASP)

A secondary outcome was the comparison between groups of platelet reactivity index (PRI) measured by vasodilator-stimulated phosphoprotein (VASP) at 24 hours after loading dose. (NCT01852175)
Timeframe: 24 hours

InterventionPRI% (Least Squares Mean)
Prasugrel14.2
Ticagrelor26.4

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Platelet Reactivity Measured by Vasodilator-stimulated Phosphoprotein (VASP)

A secondary outcome was the comparison between groups of platelet reactivity index (PRI) measured by vasodilator-stimulated phosphoprotein (VASP) at 2 hours after loading dose. (NCT01852175)
Timeframe: 2 hours

InterventionPRI% (Least Squares Mean)
Prasugrel13.4
Ticagrelor15.6

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Platelet Reactivity by Vasodilator-stimulated Phosphoprotein (VASP)

The primary end-point of the study was the comparison in the platelet reactivity index (PRI%) determined by vasodilator-stimulated phosphoprotein (VASP) at 1 week between prasugrel and ticagrelor. (NCT01852175)
Timeframe: 1 week

InterventionPRI% (Least Squares Mean)
Prasugrel32.1
Ticagrelor32.6

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Platelet Reactivity Index

The comparison of the platelet reactivity index (PRI) values determined by vasodilator-stimulated phosphoprotein (VASP) between both treatments (ticagrelor or prasugrel). VASP was measured by quantitative flow cytometry using commercially available labelled monoclonal antibodies. A low PRI is indicative of high platelet inhibition. (NCT01852214)
Timeframe: 2 hours

InterventionPRI (Least Squares Mean)
Prasugrel35
Ticagrelor37

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Platelet Reactivity Index

The comparison of the platelet reactivity index (PRI) values determined by vasodilator-stimulated phosphoprotein (VASP) between both treatments (ticagrelor or prasugrel). VASP was measured by quantitative flow cytometry using commercially available labelled monoclonal antibodies. A low PRI is indicative of high platelet inhibition. (NCT01852214)
Timeframe: 1 week

InterventionPRI (Least Squares Mean)
Prasugrel36
Ticagrelor36

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P2Y12 Reaction Units

The primary endpoint is the comparison of the P2Y12 reaction units (PRU) values determined by VerifyNow between both treatments (ticagrelor or prasugrel). Treatment effects were evaluated comparing PRU observed in the overall patient population after prasugrel treatment with those achieved after ticagrelor regardless of the sequence. (NCT01852214)
Timeframe: 1 week

InterventionPRU (Least Squares Mean)
Prasugrel83
Ticagrelor52

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P2Y12 Reaction Units

Comparison of the P2Y12 reaction units (PRU) values determined by VerifyNow between both treatments (ticagrelor or prasugrel) (NCT01852214)
Timeframe: 2 hours

InterventionPRU (Least Squares Mean)
Prasugrel97
Ticagrelor75

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Extent Of Preservation Of Platelet Inhibitory Effect Of Cangrelor Treatment After Prasugrel Or Clopidogrel Compared To Treatment With Cangrelor Alone

A reference point for cangrelor was chosen for comparison and designated as the administration time of prasugrel 60 mg or clopidogrel 600 mg (2.5, 2, 1.5, or 1 hrs). Platelet function was assessed using LTA. LTA measures the aggregation or cross linking of platelets by fibrinogen and requires the activation of platelets plus the binding of fibrinogen. The extent of aggregation was examined using LTA and expressed as % aggregation in response to 20 μM ADP at 300 sec (final/terminal aggregation response). (NCT01979445)
Timeframe: Day 1 at 1, 1.5, 2, or 2.5 hrs after administration of prasugrel or clopidogrel (reference) and Day 1 at 1.75 and 2 hrs after initiation of cangrelor infusion

,,,
Intervention% aggregation (Mean)
Cangrelor Reference (2.5, 2, 1.5, or 1 hrs)1.75 hrs2 hrs
Clopidogrel 1 Hr During Cangrelor3.01.32.3
Clopidogrel 1.5 Hrs During Cangrelor2.01.81.5
Clopidogrel Within 5 Min After Cangrelor01.0NA
Prasugrel 30 Min After Cangrelor60.00.30.3

