vorapaxar profile

vorapaxar: has antiplatelet activity; structure in first source [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

vorapaxar : A carbamate ester that is the ethyl ester of [(1R,3aR,4aR,6R,8aR,9S,9aS)-9-{(E)-2-[5-(3-fluorophenyl)pyridin-2-yl]ethynyl}-1-methyl-3-oxododecahydronaphtho[2,3-c]furan-6-yl]carbamic acid. A protease-activated receptor-1 antagonist used (as its sulfate salt) for the reduction of thrombotic cardiovascular events in patients with a history of myocardial infarction (MI) or with peripheral arterial disease. It has been shown to reduce the rate of a combined endpoint of cardiovascular death, MI, stroke and urgent coronary revascularisation. [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]

ID Source	ID
PubMed CID	10077130
CHEMBL ID	493982
CHEBI ID	82702
SCHEMBL ID	3399110
SCHEMBL ID	471187
MeSH ID	M0523308

Synonym
sch-530348
vorapaxar
mk-5348
SCHEMBL3399110
ethyl [(3ar,4ar,8ar,9as)-9(s)-[(e)-2-[5-(3-fluorophenyl)-2-pyridinyl]ethenyl]dodecahydro-1(r)-methyl-3-oxonaphtho[2,3-c]furan-6(r)-yl]carbamate
bdbm50261110
chebi:82702 ,
CHEMBL493982 ,
618385-01-6
vorapaxar (usan/inn)
D09765
carbamic acid, ((1r,3ar,4ar,6r,8ar,9s,9as)-9-((1e)-2-(5-(3-fluorophenyl)-2- pyridinyl)ethenyl)dodecahydro-1-methyl-3-oxonaphtho(2,3-c)furan-6-yl)-, ethyl ester
sch530348
vorapaxar [usan:inn]
unii-zce93644n2
ethyl ((1r,3ar,4ar,6r,8ar,9s,9as)-9-((1e)-2-(5-(3-fluorophenyl)pyridin-2-yl)ethenyl)- 1-methyl-3-oxododecahydronaphtho(2,3-c)furan-6-yl)carbamate
ethyl n-((1r,3ar,4ar,6r,8ar,9s)-9-((e)-2-(5-(3-fluorophenyl)pyridin-2-yl)ethenyl)-1-methyl-3-oxo-decahydro-1h-naphtho(2,3-c)furan-6-yl)carbamate
zce93644n2 ,
S8067
gtpl4047
ethyl n-[(3r,3as,4s,4ar,7r,8ar,9ar)-4-[(e)-2-[5-(3-fluorophenyl)pyridin-2-yl]ethenyl]-3-methyl-1-oxo-3a,4,4a,5,6,7,8,8a,9,9a-decahydro-3h-naphtho[6,7-c]furan-7-yl]carbamate
smr004701388
MLS006010324
vorapaxar [who-dd]
vorapaxar [mart.]
vorapaxar [inn]
ethyl ((1r,3ar,4ar,6r,8ar,9s,9as)-9-((1e)-2-(5-(3-fluorophenyl)pyridine-2-yl)ethen-1-yl)-1-methyl-3-oxododecahydronaphtho(2,3-c)furan-6-yl)carbamate
carbamic acid,((1r,3ar,4ar,6r,8ar,9s,9as)-9-((1e)-2-(5-(3-fluorophenyl)-2-pyridinyl)ethenyl)dodecahydro-1-methyl-3-oxonaphtho(2,3-c)furan-6-yl)-,ethyl ester
vorapaxar [vandf]
vorapaxar [mi]
vorapaxar [usan]
ethyl [(1r,3ar,4ar,6r,8ar,9s,9as)-9-{(e)-2-[5-(3-fluorophenyl)pyridin-2-yl]ethenyl}-1-methyl-3-oxododecahydronaphtho[2,3-c]furan-6-yl]carbamate
[(1r,3ar,4ar,6r,8ar,9s,9as)-9-[(1e)-2-[5-(3-fluorophenyl)-2-pyridinyl]ethenyl]dodecahydro-1-methyl-3-oxonaphtho[2,3-c]furan-6-yl]-carbamic acid ethyl ester
SCHEMBL471187
ethyl (1r,3ar,4ar,6r,8ar,9s,9as)-9-((e)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-1-methyl-3-oxododecahydronaphtho[2,3-c]furan-6-ylcarbamate
mk 5348
ethyl ((1r,3ar,4ar,6r,8ar,9s,9as)-9-((e)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-1-methyl-3-oxododecahydronaphtho[2,3-c]furan-6-yl)carbamate
DB09030
ethyl n-[(3r,3as,4s,4ar,7r,8ar,9ar)-4-[(e)-2-[5-(3-fluorophenyl)-2-pyridyl]vinyl]-3-methyl-1-oxo-3a,4,4a,5,6,7,8,8a,9,9a-decahydro-3h-benzo[f]isobenzofuran-7-yl]carbamate
carbamic acid, n-[(1r,3ar,4ar,6r,8ar,9s,9as)-9-[(e)-2-[5-(3-fluorophenyl)-2-pyridinyl]ethenyl]dodecahydro-1-methyl-3-oxonaphtho[2,3-c]furan-6-yl]-, ethyl ester
carbamic acid, [(1r,3ar,4ar,6r,8ar,9s,9as)-9-[(1e)-2-[5-(3-fluorophenyl)-2- pyridinyl]ethenyl]dodecahydro-1-methyl-3-oxonaphtho[2,3-c]furan-6-yl]-, ethyl ester
CS-5527
HY-10119
A1-03410
EX-A1343
AKOS027326789
A868624
[(1r,3ar,4ar,6r,8ar,9s,9as)-9-{(e)-2-[5-(3-fluorophenyl)pyridin-2-yl]ethenyl}-1-methyl-3-oxododecahydronaphtho[2,3-c]fur
an-6-yl]carbamate
618385-01-6 (free base)
vorapaxar free base
vorapaxar (sch 530348)
mfcd16038876
Q7941753
CCG-269633
DTXSID201009336 ,
AS-56098
ethyl n-[(1r,3ar,4ar,6r,8ar,9s,9as)-9-[(1e)-2-[5-(3-fluorophenyl)pyridin-2-yl]ethenyl]-1-methyl-3-oxo-dodecahydronaphtho[2,3-c]furan-6-yl]carbamate
EN300-21682214
Z2568728886
ethyl n-((3r,3as,4s,4ar,7r,8ar,9ar)-4-((e)-2-(5-(3-fluorophenyl)-2-pyridyl)vinyl)-3-methyl-1-oxo-3a,4,4a,5,6,7,8,8a,9,9a-decahydro-3h-benzo(f)isobenzofuran-7-yl)carbamate
dtxcid801436165
((1r,3ar,4ar,6r,8ar,9s,9as)-9-((e)-2-(5-(3-fluorophenyl)-2-pyridinyl)vinyl)-1-methyl-3-oxododecahydronaphto(2,3-c)furan-6-yl)carbamate d'ethyle
vorapaxar (mart.)