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Extent of Preservation of Platelet Inhibitory Effect of Cangrelor Treatment After Prasugrel or Clopidogrel Compared to Treatment With Cangrelor Alone Determined By VerifyNow P2Y12 Assay

A reference point for cangrelor was chosen for comparison and designated as the administration time of prasugrel 60 mg or clopidogrel 600 mg (2.5, 2, 1.5, or 1 hrs). Platelet function was assessed using the VerifyNow P2Y12 assay. The VerifyNow P2Y12 assay measures the aggregation or cross linking of platelets by fibrinogen and requires the activation of platelets plus the binding of fibrinogen. The extent of aggregation was assessed by PRU, determined by the VerifyNow P2Y12 assay. The VerifyNow P2Y12 assay is designed to directly measure the effects of drugs on the P2Y12 receptor, using prostaglandin E1 in addition to ADP to increase intraplatelet cAMP. Platelet reactivity was expressed in PRU. (NCT01979445)
Timeframe: Day 1 at 1, 1.5, 2, or 2.5 hrs after administration of prasugrel or clopidogrel (reference) and Day 1 at 1.75 and 2 hrs after initiation of cangrelor infusion

,,,
InterventionPRU (Mean)
Cangrelor Reference (2.5, 2, 1.5, or 1 hrs)1.75 hrs2 hrs
Clopidogrel 1 Hr During Cangrelor7.06.35.7
Clopidogrel 1.5 Hrs During Cangrelor17.725.028.8
Clopidogrel Within 5 Min After Cangrelor7.33.7NA
Prasugrel 30 Min After Cangrelor208.03.35.3

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Bleeding Events In Accordance With GUSTO Scale

"Bleeding was assessed by history, physical exam, and complete blood count (CBC) that was performed on study Day 1. Reports of bleeding were to be evaluated by performance of a CBC. Participants were assessed for bleeding events in accordance with the Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO) scale.~The severity of bleeding events by GUSTO Criteria is defined as the following:~Severe/life-threatening: fatal, intracranial hemorrhage, or if hemodynamic compromise results~Moderate: transfusion required~Mild: no transfusion or hemodynamic compromise~A summary of serious and all other non-serious adverse events regardless of causality is located in the Reported Adverse Events module." (NCT01979445)
Timeframe: Screening through the follow-up period (5 to 7 days after Day 1)

,,,
Interventionbleeding events (Number)
MildModerateLife-threatening/Severe
Clopidogrel 1 Hr During Cangrelor000
Clopidogrel 1.5 Hrs During Cangrelor000
Clopidogrel Within 5 Min After Cangrelor000
Prasugrel 30 Min After Cangrelor000

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Extent of Preservation Of Platelet Inhibitory Effect After Transition From Cangrelor To Prasugrel Or Clopidogrel Compared With Effect Observed With Prasugrel Or Clopidogrel Alone

A reference point for prasugrel or clopidogrel was chosen for comparison and designated at 6 or 5.5 hrs after the administration of prasugrel or clopidogrel as the reference for the effect of the oral drug. Platelet function was assessed using light transmittance aggregometry (LTA). LTA measures the aggregation or cross linking of platelets by fibrinogen and requires the activation of platelets plus the binding of fibrinogen. The extent of aggregation was expressed as % aggregation in response to 20 micromolar (μM) adenosine diphosphate (ADP) at 300 seconds (sec) (final/terminal aggregation response). (NCT01979445)
Timeframe: Day 1 at 5.5 or 6 hrs after administration of prasugrel or clopidogrel (reference) and Day 1 at 2.25, 2.5, 2.75, 3, 4, and 5.5 hrs after initiation of cangrelor infusion

,,,
Intervention% aggregation (Mean)
Prasugrel/Clopidogrel Reference (6 or 5.5 hrs)2.25 hrs2.5 hrs2.75 hrs3 hrs4 hrs5.5 hrs
Clopidogrel 1 Hr During Cangrelor50.333.362.067.765.062.7NA
Clopidogrel 1.5 Hrs During Cangrelor50.022.254.356.856.251.2NA
Clopidogrel Within 5 Min After Cangrelor21.726.049.758.356.038.026.7
Prasugrel 30 Min After Cangrelor1.316.360.063.365.016.31.3