ethyl ((1r,3ar,4ar,6r,8ar,9s,9as)-9-((e)-2-(5-(3-fluorophenyl)pyridin-2-yl)ethenyl)-1-methyl-3-oxododecahydronaphtho(2,3-c)furan-6-yl)carbamate
vorapaxarum
b01ac26
carbamic acid, n-((1r,3ar,4ar,6r,8ar,9s,9as)-9-((e)-2-(5-(3-fluorophenyl)-2-pyridinyl)ethenyl)dodecahydro-1-methyl-3-oxonaphtho(2,3-c)furan-6-yl)-, ethyl ester

Excerpt	Reference	Relevance
"Vorapaxar is a novel antiplatelet therapy that inhibits thrombin-mediated platelet aggregation to prevent recurrence of ischemic events."	( Protease-Activated Receptor Antagonist for Reducing Cardiovascular Events - A Review on Vorapaxar. Aedma, SK; Combs, WG; Gupta, R; Kluck, B; Lin, M; Mehta, A; Patel, NC; Ranchal, P; Shah, R; Singh, S; Vyas, AV, 2023)	1.85
"Vorapaxar is a clinically approved PAR-1 antagonist for cardiovascular protection."	( Vorapaxar proven to be a promising candidate for pulmonary fibrosis by intervening in the PAR1/JAK2/STAT1/3 signaling pathway-an experimental in vitro and vivo study. Bao, J; Chen, S; Gao, D; Gao, J; Gu, X; Jin, J; Ren, S; Sun, R; Wei, L; Wu, C; Xiao, T; Yang, C; Yang, G; Zhou, H, 2023)	3.07
"Vorapaxar is an approved inhibitor of PAR1, used for treatment of patients with myocardial infarction or peripheral arterial disease."	( Proteinase-activated receptor 1: A target for repurposing in the treatment of COVID-19? Insel, PA; Sriram, K, 2020)	1.28
"Vorapaxar is a direct inhibitor of PAR-1 and the only agent of this class approved for the prevention of recurrent ischemic events in patients with prior myocardial infarction or peripheral artery disease."	( Role for Thrombin Receptor Antagonism With Vorapaxar in Secondary Prevention of Atherothrombotic Events: From Bench to Bedside. Angiolillo, DJ; Franchi, F; Moon, JY; Rollini, F, 2018)	1.46
"Vorapaxar is a reversible, orally active, low molecular weight, competitive antagonist of PAR-1.We investigated the effects of PAR-1 inhibition by vorapaxar on the inflammatory response, the activation of coagulation, fibrinolysis and endothelium during experimental endotoxemia."	( Inhibition of Protease-Activated Receptor (PAR1) Reduces Activation of the Endothelium, Coagulation, Fibrinolysis and Inflammation during Human Endotoxemia. Buchtele, N; Gelbenegger, G; Jilma, B; Jilma-Stohlawetz, P; Mussbacher, M; Schabbauer, G; Schoergenhofer, C; Schwameis, M; Thaler, B; Wojta, J, 2018)	1.2
"Vorapaxar is a novel antagonist of protease-activated receptor-1, the primary receptor for thrombin on human platelets that is also present on vascular endothelium and smooth muscle. "	( Vorapaxar in patients with peripheral artery disease: results from TRA2{degrees}P-TIMI 50. Bonaca, MP; Bounameaux, H; Braunwald, E; Creager, MA; Dellborg, M; Lamp, JM; Morrow, DA; Murphy, SA; Olin, J; Scirica, BM, 2013)	3.28
"Vorapaxar is an antagonist of the protease activated receptor-1 (PAR-1), the principal platelet thrombin receptor. "	( Effects of vorapaxar on platelet reactivity and biomarker expression in non-ST-elevation acute coronary syndromes. The TRACER Pharmacodynamic Substudy. Becker, RC; Chen, E; Cornel, JH; Dery, JP; Harrington, RA; Hord, E; Huber, K; Jennings, LK; Judge, HM; Kotha, J; Mahaffey, KW; Moccetti, T; Moliterno, DJ; Rorick, TL; Smyth, SS; Storey, RF; Strony, J; Thomas, GS; Tricoci, P; Valgimigli, M, 2014)	2.23
"Vorapaxar is a novel, oral, protease-activated receptor-1 antagonist that inhibits thrombin-induced platelet activation."	( PAR-1 antagonist vorapaxar favorably improves global thrombotic status in patients with coronary disease. Christopoulos, C; Gorog, DA; Kozarski, R; Morrow, D; Niespialowska-Steuden, MN; Rosser, G; Tricoci, P; Wilcox, R, 2014)	1.46
"Vorapaxar is a proteaseactivated receptor (PAR)-1 antagonist being developed for the prevention and treatment of thrombotic vascular events. "	( Pharmacokinetics of vorapaxar and its metabolite following oral administration in healthy Chinese and American subjects. Chen, X; Cutler, DL; Dockendorf, MF; Hu, P; Jiang, J; Kosoglou, T; Kumar, B; Li, J; Liu, H; Lowe, RS; Statkevich, P; Wang, G; Wang, Z, 2014)	2.17
"Vorapaxar is a novel platelet inhibitor that potently and selectively inhibits thrombin-mediated platelet activation without interfering with thrombin-mediated cleavage of fibrinogen via antagonism of the platelet proteinase-activated receptor PAR1. "	( Vorapaxar for the reduction of atherothrombotic events. Diaz-Ricart, M; Escolar, G, 2014)	3.29
"Vorapaxar is a protease-activated receptor-1 antagonist approved by the U.S. "	( Efficacy and safety of vorapaxar as approved for clinical use in the United States. Bonaca, MP; Braunwald, E; Dalby, AJ; Fox, KA; Magnani, G; Morrow, DA; Murphy, SA; Nicolau, JC; Oude Ophuis, T; Scirica, BM; Spinar, J; Theroux, P, 2015)	2.17
"Vorapaxar is a novel protease-activated receptor-1 (PAR-1) antagonist recently approved for the reduction of thrombotic cardiovascular events in patients with a history of myocardial infarction or with peripheral arterial disease. "	( Platelet transfusion reverses bleeding evoked by triple anti-platelet therapy including vorapaxar, a novel platelet thrombin receptor antagonist. Cai, TQ; Chintala, M; Forrest, M; Handt, L; Michener, MS; Raubertas, R; Seiffert, D; Sitko, G; Wickham, LA, 2015)	2.08
"Vorapaxar (Zontivity®) is a first-in-class, potent and orally-active protease-activated receptor 1 (PAR-1) antagonist that blocks thrombin-mediated platelet activation without interfering with thrombin-mediated fibrin deposition. "	( Vorapaxar: a review of its use in the long-term secondary prevention of atherothrombotic events. Frampton, JE, 2015)	3.3
"Vorapaxar is a novel protease-activated receptor-1 (PAR1) antagonist recently approved for the reduction of thrombotic cardiovascular events in patients with a history of myocardial infarction or with peripheral arterial disease. "	( In vitro pharmacological characterization of vorapaxar, a novel platelet thrombin receptor antagonist. Chintala, M; Hawes, BE; Hesk, D; Seiffert, D; Wei, H; Wirth, M; Zhai, Y, 2015)	2.12