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Extent of Preservation Of Platelet Inhibitory Effect After Transition From Cangrelor to Prasugrel Or Clopidogrel Compared With Effect Observed With Prasugrel Or Clopidogrel Alone Determined By VerifyNow P2Y12 Assay

A reference point for prasugrel or clopidogrel was chosen for comparison and designated at 6 or 5.5 hrs after the administration of prasugrel or clopidogrel as the reference for the effect of the oral drug. Platelet function was assessed using the VerifyNow P2Y12 assay. The VerifyNow P2Y12 assay measures the aggregation or cross linking of platelets by fibrinogen and requires the activation of platelets plus the binding of fibrinogen. The extent of aggregation was assessed by platelet reaction units (PRU), determined by the VerifyNow P2Y12 assay. The VerifyNow P2Y12 assay is designed to directly measure the effects of drugs on the P2Y12 receptor, using prostaglandin E1 in addition to ADP to increase intraplatelet cyclic adenosine monophosphate (cAMP). Platelet reactivity was expressed in PRU. (NCT01979445)
Timeframe: Day 1 at 5.5 or 6 hrs after administration of prasugrel or clopidogrel (reference) and Day 1 at 2.25, 2.5, 2.75, 3, 4, and 5.5 hrs after initiation of cangrelor infusion

,,,
InterventionPRU (Mean)
Prasugrel/Clopidogrel Reference (6 or 5.5 hrs)2.25 hrs2.5 hrs2.75 hrs3 hrs4 hrs5.5 hrs
Clopidogrel 1 Hr During Cangrelor197.398.7206.3214.3212.7203.7NA
Clopidogrel 1.5 Hrs During Cangrelor211.390.3229.8255.8234.5215.5NA
Clopidogrel Within 5 Min Post Cangrelor159.099.0220.7233.0215.7182.0155.0
Prasugrel 30 Min After Cangrelor8.076.7208.0225.7226.077.024.5

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Platelet Reactivity Measured as P2Y12 Reaction Units (PRU) Determined by Verify Now-P2Y12 Assay

The primary hypothesis of our study was that after 1 week of randomized treatment PRU levels would be non-inferior in patients switched from prasugrel to ticagrelor (two arms combined) compared with patients remaining on prasugrel. (NCT02016170)
Timeframe: 7 days

InterventionPRU (Least Squares Mean)
Ticagrelor45
Prasugrel63

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Platelet Reactivity Index (PRI) Measured by Whole Blood Vasodilator-stimulated Phosphoprotein (VASP).

The secondary hypothesis of our study was that after 1 week of randomized treatment PRI levels would be non-inferior in patients switched from prasugrel to ticagrelor (two arms combined) compared with patients remaining on prasugrel. VASP was measured by quantitative flow cytometry using commercially available labelled monoclonal antibodies. (NCT02016170)
Timeframe: 7 days

InterventionPRI (Least Squares Mean)
Ticagrelor25
Prasugrel36

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Platelet Reactivity

The primary endpoint is P2Y12 reaction unit (PRU) measured by the Verify Now P2Y12 assay 24hours/hospital discharge post randomization to prasugrel vs ticagrelor. PRU is is an arbitrary unit of measure to assess ADP-induced platelet aggregation. (NCT02065479)
Timeframe: 24 hours post loading dose

InterventionPRU (Mean)
Ticagrelor36
Prasugrel33

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Bleeding Event

Any event related to bleeding including access site bleeding and peri-procedural bleeding based on Bleeding Academic Research Consortium (BARC) criteria. (NCT02075125)
Timeframe: 30 days

Interventionparticipants (Number)
Prasugrel0
Ticagrelor0

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Pre-procedure Platelet Reactivity Index (PRI)

Platelet reactivity was measured using vasodilator-stimulated phosphoprotein (VASP) phosphorylation P2Y12 assay. Platelet reactivity values were presented as platelet reactivity index (PRI). (NCT02075125)
Timeframe: Baseline

Interventionpercentage (Median)
Prasugrel51.2
Ticagrelor47.5

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Number of Participants With High Platelet Reactivity

Platelet reactivity were measured by VerifyNow (volumetrics accuretic,San Diego, California, USA), and vasodilator-stimulated phosphoprotein (VASP) phosphorylation P2Y12 assay (BioCytex, Marseille, France) with FACSCalibur flow cytometer (BD Biosciences, San Jose, California, USA) using. Measurement time gap +/- 12 hours were allowed. High platelet reactivity (HPR) is defined as the result of P2Y12 reaction units (PRU) >235 and platelet reactivity index (PRI) >50%. (NCT02075125)
Timeframe: 48 hours after loading dose of study drug

,
Interventionparticipants (Number)
PRU>235VASP-PRI>50%
Prasugrel00
Ticagrelor00

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Number of Participants With Low Platelet Reactivity

Platelet reactivity were measured using VerifyNow (volumetrics accuretic, San Diego, California, USA), and vasodilator-stimulated phosphoprotein (VASP) phosphorylation P2Y12 assay (BioCytex, Marseille, France) with FACSCalibur flow cytometer (BD Biosciences, San Jose, California, USA) using. Measurement time gap +/- 12 hours were allowed. Low platelet reactivity (LPR) is defined as the result of P2Y12 reaction units (PRU) <85 and platelet reactivity index (PRI)<16%. The PRU value for LPR, 18 patients were in prasugrel groups and 19 patients in ticagrelor groups, regarding the PRI value for LPR, 16 patients were in each groups. (NCT02075125)
Timeframe: 48 hours after loading dose of study drug

,
Interventionparticipants (Number)
PRU<85VASP-PRI<16%
Prasugrel1816
Ticagrelor1916

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Adverse Drug Reaction

Any adverse reaction related to study drug until 30 days after percutaneous coronary intervention. (NCT02075125)
Timeframe: 30 days

Interventionparticipants (Number)
Prasugrel0
Ticagrelor0

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Major Adverse Cardiac and Cerebrovascular Events

Any major adverse cardiac and cerebrovascular event including (death, myocardial infarction, or revascularization and stroke) until day 30. (NCT02075125)
Timeframe: 30 days

Interventionparticipants (Number)
Prasugrel0
Ticagrelor0

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Pre-procedure P2Y12 Reaction Units (PRU)

Platelet reactivity was measured using VerifyNow (volumetrics accuretic, San Diego, California, USA). Platelet reactivity values were presented as P2Y12 reaction units (PRU). (NCT02075125)
Timeframe: Baseline

InterventionPRU units (Median)
Prasugrel259
Ticagrelor261

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P2Y12 Reaction Units (PRU)

The primary end-point of the study is the comparison in platelet reactivity expressed as PRU determined by VerifyNow P2Y12 between prasugrel 60 mg and crushed prasugrel 60 mg at 2 hours after LD administration (NCT02212028)
Timeframe: 2 hrs

InterventionPRU (Least Squares Mean)
Prasugrel Crush95
Prasugrel Tablets164

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Platelet Reactivity Index (PRI)

The secondary end-point of the study is the comparison in platelet reactivity expressed as PRI determined by whole blood vasodilator-stimulated phosphoprotein (VASP) between prasugrel 60 mg and crushed prasugrel 60 mg at 2 hours after LD administration (NCT02212028)
Timeframe: 2 hrs

InterventionPRI (Least Squares Mean)
Prasugrel Crush33
Prasugrel Tablets61

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Pharmacokinetic Quantification of Plasma Concentration of Clopidogrel and Prasugrel Active Metabolite and Ticagrelor Parent Compound and Active Metabolite Assessed Using Liquid Chromatography in Tandem With Mass Spectrometry (LC-MS/MS) Expressed as ng/ml

The parent compound of Ticagrelor was also analysed within the same patient group of Ticagrelor as it is a directly acting agent that does not require metabolic conversion to its active form. (NCT02376283)
Timeframe: Balloon Inflation as Baseline, 20, 60, 240 minutes