"Vorapaxar is a newer drug recommended along with aspirin or clopidogril for prevention of recurrence of cardiac events."	( Vorapaxar, a Protease-Activated Receptor-1 Antagonist, a Double-Edged Sword! Bhandari, B; Mehta, B, 2014)	2.57
"Vorapaxar is a highly selective, reversible antagonist of protease-activated receptor-1 expressed on platelets. "	( Vorapaxar for reduction of thrombotic cardiovascular events in myocardial infarction and peripheral artery disease. Arif, SA; D'Souza, J; Gil, M; Gim, S, 2015)	3.3
"Vorapaxar is a novel antiplatelet agent that has demonstrated efficacy in reducing atherosclerotic events in patients with a history of MI or PAD without a history of stroke, transient ischemic attack, or ICH when taken in combination with aspirin and clopidogrel."	( Vorapaxar for reduction of thrombotic cardiovascular events in myocardial infarction and peripheral artery disease. Arif, SA; D'Souza, J; Gil, M; Gim, S, 2015)	3.3
"Vorapaxar is a protease activated receptor-1 (PAR-1) antagonist, and prevents thrombin activation of PAR-1 receptors on platelets."	( Review of vorapaxar for the prevention of atherothrombotic events. Wang, A, 2015)	1.54
"Vorapaxar is a first-in-class protease-activated receptor-1 antagonist indicated for secondary prevention in stable patients with previous myocardial infarction (MI) or peripheral artery disease and no cerebrovascular disease. "	( Outcomes in Stable Patients With Previous Atherothrombotic Events Receiving Vorapaxar Who Experience a New Acute Coronary Event (from TRA2°P-TIMI 50). Berg, DD; Bonaca, MP; Braunwald, E; Corbalan, R; Goto, S; Kiss, RG; Morrow, DA; Murphy, SA; Scirica, BM; Spinar, J, 2016)	2.11
"Vorapaxar is a first-in-class PAR-1 antagonistic drug based on the ent-himbacine scaffold. "	( Synthesis of novel and potent vorapaxar analogues. Aliev, AE; Caddick, S; Chambers, RC; Chudasama, V; Inglis, GG; Knight, E; Robinson, E; Smoktunowicz, N, 2016)	2.17
"Vorapaxar is a first-in-class protease-activated receptor-1 antagonist indicated for the reduction of cardiovascular death, myocardial infarction, and stroke in stable patients with prior atherothrombosis, who have not had a prior stroke or transient ischemic attack. "	( Vorapaxar in patients with coronary artery bypass grafting: Findings from the TRA 2°P-TIMI 50 trial. Bonaca, MP; Braunwald, E; Dellborg, M; He, P; Kosova, EC; Morais, J; Morrow, DA; Oude Ophuis, T; Scirica, BM; Tendera, M; Theroux, P, 2017)	3.34
"Vorapaxar is a tricyclic himbacine-derived reversible inhibitor of platelet surface protease activator receptor-1, which prevents thrombin from activating platelets."	( Impact of selective platelet inhibition in reducing cardiovascular risk - role of vorapaxar. Cheng, JW, 2016)	1.38
"Vorapaxar is a first-in-class, novel antiplatelet agent that acts by antagonizing the PAR-1 receptor, inhibiting thrombin-mediated platelet activation."	( Vorapaxar: emerging evidence and clinical questions in a new era of PAR-1 inhibition. Mahaffey, KW; Rodriguez, F; Ungar, L, 2016)	2.6
"Vorapaxar is a first-in-class, protease-activated receptor-1 antagonist. "	( Vorapaxar: The Current Role and Future Directions of a Novel Protease-Activated Receptor Antagonist for Risk Reduction in Atherosclerotic Disease. Anderson, SM; Buckley, LF; Gryka, RJ, 2017)	3.34
"Vorapaxar is a new oral protease-activated-receptor 1 (PAR-1) antagonist that inhibits thrombin-induced platelet activation."	( Thrombin-receptor antagonist vorapaxar in acute coronary syndromes. Ambrosio, G; Armstrong, PW; Aylward, PE; Bode, C; Cequier, A; Chen, E; Cornel, JH; Diaz, R; Erkan, A; Harrington, RA; Held, C; Huang, Z; Huber, K; Hudson, MP; Jennings, LH; Jiang, L; Jukema, JW; Kilian, AM; Leonardi, S; Lewis, BS; Lincoff, AM; Lokhnygina, Y; Mahaffey, KW; Moliterno, DJ; Montalescot, G; Nicolau, JC; Ogawa, H; Pei, J; Pfisterer, M; Prieto, JC; Rorick, TL; Ruzyllo, W; Sinnaeve, PR; Storey, RF; Strony, J; Tricoci, P; Valgimigli, M; Van de Werf, F; Wallentin, L; Whellan, DJ; White, HD; Widimsky, P, 2012)	2.11
"Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1."	( Vorapaxar in the secondary prevention of atherothrombotic events. Ameriso, SF; Bonaca, MP; Braunwald, E; Dalby, AJ; Fish, MP; Fox, KA; Lipka, LJ; Liu, X; Morrow, DA; Murphy, SA; Nicolau, JC; Ophuis, AJ; Paolasso, E; Scirica, BM; Spinar, J; Strony, J; Theroux, P; Wiviott, SD, 2012)	2.54
"Vorapaxar is an orally active protease-activated receptor 1 (PAR-1) antagonist that inhibits thrombin-induced platelet aggregation. "	( Vorapaxar, an oral PAR-1 receptor antagonist, does not affect the pharmacokinetics and pharmacodynamics of warfarin. Black, L; Cutler, DL; Johnson-Levonas, AO; Kosoglou, T; Martinho, M; Statkevich, P; Xuan, F; Zhu, Y, 2012)	3.26
"Vorapaxar is an antiplatelet agent that antagonizes thrombin-mediated activation of the protease-activated receptor-1 on platelets. "	( Efficacy and safety of vorapaxar in patients with prior ischemic stroke. Alberts, MJ; Ameriso, SF; Bonaca, MP; Braunwald, E; Goto, S; Hankey, GJ; Mohr, JP; Morrow, DA; Murphy, SA; Scirica, BM, 2013)	2.14

Excerpt	Reference	Relevance
"Vorapaxar treatment significantly inhibited thrombin-induced calcium mobilisation, leaving a residual, delayed response."	( PAR1 antagonists inhibit thrombin-induced platelet activation whilst leaving the PAR4-mediated response intact. Ecob, R; Hord, E; Jennings, LK; Judge, HM; Kotha, J; Moliterno, DJ; Rorick, T; Storey, RF; Tricoci, P, 2015)	1.14

Excerpt	Reference	Relevance
" Previous phase II studies of patients undergoing urgent or scheduled percutaneous coronary intervention treated with vorapaxar plus aspirin and clopidogrel or ticlopidine showed a trend toward reducing major adverse cardiac events, particularly myocardial infarction, without increasing bleeding risk."	( Safety of the novel protease-activated receptor-1 antagonist vorapaxar in Japanese patients with a history of ischemic stroke. Doi, M; Goto, S; Jensen, P; Shinohara, Y, 2012)	0.83
" The primary endpoint was overall incidence of adverse events during the protocol-defined treatment phase (60 days)."	( Safety of the novel protease-activated receptor-1 antagonist vorapaxar in Japanese patients with a history of ischemic stroke. Doi, M; Goto, S; Jensen, P; Shinohara, Y, 2012)	0.62
"Addition of vorapaxar to aspirin did not significantly increase the overall incidence of adverse events, including serious adverse events."	( Safety of the novel protease-activated receptor-1 antagonist vorapaxar in Japanese patients with a history of ischemic stroke. Doi, M; Goto, S; Jensen, P; Shinohara, Y, 2012)	1
"Vorapaxar used in combination with standard doses of aspirin was safe and well tolerated in Japanese subjects with a history of ischemic stroke."	( Safety of the novel protease-activated receptor-1 antagonist vorapaxar in Japanese patients with a history of ischemic stroke. Doi, M; Goto, S; Jensen, P; Shinohara, Y, 2012)	2.06

Excerpt	Reference	Relevance
" Early appraisal of drug metabolism and pharmacokinetic (DMPK) parameters is now possible due to several higher throughput in vitro and in vivo screens."	( The role of exploratory drug metabolism and pharmacokinetics in new drug research: case study-selection of a thrombin receptor antagonist for development. Chackalamannil, S; Cheng, KC; Hsieh, Y; Korfmacher, WA; Wang, Y; White, RE; Xia, Y, 2009)	0.35
" Pharmacodynamic and pharmacokinetic profiles of vorapaxar in the two racial/ethnic groups were similar."	( No differences in the pharmacodynamics and pharmacokinetics of the thrombin receptor antagonist vorapaxar between healthy Japanese and Caucasian subjects. Cutler, DL; Jennings, LK; Kasserra, C; Kosoglou, T; Maxwell, SE; Meehan, AG; Pei, J; Reyderman, L; Schiller, J; Xuan, F; Young, S, 2012)	0.85
" Blood samples for vorapaxar PK and pharmacodynamic analysis were collected predose and at frequent intervals up to 6 weeks postdose."	( Pharmacokinetics and pharmacodynamics of the novel PAR-1 antagonist vorapaxar in patients with end-stage renal disease. Cutler, DL; Jennings, LK; Kosoglou, T; Kraft, WK; Kumar, B; Langdon, RB; Ma, L; Schiller, JE; Statkevich, P; Xuan, F, 2012)	0.94
" The observed means for elimination half-life were 186 and 231 h in the ESRD and control groups, respectively."	( Pharmacokinetics and pharmacodynamics of the novel PAR-1 antagonist vorapaxar in patients with end-stage renal disease. Cutler, DL; Jennings, LK; Kosoglou, T; Kraft, WK; Kumar, B; Langdon, RB; Ma, L; Schiller, JE; Statkevich, P; Xuan, F, 2012)	0.61
"Results of this study indicate that vorapaxar has no meaningful effect on the pharmacokinetics or pharmacodynamics of warfarin, suggesting that the coadministration of these two drugs or vorapaxar coadministered with other CYP2C9/CYP2C19 substrates is unlikely to cause a clinically significant pharmacokinetic drug interaction."	( Vorapaxar, an oral PAR-1 receptor antagonist, does not affect the pharmacokinetics and pharmacodynamics of warfarin. Black, L; Cutler, DL; Johnson-Levonas, AO; Kosoglou, T; Martinho, M; Statkevich, P; Xuan, F; Zhu, Y, 2012)	2.1
" It was the study's objective to assess the pharmacodynamic effects of vorapaxar versus placebo that included aspirin or a thienopyridine or, frequently, a combination of both agents in NSTE-ACS patients."	( Effects of vorapaxar on platelet reactivity and biomarker expression in non-ST-elevation acute coronary syndromes. The TRACER Pharmacodynamic Substudy. Becker, RC; Chen, E; Cornel, JH; Dery, JP; Harrington, RA; Hord, E; Huber, K; Jennings, LK; Judge, HM; Kotha, J; Mahaffey, KW; Moccetti, T; Moliterno, DJ; Rorick, TL; Smyth, SS; Storey, RF; Strony, J; Thomas, GS; Tricoci, P; Valgimigli, M, 2014)	1.03
" To evaluate race/ethnic differences between Caucasians and Chinese in the pharmacokinetics of vorapaxar and its active metabolite SCH 2046273 (M20) or in the metabolite/parent ratio, we conducted a cross-study comparison on pharmacokinetic data of vorapaxar and M20 obtained from two similarly designed studies: one in healthy Chinese subjects and the other in a healthy Western (United States, [U."	( Pharmacokinetics of vorapaxar and its metabolite following oral administration in healthy Chinese and American subjects. Chen, X; Cutler, DL; Dockendorf, MF; Hu, P; Jiang, J; Kosoglou, T; Kumar, B; Li, J; Liu, H; Lowe, RS; Statkevich, P; Wang, G; Wang, Z, 2014)	0.94
"The pharmacokinetic profiles of vorapaxar and M20 were characterized using open label, two treatment parallel group designs in men and women aged 18 - 45 years."	( Pharmacokinetics of vorapaxar and its metabolite following oral administration in healthy Chinese and American subjects. Chen, X; Cutler, DL; Dockendorf, MF; Hu, P; Jiang, J; Kosoglou, T; Kumar, B; Li, J; Liu, H; Lowe, RS; Statkevich, P; Wang, G; Wang, Z, 2014)	1.01
"The pharmacokinetic profiles of vorapaxar and M20 and the metabolite/parent ratios in healthy Chinese were generally comparable to those in a healthy Western population."	( Pharmacokinetics of vorapaxar and its metabolite following oral administration in healthy Chinese and American subjects. Chen, X; Cutler, DL; Dockendorf, MF; Hu, P; Jiang, J; Kosoglou, T; Kumar, B; Li, J; Liu, H; Lowe, RS; Statkevich, P; Wang, G; Wang, Z, 2014)	1.01
" The ratio of geometric means (GMR) and 90% confidence intervals (CI) of the coadministration versus monotherapy for Cmax (GMR 95; 90% CI 88, 103) and AUC0-24 h (GMR 103; 90% CI 98, 108) were within the 80-125% bioequivalence criteria."	( Vorapaxar, an oral PAR-1 receptor antagonist, does not affect the pharmacokinetics of rosiglitazone. Cutler, DL; Hanson, ME; Kantesaria, B; Kosoglou, T; Kumar, B; Schiller, JE; Sisk, CM; Statkevich, P, 2015)	1.86
"Coadministration of vorapaxar with rosiglitazone or drugs metabolized via CYP2C8 is unlikely to cause a significant pharmacokinetic interaction."	( Vorapaxar, an oral PAR-1 receptor antagonist, does not affect the pharmacokinetics of rosiglitazone. Cutler, DL; Hanson, ME; Kantesaria, B; Kosoglou, T; Kumar, B; Schiller, JE; Sisk, CM; Statkevich, P, 2015)	2.18