,,,
Interventionng/ml (Mean)
STEMI at 20 minsSTEMI at balloon inflationSTEMI at 60 minsSTEMI at 240 minsNSTEMI at 20 minsNSTEMI at 60 minsNSTEMI at 240 mins
Clopidogrel39.12107.8371.0232.4141.9993.3527.71
Prasugrel14.2724.2036.8638.44515.80194.5936.80
Ticagrelor0.161.6414.4353.387.7258.40113.59
Ticagrelor Parent Compound9.0428.5647.1384.9222.7884.13140.61

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Pharmacodynamic Assessment of Degree of Platelet Inhibition as Determined by Verify Now Point of Care Assay and Expressed as P2Y12 Reaction Units (PRU)

(NCT02376283)
Timeframe: Balloon Inflation as Baseline, 20, 60, 240 minutes

,,
InterventionP2Y12 reaction units (PRU) (Mean)
STEMI at 20 minsSTEMI at balloon inflationSTEMI at 60 minsSTEMI at 240 minsNSTEMI at 20 minsNSTEMI at 60 minsNSTEMI at 240 mins
Clopidogrel270.23286.46293.46226.42213.21227.36214.00
Prasugrel247.73253.73262.87128.64125.8076.9331.87
Ticagrelor256.73257.93225.20176.27172.80114.2023.00

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Pharmacodynamic Assessment of Degree of Platelet Inhibition as Determined by VASP (Vasodilator Stimulated Phosphoprotein Phosphorylation) Flow Cytometry and Expressed as %PRI (Platelet Reactivity Index)

(NCT02376283)
Timeframe: Balloon Inflation as Baseline, 20, 60, 240 minutes

,,
Intervention%PRI (Mean)
STEMI at 20 minsSTEMI at balloon inflationSTEMI at 60 minsSTEMI at 240 minsNSTEMI at 20 minsNSTEMI at 60 minsNSTEMI at 240 mins
Clopidogrel76.2974.8671.5763.1475.1776.7561.83
Prasugrel46.2541.1350.5057.0033.2721.9115.18
Ticagrelor79.7574.6376.2551.3862.0033.1720.17

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Maximal Platelet Aggregation

The primary end point of our study is the comparison of maximal platelet aggregation measured by light transmittance aggregometry using CAT (collagen-ADP-TRAP) between DAPT and DAPT plus vorapaxar after 30 days of treatment. (NCT02545933)
Timeframe: 30 days

Interventionpercent aggregation (Mean)
DAPT Plus Vorapaxar52
Prasugrel/Ticagrelor Plus Vorapaxar64
DAPT74

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Number of Participants With Bleeding Academic Research Consortium (BARC) Type 1, 2, 3, and 5 Bleeding According to the BARC Definitions Following Edoxaban-based Regimen Compared With Vitamin K Antagonist (VKA)-Based Regimen

"Bleeding Academic Research Consortium (BARC) bleeding events included: Bleeding (defined by BARC type 3 or 5), bleeding (defined by BARC type 2, 3, or 5), and any bleeding (defined as the composite of BARC type 1, 2, 3, or 5), where increases in BARC type indicate worse outcome.~Type 1: bleeding that is not actionable and does not cause the patient to seek unscheduled performance of studies, hospitalization, or treatment by a healthcare professional; may include episodes leading to self-discontinuation of medical therapy by the patient without consultation; Type 2: any overt, actionable sign of hemorrhage that does not fit the criteria for type 3, 4, or 5 but does meet at least one of the following criteria: (1) requiring nonsurgical, medical intervention, (2) leading to hospitalization or increased level of care, or (3) prompting evaluation; Type 3: Overt bleeding plus hemoglobin drop of 3 to ≤5 g/dL (3a), ≥5 g/dl (3b), and intracranial hemorrhage (3c) Type 5: Fatal bleeding" (NCT02866175)
Timeframe: Day 1 to 12 months postdose

,
InterventionParticipants (Count of Participants)
Bleeding (BARC Type 3 or 5)Bleeding (BARC Type 2, 3, or 5)Bleeding (BARC Type 1, 2, 3, or 5)
Edoxaban Regimen36124207
Vitamin K Antagonist Regimen42144242

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Number of Participants With Adjudicated Major, Minor, and Minimal Bleeding by Thrombolysis in Myocardial Infarction (TIMI) Definition Following Edoxaban-based Regimen Compared With Vitamin K Antagonist (VKA)-Based Regimen

Thrombolysis in Myocardial Infarction (TIMI) defined bleeding events included: Major bleeding (including fatal bleeding and non-fatal bleeding [fulfilling the TIMI major bleeding definition], major or minor bleeding, minor bleeding, minimal bleeding, and any bleeding (defined as composite of major, minor, and minimal bleeding) (NCT02866175)
Timeframe: Day 1 to 12 months postdose

,
InterventionParticipants (Count of Participants)
Major bleedingFatal bleedingMajor or minor bleedingMinor bleedingMinimal bleeding
Edoxaban Regimen151124113117
Vitamin K Antagonist Regimen244144126131

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Number of Participants With Adjudicated Major, Clinically Relevant Non-major and Minor Bleeding (All Events) Defined by International Society on Thrombosis and Haemostasis Following Edoxaban-based Regimen Compared With Vitamin K Antagonist-Based Regimen

All major, clinically relevant non-major and minor bleeding are reported for the secondary outcome. Participants may have experiences more than 1 bleeding event, all occurrences are reported. Participants with International Society on Thrombosis and Hemostasis (ISTH) defined bleeding events included: major or clinically relevant non-major bleeding (MCRB), major bleeding, including fatal bleeding (intracranial and non-intracranial), symptomatic intracranial hemorrhage, symptomatic bleeding in a critical area or organ, and clinically overt and causing ≥2.0 g/dL adjusted hemoglobin loss, clinically relevant non-major (CRNM) bleeding, minor bleedings, any bleeding (defined as the composite of major, CRNM, and minor bleeding), life-threatening bleeding, provoked (spontaneous, instrumental/traumatic, unknown) bleeding, and spontaneous bleeding. (NCT02866175)
Timeframe: Day 1 to 12 months postdose

,
InterventionParticipants (Count of Participants)
Major bleedingClinically relevant non-major bleedingMinor bleedingSymptomatic intracranial hemorrhageFatal major bleedingFatal intracranial hemorrhageLife-threatening bleedingSpontaneous bleeding
Edoxaban Regimen45971164105184
Vitamin K Antagonist Regimen481141259748210

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Number of Participants With Treatment-emergent Adverse Events (TEAEs) Following Edoxaban-based Regimen Compared With Vitamin K Antagonist (VKA)-Based Regimen

Treatment-emergent adverse events (TEAEs) in >1.0% of participants were defined as events which started on or after first dose of the assigned study drug (edoxaban and VKA) or started prior to but then worsened after the first dose of the assigned study drug. (NCT02866175)
Timeframe: Day 1 to 30 days after the last dose

,
InterventionParticipants (Count of Participants)
Any TEAEInfections and InfestationsNasopharyngitisPneumoniaBronchitisUrinary tract infectionRespiratory tract infectionInfluenzaCardiac DisordersCardiac failureAtrial fibrillationBradycardiaCardiac failure congestiveVentricular extrasystolesTachycardiaGeneral Disorders & Administration Site ConditionNon-cardiac chest painOedema peripheralAstheniaChest painFatigueGastrointestinal DisordersDiarrhoeaConstipationAbdominal pain upperGastritisNauseaDyspepsiaRespiratory,Thoracic, and Mediastinal DisordersDyspnoeaCoughDyspnoea exertionalChronic obstructive pulmonary diseaseMusculoskeletal and Connective Tissue DisordersBack painArthralgiaPain in extremityMyalgiaOsteoarthritisInvestigationsBlood creatinine increasedAlanine aminotransferase increasedBlood pressure increasedCreatinine renal clearance decreasedAspartate aminotransferase increasedInternational normalised ratio increasedNervous System DisordersDizzinessHeadacheSyncopeVascular DisordersHypertensionHypotensionHypertensive crisisRenal and Urinary DisordersRenal failureAcute kidney injuryRenal impairmentInjury, Poisoning, and Procedural ComplicationsFallSkin and Subcutaneous Tissue DisordersPruritusRashMetabolism and Nutrition DisordersGoutBlood and Lymphatic System DisordersAnaemiaPsychiatric DisorderInsomniaEar and Labyrinth DisordersVertigo
Edoxaban Regimen4571452520191412101364039108711113303121711110231169888722211866914115897015812127083301985523141149118744855121042114119238128
Vitamin K Antagonist Regimen44714022222019157134474178839824221411683197105537226115108314121385791313871112652212662231485512138441233794243520208165