Excerpt	Reference	Relevance
" In conclusion, GP IIb/IIIa receptor inhibitor use plus dual antiplatelet therapy in a population with non-ST-segment elevation myocardial infarction planned for PCI was frequent but did not interact with vorapaxar's efficacy or safety."	( Glycoprotein IIb/IIIa Receptor Inhibitors in Combination With Vorapaxar, a Platelet Thrombin Receptor Antagonist, Among Patients With Non-ST-Segment Elevation Acute Coronary Syndromes (from the TRACER Trial). Armstrong, PW; Aylward, PE; Chen, E; Clare, RM; Cornel, JH; Harrington, RA; Held, C; Leonardi, S; Lokhnygina, Y; Mahaffey, KW; Moliterno, DJ; Strony, J; Tricoci, P; Van de Werf, F; Wallentin, L; White, HD, 2015)	0.85
" Here, we have performed robust virtual screening combined with biased-force pulling molecular dynamic (MD) simulations to predict high-affinity GPR17 modulators followed by experimental validation."	( Bias-force guided simulations combined with experimental validations towards GPR17 modulators identification. Kandhavelu, M; Kari, S; Kidambi, S; Marimuthu, P; Murugesan, A; Razzokov, J; Selvaraj, C; Thiyagarajan, R, 2023)	0.91

Excerpt	Reference	Relevance
" In both cynomolgus monkeys and humans, the compound had high bioavailability and inhibited ex vivo TRAP (thrombin receptor-activating peptide)-stimulated platelet aggregation in a potent and long-lasting manner."	( SCH-530348, a thrombin receptor (PAR-1) antagonist for the prevention and treatment of atherothrombosis. Oestreich, J, 2009)	0.35
" Preclinical and initial clinical studies have demonstrated this compound to be a highly potent inhibitor of thrombin-induced platelet activation, to have excellent oral bioavailability and to have a favorable safety profile."	( SCH 530348: a novel oral thrombin receptor antagonist. Bonaca, MP; Morrow, DA, 2009)	0.35
"Vorapaxar, a novel antiplatelet agent in advanced clinical development for the prevention and treatment of atherothrombotic disease, is a potent, orally bioavailable thrombin receptor antagonist selective for the protease-activated receptor 1 (PAR-1)."	( No differences in the pharmacodynamics and pharmacokinetics of the thrombin receptor antagonist vorapaxar between healthy Japanese and Caucasian subjects. Cutler, DL; Jennings, LK; Kasserra, C; Kosoglou, T; Maxwell, SE; Meehan, AG; Pei, J; Reyderman, L; Schiller, J; Xuan, F; Young, S, 2012)	2.04
"Mean vorapaxar bioavailability (based on area under the curve of plasma vorapaxar concentration over time) was identical in the two subject groups; the ESRD/healthy geometric mean ratio (GMR, expressed in percent) was 98."	( Pharmacokinetics and pharmacodynamics of the novel PAR-1 antagonist vorapaxar in patients with end-stage renal disease. Cutler, DL; Jennings, LK; Kosoglou, T; Kraft, WK; Kumar, B; Langdon, RB; Ma, L; Schiller, JE; Statkevich, P; Xuan, F, 2012)	1.13

Excerpt	Relevance	Reference
" Clinical study results suggest that SCH 530348 dosage at 20 mg or 40 mg is feasible to achieve rapid maximum platelet inhibition following an acute coronary event or intervention procedure."	( Determination of a novel thrombin receptor antagonist (SCH 530348) in human plasma: evaluation of Ultra Performance Liquid Chromatography™-tandem mass spectrometry for routine bioanalytical analysis. Clement, RP; Hayes, RN; Schiller, JE; Shen, JX; Tama, CI, 2011)	0.37
"Since race/ethnicity may affect the safety, efficacy and dosage of drugs, this study was conducted to evaluate potential differences in the pharmacodynamics, pharmacokinetics and safety of vorapaxar after single (5, 10, 20, or 40 mg) or multiple (0."	( No differences in the pharmacodynamics and pharmacokinetics of the thrombin receptor antagonist vorapaxar between healthy Japanese and Caucasian subjects. Cutler, DL; Jennings, LK; Kasserra, C; Kosoglou, T; Maxwell, SE; Meehan, AG; Pei, J; Reyderman, L; Schiller, J; Xuan, F; Young, S, 2012)	0.79
" No dose or dosage adjustment of vorapaxar will be required in patients with mild to moderate hepatic impairment."	( Pharmacokinetics of the novel PAR-1 antagonist vorapaxar in patients with hepatic impairment. Cutler, DL; Kosoglou, T; Kumar, B; Langdon, RB; Preston, RA; Schiller, JE; Statkevich, P; Trusley, C; Xuan, F, 2012)	0.92
"The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, dosage and administration, cost, and place in therapy of vorapaxar in the secondary prevention of atherosclerotic events are reviewed."	( Vorapaxar for reduction of thrombotic cardiovascular events in myocardial infarction and peripheral artery disease. Arif, SA; D'Souza, J; Gil, M; Gim, S, 2015)	2.06
" Vorapaxar dosing was guided by thrombin receptor-activating peptide-6-induced whole blood aggregometry."	( Inhibition of Protease-Activated Receptor (PAR1) Reduces Activation of the Endothelium, Coagulation, Fibrinolysis and Inflammation during Human Endotoxemia. Buchtele, N; Gelbenegger, G; Jilma, B; Jilma-Stohlawetz, P; Mussbacher, M; Schabbauer, G; Schoergenhofer, C; Schwameis, M; Thaler, B; Wojta, J, 2018)	1.39

Role	Description
protease-activated receptor-1 antagonist	An antagonist at the protease-activated receptor-1.
platelet aggregation inhibitor	A drug or agent which antagonizes or impairs any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system.
cardiovascular drug	A drug that affects the rate or intensity of cardiac contraction, blood vessel diameter or blood volume.
[role information is derived from 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]

Class	Description
pyridines	Any organonitrogen heterocyclic compound based on a pyridine skeleton and its substituted derivatives.
carbamate ester	Any ester of carbamic acid or its N-substituted derivatives.
organofluorine compound	An organofluorine compound is a compound containing at least one carbon-fluorine bond.
naphthofuran
lactone	Any cyclic carboxylic ester containing a 1-oxacycloalkan-2-one structure, or an analogue having unsaturation or heteroatoms replacing one or more carbon atoms of the ring.
[compound class information is derived from 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]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Proteinase-activated receptor 1	Homo sapiens (human)	IC50 (µMol)	0.0626	0.0011	1.0069	10.0000	AID1056259; AID1056260; AID1458226; AID1458242; AID1458243; AID1667457; AID407982; AID407983
Proteinase-activated receptor 1	Homo sapiens (human)	Ki	0.0077	0.0011	0.0287	0.1600	AID1065174; AID407981; AID407996; AID407997; AID527581
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Process	via Protein(s)	Taxonomy
connective tissue replacement involved in inflammatory response wound healing	Proteinase-activated receptor 1	Homo sapiens (human)
negative regulation of glomerular filtration	Proteinase-activated receptor 1	Homo sapiens (human)
activation of cysteine-type endopeptidase activity involved in apoptotic process	Proteinase-activated receptor 1	Homo sapiens (human)
inflammatory response	Proteinase-activated receptor 1	Homo sapiens (human)
G protein-coupled receptor signaling pathway	Proteinase-activated receptor 1	Homo sapiens (human)
phospholipase C-activating G protein-coupled receptor signaling pathway	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of cytosolic calcium ion concentration	Proteinase-activated receptor 1	Homo sapiens (human)
protein kinase C-activating G protein-coupled receptor signaling pathway	Proteinase-activated receptor 1	Homo sapiens (human)
establishment of synaptic specificity at neuromuscular junction	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of cell population proliferation	Proteinase-activated receptor 1	Homo sapiens (human)
negative regulation of cell population proliferation	Proteinase-activated receptor 1	Homo sapiens (human)
response to wounding	Proteinase-activated receptor 1	Homo sapiens (human)
anatomical structure morphogenesis	Proteinase-activated receptor 1	Homo sapiens (human)
platelet activation	Proteinase-activated receptor 1	Homo sapiens (human)
regulation of blood coagulation	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of blood coagulation	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of cell migration	Proteinase-activated receptor 1	Homo sapiens (human)
response to lipopolysaccharide	Proteinase-activated receptor 1	Homo sapiens (human)
regulation of interleukin-1 beta production	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of interleukin-6 production	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of interleukin-8 production	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of collagen biosynthetic process	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of Rho protein signal transduction	Proteinase-activated receptor 1	Homo sapiens (human)
dendritic cell homeostasis	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of canonical NF-kappaB signal transduction	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of cysteine-type endopeptidase activity involved in apoptotic process	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of MAPK cascade	Proteinase-activated receptor 1	Homo sapiens (human)
negative regulation of neuron apoptotic process	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of GTPase activity	Proteinase-activated receptor 1	Homo sapiens (human)
cell-cell junction maintenance	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of DNA-templated transcription	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of vasoconstriction	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of smooth muscle contraction	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of receptor signaling pathway via JAK-STAT	Proteinase-activated receptor 1	Homo sapiens (human)
regulation of synaptic plasticity	Proteinase-activated receptor 1	Homo sapiens (human)
homeostasis of number of cells within a tissue	Proteinase-activated receptor 1	Homo sapiens (human)
release of sequestered calcium ion into cytosol	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of release of sequestered calcium ion into cytosol	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transduction	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of calcium ion transport	Proteinase-activated receptor 1	Homo sapiens (human)
regulation of sensory perception of pain	Proteinase-activated receptor 1	Homo sapiens (human)
platelet dense granule organization	Proteinase-activated receptor 1	Homo sapiens (human)
positive regulation of ERK1 and ERK2 cascade	Proteinase-activated receptor 1	Homo sapiens (human)
thrombin-activated receptor signaling pathway	Proteinase-activated receptor 1	Homo sapiens (human)
trans-synaptic signaling by endocannabinoid, modulating synaptic transmission	Proteinase-activated receptor 1	Homo sapiens (human)
negative regulation of renin secretion into blood stream	Proteinase-activated receptor 1	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
G-protein alpha-subunit binding	Proteinase-activated receptor 1	Homo sapiens (human)
G protein-coupled receptor activity	Proteinase-activated receptor 1	Homo sapiens (human)
signaling receptor binding	Proteinase-activated receptor 1	Homo sapiens (human)
protein binding	Proteinase-activated receptor 1	Homo sapiens (human)
thrombin-activated receptor activity	Proteinase-activated receptor 1	Homo sapiens (human)
G-protein beta-subunit binding	Proteinase-activated receptor 1	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
plasma membrane	Proteinase-activated receptor 1	Homo sapiens (human)
extracellular region	Proteinase-activated receptor 1	Homo sapiens (human)
early endosome	Proteinase-activated receptor 1	Homo sapiens (human)
late endosome	Proteinase-activated receptor 1	Homo sapiens (human)
Golgi apparatus	Proteinase-activated receptor 1	Homo sapiens (human)
plasma membrane	Proteinase-activated receptor 1	Homo sapiens (human)
caveola	Proteinase-activated receptor 1	Homo sapiens (human)
cell surface	Proteinase-activated receptor 1	Homo sapiens (human)
platelet dense tubular network	Proteinase-activated receptor 1	Homo sapiens (human)
neuromuscular junction	Proteinase-activated receptor 1	Homo sapiens (human)
postsynaptic membrane	Proteinase-activated receptor 1	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (110)

Assay ID	Title	Year	Journal	Article
AID1347411	qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary	2020	ACS chemical biology, 07-17, Volume: 15, Issue:7	High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1217224	Activity of human recombinant CYP2B6 assessed as enzyme-mediated drug metabolism at 10 uM after 120 mins by LC-MS/MS analysis in presence of NADPH	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1217272	Drug metabolism in human liver microsomes assessed as (3R,3aS,4S,4aR,7R,8aR,9aR)-7-amino-4-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-3-methyldecahydronaphtho[2,3-c]furan-1(3H)-one formation at 10 to 25 uM after 120 mins by LC-MS/MS analysis in presenc	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID527570	Ex-vivo inhibition of PAR1-mediated aggregation of high affinity TRAP-stimulated cynomolgus monkey platelet at 0.1 mg/kg, po administered as single dose measured after 24 hrs	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Discovery of a vorapaxar analog with increased aqueous solubility.
AID1217223	Activity of human recombinant CYP1A2 assessed as enzyme-mediated drug metabolism at 10 uM after 120 mins by LC-MS/MS analysis in presence of NADPH	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1217285	Drug metabolism in human liver microsomes assessed as 2-hydroxyethyl (1R,3aR,4aR,6R,8aR,9S,9aS)-9-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-1-methyl-3-oxododecahydronaphtho[2,3-c]furan-6-ylcarbamate formation at 25 uM after 120 mins by LC-MS/MS analys	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID408024	Cmax in cynomolgus monkey at 0.1 mg/kg, po after >24 hrs	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1217259	Activity of human recombinant CYP2J2 assessed as enzyme-mediated ((4aR,6R)-9-{2-[(1R,4S)-5-((S)-3-Fluoro-phenyl)-pyridin-2-yl]-vinyl}-1-methyl-3-oxo-dodecahydro-naphtho[2,3-c]furan-6-yl)-carbamic acid(R)-2-hydroxy-ethyl ester formation at 10 uM after 120	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1217276	Drug metabolism in human liver microsomes assessed as (3R,3aS,4S,4aR,7R,8aR,9aR)-7-amino-4-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-3-methyldecahydronaphtho[2,3-c]furan-1(3H)-one formation at 10 to 25 uM after 120 mins by LC-MS/MS analysis in presenc	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID527582	Equilibrium solubility of the compound after 24 hrs	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Discovery of a vorapaxar analog with increased aqueous solubility.
AID1458243	Antagonist activity at PAR1 in human platelet-rich plasma assessed as reduction in thrombin-stimulated platelet aggregation preincubated for 3 mins followed by thrombin stimulation measured after 5 mins by aggregometric analysis	2017	Journal of medicinal chemistry, 08-24, Volume: 60, Issue:16	Discovery of Potent Orally Active Protease-Activated Receptor 1 (PAR1) Antagonists Based on Andrographolide.
AID1065174	Displacement of [3H]haTRAP from PAR-1 isolated from human platelets by liquid scintillation counting analysis	2014	ACS medicinal chemistry letters, Feb-13, Volume: 5, Issue:2	Himbacine-derived thrombin receptor antagonists: c7-aminomethyl and c9a-hydroxy analogues of vorapaxar.