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Number of Participants With Main Efficacy Endpoints For the Overall Study Period Following Edoxaban-based Regimen Compared With Vitamin K Antagonist (VKA)-Based Regimen

The main efficacy endpoints were defined as the composite of cardiovascular death (ARC), stroke (protocol defined), systemic embolic event (SEE), myocardial infarction (MI), or definite stent thrombosis. (NCT02866175)
Timeframe: Day 1 to 12 months postdose

,
InterventionParticipants (Count of Participants)
Composite MEE eventCardiovascular death (ARC)Stroke (Protocol definition)Systemic Embolic EventMyocardial infarctionDefinite stent thrombosis
Edoxaban Regimen4910100227
Vitamin K Antagonist Regimen4612110185

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Number of Participants With Adjudicated Major or Clinically Relevant Non-major Bleeding As First Event Defined by International Society on Thrombosis and Haemostasis Following Edoxaban-based Regimen Compared With Vitamin K Antagonist (VKA)-Based Regimen

Participants' first major or clinically relevant non-major bleeding (MCRB) events were reported. International Society on Thrombosis and Hemostasis (ISTH) defined bleeding events included: MCRB, major bleeding, including fatal bleeding (intracranial and non-intracranial), symptomatic intracranial hemorrhage, symptomatic bleeding in a critical area or organ, and clinically overt and causing ≥2.0 g/dL adjusted hemoglobin loss, clinically relevant non-major (CRNM) bleeding, minor bleedings, any bleeding (defined as the composite of major, CRNM, and minor bleeding), life-threatening bleeding, provoked (spontaneous, instrumental/traumatic, unknown) bleeding, and spontaneous bleeding. (NCT02866175)
Timeframe: Day 1 to 12 months postdose

,
InterventionParticipants (Count of Participants)
Composite MCRBMajor bleedingClinically relevant non-major bleeding
Edoxaban Regimen1283989
Vitamin K Antagonist Regimen15244108

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P2Y12 Reaction Unit (PRU)

Platelet reactivity measured by VerifyNow and reported as PRU (NCT03489863)
Timeframe: at 24 hours post loading dose

InterventionPRU (Mean)
Prasugrel5
Ticagrelor24

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Mean Change From Baseline to Week 4 in P2Y12 Reaction Units During Period 1

The mean change in the P2Y12 reaction unit value assessed from baseline to the end of the 4-week maintenance dose treatment period, after switching from clopidogrel maintenance dose to prasugrel maintenance dose was analyzed with a paired t-test model. Mean changes (including standard deviations) are presented. (NCT03672097)
Timeframe: Baseline up to Week 4 post-maintenance dose prasugrel treatment period

InterventionP2Y12 reaction unit (Mean)
Prasugrel-18.2

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Mean Percentage Change From Baseline to Week 4 in Platelet Inhibition During Period 1

The mean percentage change in platelet inhibition at the end of the 4-week maintenance dose prasugrel treatment period, after switching from clopidogrel maintenance dose to prasugrel maintenance dose is reported. (NCT03672097)
Timeframe: Baseline up to Week 4 post-maintenance dose prasugrel treatment period

Interventionpercentage of platelet inhibition (Mean)
Prasugrel7.2

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Number of Participants With High On-Treatment Platelet Reactivity (HTPR) During Period 1

High On-Treatment Platelet Reactivity (HTPR) was defined as PRU >235. (NCT03672097)
Timeframe: Baseline up to Week 4 post-maintenance dose prasugrel treatment period