AID1458249	Toxicity in guinea pig assessed as inhibition of collagen-stimulated platelet aggregation at 10 mg/kg, po pretreated for 2 hrs followed by collagen stimulation measured after 5 mins	2017	Journal of medicinal chemistry, 08-24, Volume: 60, Issue:16	Discovery of Potent Orally Active Protease-Activated Receptor 1 (PAR1) Antagonists Based on Andrographolide.
AID1667457	Antagonist activity at human PAR1 expressed in KNRK cells assessed as inhibition of agonist-induced intracellular calcium mobilization by fluorimetric assay	2020	Bioorganic & medicinal chemistry letters, 04-15, Volume: 30, Issue:8	Design and synthesis of potent PAR-1 antagonists based on vorapaxar.
AID1667459	AUC (0 to infinity) in Sprague-Dawley rat at 5 mg/kg, po or 1 mg/kg, iv	2020	Bioorganic & medicinal chemistry letters, 04-15, Volume: 30, Issue:8	Design and synthesis of potent PAR-1 antagonists based on vorapaxar.
AID1217280	Drug metabolism in human liver microsomes assessed as (3R,3aS,4S,4aR,7R,8aR,9aR)-7-amino-4-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-3-methyldecahydronaphtho[2,3-c]furan-1(3H)-one formation at 10 to 25 uM after 120 mins by LC-MS/MS analysis in presenc	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1217221	Drug metabolism in human liver S9 fraction assessed as compound remaining at 10 uM after 120 mins by LC-MS/MS analysis in presence of NADPH	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1217335	Drug metabolism in human lung microsomes assessed as 2-hydroxyethyl (1R,3aR,4aR,6R,8aR,9S,9aS)-9-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-1-methyl-3-oxododecahydronaphtho[2,3-c]furan-6-ylcarbamate formation at 25 uM after 120 mins by LC-MS/MS analysi	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID408023	AUC (0 to 24 hrs) in cynomolgus monkey at 0.1 mg/kg, po after >24 hrs	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1217229	Activity of human recombinant CYP3A5 assessed as enzyme-mediated drug metabolism at 10 uM after 120 mins by LC-MS/MS analysis in presence of NADPH	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1667456	Antagonist activity at human PAR1 expressed in KNRK cells assessed as inhibition of agonist-induced intracellular calcium mobilization at 10'-5 M by fluorimetric assay relative to control	2020	Bioorganic & medicinal chemistry letters, 04-15, Volume: 30, Issue:8	Design and synthesis of potent PAR-1 antagonists based on vorapaxar.
AID1056259	Antagonist activity at PAR1 in washed human platelets assessed as inhibition of haTRAP-induced platelet aggregation preincubated for 1 hr followed by haTRAP addition measured for 10 mins by spectrophotometric analysis	2013	ACS medicinal chemistry letters, Nov-14, Volume: 4, Issue:11	Discovery of Octahydroindenes as PAR1 Antagonists.
AID1217222	Activity of human recombinant CYP1A1 assessed as enzyme-mediated drug metabolism at 10 uM after 120 mins by LC-MS/MS analysis in presence of NADPH	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1552687	Negative allosteric modulation of PAR2 in human EAhy926 cells assessed as reduction in SLIGKV-NH2-induced intracellular calcium mobilization at 0.316 to 10 uM incubated for 15 mins followed by TFLLRN-NH2 addition by Fluo-4-AM dye based fluorescence assay	2019	Bioorganic & medicinal chemistry, 09-01, Volume: 27, Issue:17	The parmodulin NRD-21 is an allosteric inhibitor of PAR1 Gq signaling with improved anti-inflammatory activity and stability.
AID1217270	Drug metabolism in human liver microsomes assessed as (3R,3aS,4S,4aR,7R,8aR,9aR)-7-amino-4-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-3-methyldecahydronaphtho[2,3-c]furan-1(3H)-one formation at 10 to 25 uM after 120 mins by LC-MS/MS analysis in presenc	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID407996	Antagonist activity at human PAR1 in HCASMC assessed as inhibition of thrombin-induced calcium efflux	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID408007	Tmax in monkey 1 mg/kg, po	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID408013	Inhibition of CYP1A2 in human liver microsomes at 90 uM	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID408010	Binding affinity to PAR2	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1056257	Cytotoxicity against human HepG2 cells assessed as ATP contents at 30 uM after 24 hrs relative to control	2013	ACS medicinal chemistry letters, Nov-14, Volume: 4, Issue:11	Discovery of Octahydroindenes as PAR1 Antagonists.
AID1217254	Drug metabolism in human liver microsomes assessed as 2-hydroxyethyl (1R,3aR,4aR,6R,8aR,9S,9aS)-9-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-1-methyl-3-oxododecahydronaphtho[2,3-c]furan-6-ylcarbamate formation at 25 uM after 120 mins by LC-MS/MS analys	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1217333	Drug metabolism in human intestine microsomes assessed as 2-hydroxyethyl (1R,3aR,4aR,6R,8aR,9S,9aS)-9-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-1-methyl-3-oxododecahydronaphtho[2,3-c]furan-6-ylcarbamate formation at 25 uM after 120 mins by LC-MS/MS an	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1217269	Drug metabolism in human liver microsomes assessed as (3R,3aS,4S,4aR,7R,8aR,9aR)-7-amino-4-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-3-methyldecahydronaphtho[2,3-c]furan-1(3H)-one formation at 10 to 25 uM after 120 mins by LC-MS/MS analysis in presenc	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1217279	Drug metabolism in human liver microsomes assessed as (3R,3aS,4S,4aR,7R,8aR,9aR)-7-amino-4-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-3-methyldecahydronaphtho[2,3-c]furan-1(3H)-one formation at 10 to 25 uM after 120 mins by LC-MS/MS analysis in presenc	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1667460	Cmax in Sprague-Dawley rat at 5 mg/kg, po or 1 mg/kg, iv	2020	Bioorganic & medicinal chemistry letters, 04-15, Volume: 30, Issue:8	Design and synthesis of potent PAR-1 antagonists based on vorapaxar.
AID408012	Activity at PAR4	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID408006	Tmax in rat 10 mg/kg, po	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1217268	Drug metabolism in human liver microsomes assessed as (3R,3aS,4S,4aR,7R,8aR,9aR)-7-amino-4-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-3-methyldecahydronaphtho[2,3-c]furan-1(3H)-one formation at 10 to 25 uM after 120 mins by LC-MS/MS analysis in presenc	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1217228	Activity of human recombinant CYP3A4 assessed as enzyme-mediated drug metabolism at 10 uM after 120 mins by LC-MS/MS analysis in presence of NADPH	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID527585	Cmax in rat	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Discovery of a vorapaxar analog with increased aqueous solubility.
AID407994	Ex vivo inhibition of haTRAP-induced platelet aggregation in cynomolgus monkey at 0.3 mg/kg, po after 24 hrs by impedance aggregometry	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID527583	Kinetic solubility of the compound	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Discovery of a vorapaxar analog with increased aqueous solubility.
AID1552688	Reversible inhibition of PAR1 in human EAhy926 cells assessed as reduction in TFLLRN-NH2-induced intracellular calcium mobilization at 10 uM incubated for 15 mins and washed in buffer followed by TFLLRN-NH2 addition by Fluo-4-AM dye based fluorescence ass	2019	Bioorganic & medicinal chemistry, 09-01, Volume: 27, Issue:17	The parmodulin NRD-21 is an allosteric inhibitor of PAR1 Gq signaling with improved anti-inflammatory activity and stability.