InterventionParticipants (Count of Participants)
BaselineWeek 4
Prasugrel236

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Number of Participants With Thrombolysis In Myocardial Infarction (TIMI) Major Bleeding Events During Period 2

All safety events were assessed in the overall Safety Population, regardless of the study period. The incidence of major bleeding events (defined as non-coronary artery bypass grafting [CABG] thrombolysis in myocardial infarction (TIMI) major) after 28 maintenance dose treatment weeks (optional maximum 12-month P2Y12 inhibitor treatment after ACS participants underwent PCI) are reported. Non-CABG TIMI major bleeding was defined as any intracranial bleeding (excluding microhemorrhages less than 10 millimeter evident only on gradient-echo magnetic resonance imaging); clinically overt signs of hemorrhage associated with a drop in hemoglobin of greater than or equal to 5 g/dL; and fatal bleeding (bleeding that directly results in death within 7 days) (NCT03672097)
Timeframe: End of Week 4 up to Week 28 post-maintenance dose prasugrel treatment period

InterventionParticipants (Count of Participants)
Prasugrel4

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Number of Participants With Adverse Events of Special Interest During Period 1

Adverse events of special interest were defined as major and minor bleeding events, clinically relevant bleeding events, and any major adverse cardiovascular events (MACE). Non-CABG TIMI major bleeding was defined as any intracranial bleeding (excluding microhemorrhages less than 10 millimeter evident only on gradient-echo magnetic resonance imaging); clinically overt signs of hemorrhage associated with a drop in hemoglobin of greater than or equal to 5 g/dL; and fatal bleeding (bleeding that directly results in death within 7 days). Non-CABG TIMI minor bleeding was defined as clinically overt (including imaging), resulting in hemoglobin drop of 3 to less than 5 g/dL. (NCT03672097)
Timeframe: Baseline up to Week 4 post-maintenance dose prasugrel treatment period

InterventionParticipants (Count of Participants)
Any major bleeding adverse events (AE)Any minor bleeding AEAny clinically relevant bleeding AEAny MACE, Cardiovascular deathAny MACE, Non-fatal myocardial infarctionAny MACE, Non-fatal strokeAny MACE, Stent thrombosisAny MACE, Revascularization
Prasugrel01200000

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Number of Participants With Adverse Events of Special Interest During Period 2

All safety events were assessed in the overall Safety Population, regardless of the study period. Adverse events of special interest were defined as major and minor bleeding events, clinically relevant bleeding events, and any major adverse cardiovascular events (MACE). Non-CABG TIMI major bleeding was defined as any intracranial bleeding (excluding microhemorrhages less than 10 millimeter evident only on gradient-echo magnetic resonance imaging); clinically overt signs of hemorrhage associated with a drop in hemoglobin of greater than or equal to 5 g/dL; and fatal bleeding (bleeding that directly results in death within 7 days). Non-CABG TIMI minor bleeding was defined as clinically overt (including imaging), resulting in hemoglobin drop of 3 to less than 5 g/dL. (NCT03672097)
Timeframe: End of Week 4 up to Week 28 post-maintenance dose prasugrel treatment period

InterventionParticipants (Count of Participants)
Any major bleeding AEAny minor bleeding AEAny clinically relevant bleeding AEAny MACE, Cardiovascular deathAny MACE, Non-fatal myocardial infarctionAny MACE, Non-fatal strokeAny MACE, Stent thrombosisAny MACE, Revascularization
Prasugrel412402000

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Maximal Platelet Aggregation (MPA%) by Light Transmittance Aggregometry (LTA)

The primary end point of this study will be the comparison of MPA% measured by LTA using the CATF cocktail as agonist between DAPT and low-dose rivaroxaban plus aspirin for each DAPT regimen (NCT04006288)
Timeframe: 30 days

Interventionpercentage of MPA (Median)
Aspirin and Clopidogrel27
Aspirin and Rivaroxaban From Aspirin and Clopidogrel53
Aspirin and Prasugrel20
Aspirin and Rivaroxaban From Aspirin and Prasugrel4
Aspirin and Ticagrelor15
Aspirin and Rivaroxaban From Aspirin and Ticagrelor20

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