AID1217332	Drug metabolism in human liver microsomes assessed as 2-hydroxyethyl (1R,3aR,4aR,6R,8aR,9S,9aS)-9-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-1-methyl-3-oxododecahydronaphtho[2,3-c]furan-6-ylcarbamate formation at 25 uM after 120 mins by LC-MS/MS analys	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID527584	AUC in rat	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Discovery of a vorapaxar analog with increased aqueous solubility.
AID1217331	Drug metabolism in human liver microsomes assessed as 2-hydroxyethyl (1R,3aR,4aR,6R,8aR,9S,9aS)-9-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-1-methyl-3-oxododecahydronaphtho[2,3-c]furan-6-ylcarbamate formation at 25 uM after 120 mins by LC-MS/MS analys	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1217220	Drug metabolism in human liver microsomes assessed as compound remaining at 10 uM after 120 mins by LC-MS/MS analysis in presence of NADPH	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1458247	In vivo antagonist activity at PAR1 in guinea pig assessed as inhibition of thrombin-stimulated platelet aggregation at 10 mg/kg, po pretreated for 2 hrs followed by thrombin stimulation measured after 5 mins	2017	Journal of medicinal chemistry, 08-24, Volume: 60, Issue:16	Discovery of Potent Orally Active Protease-Activated Receptor 1 (PAR1) Antagonists Based on Andrographolide.
AID1065173	AUC (0 to 6 hrs) in rat plasma at 10 mg/kg, po	2014	ACS medicinal chemistry letters, Feb-13, Volume: 5, Issue:2	Himbacine-derived thrombin receptor antagonists: c7-aminomethyl and c9a-hydroxy analogues of vorapaxar.
AID1552686	Negative allosteric modulation of PAR1 in human EAhy926 cells assessed as reduction in TFLLRN-NH2-induced intracellular calcium mobilization at 0.316 uM incubated for 15 mins followed by TFLLRN-NH2 addition by Fluo-4-AM dye based fluorescence assay relati	2019	Bioorganic & medicinal chemistry, 09-01, Volume: 27, Issue:17	The parmodulin NRD-21 is an allosteric inhibitor of PAR1 Gq signaling with improved anti-inflammatory activity and stability.
AID1458226	Antagonist activity at human PAR1 expressed in HEK293 cells co-expressing Galpha15 assessed as inhibition of haTRAP-induced calcium mobilization preincubated for 15 mins followed by haTRAP addition by calcium-4 dye based FLIPR assay	2017	Journal of medicinal chemistry, 08-24, Volume: 60, Issue:16	Discovery of Potent Orally Active Protease-Activated Receptor 1 (PAR1) Antagonists Based on Andrographolide.
AID1667458	Half life in Sprague-Dawley rat at 5 mg/kg, po or 1 mg/kg, iv	2020	Bioorganic & medicinal chemistry letters, 04-15, Volume: 30, Issue:8	Design and synthesis of potent PAR-1 antagonists based on vorapaxar.
AID1217278	Drug metabolism in human liver microsomes assessed as (3R,3aS,4S,4aR,7R,8aR,9aR)-7-amino-4-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-3-methyldecahydronaphtho[2,3-c]furan-1(3H)-one formation at 10 to 25 uM after 120 mins by LC-MS/MS analysis in presenc	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1056261	Metabolic stability in human liver microsomes assessed as time when 50% of compound remains	2013	ACS medicinal chemistry letters, Nov-14, Volume: 4, Issue:11	Discovery of Octahydroindenes as PAR1 Antagonists.
AID1056258	Antagonist activity at PAR1 in human platelet rich plasma assessed as inhibition of haTRAP-induced platelet aggregation preincubated for 1 hr followed by haTRAP addition measured for 10 mins by spectrophotometric analysis	2013	ACS medicinal chemistry letters, Nov-14, Volume: 4, Issue:11	Discovery of Octahydroindenes as PAR1 Antagonists.
AID1217261	Drug metabolism in human intestine microsomes assessed as ((4aR,6R)-9-{2-[(1R,4S)-5-((S)-3-Fluoro-phenyl)-pyridin-2-yl]-vinyl}-1-methyl-3-oxo-dodecahydro-naphtho[2,3-c]furan-6-yl)-carbamic acid(R)-2-hydroxy-ethyl ester formation by LC-MS/MS analysis in pr	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID407983	Antagonist activity at PAR1 in human platelets assessed as inhibition of thrombin-induced platelet aggregation	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID407982	Antagonist activity at PAR1 in human platelets assessed as inhibition of haTRAP-induced platelet aggregation	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1667455	Antagonist activity at human PAR1 expressed in KNRK cells assessed as inhibition of agonist-induced intracellular calcium mobilization at 10'-6 M by fluorimetric assay relative to control	2020	Bioorganic & medicinal chemistry letters, 04-15, Volume: 30, Issue:8	Design and synthesis of potent PAR-1 antagonists based on vorapaxar.
AID407981	Displacement of [3H]haTRAP from PAR1 in human platelets	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID407998	AUC (0 to 24 hrs) in rat 10 mg/kg, po	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID408017	Inhibition of CYP3A4 in human liver microsomes at 90 uM	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID408002	AUC (0 to 24 hrs) in monkey 1 mg/kg, po	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID407999	Cmax in rat 10 mg/kg, po	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID408026	Oral absorption in rat 10 mg/kg, po	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID408001	Half life in rat 10 mg/kg, iv	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID408015	Inhibition of CYP2C19 in human liver microsomes at 90 uM	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1217283	Drug metabolism in human liver microsomes overexpressing CYP3A4 assessed as (3R,3aS,4S,4aR,7R,8aR,9aR)-7-amino-4-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-3-methyldecahydronaphtho[2,3-c]furan-1(3H)-one formation at 25 uM after 120 mins by LC-MS/MS ana	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1217227	Activity of human recombinant CYP2D6 assessed as enzyme-mediated drug metabolism at 10 uM after 120 mins by LC-MS/MS analysis in presence of NADPH	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1667454	Antagonist activity at human PAR1 expressed in KNRK cells assessed as inhibition of agonist-induced intracellular calcium mobilization at 10'-7 M by fluorimetric assay relative to control	2020	Bioorganic & medicinal chemistry letters, 04-15, Volume: 30, Issue:8	Design and synthesis of potent PAR-1 antagonists based on vorapaxar.
AID408008	Anticoagulant activity in human plasma assessed as prothrombin time	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1217274	Drug metabolism in human liver microsomes assessed as (3R,3aS,4S,4aR,7R,8aR,9aR)-7-amino-4-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-3-methyldecahydronaphtho[2,3-c]furan-1(3H)-one formation at 10 to 25 uM after 120 mins by LC-MS/MS analysis in presenc	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1056260	Displacement of [3H]haTRAP from PAR1 in human platelet membranes after 60 mins by scintillation counting analysis	2013	ACS medicinal chemistry letters, Nov-14, Volume: 4, Issue:11	Discovery of Octahydroindenes as PAR1 Antagonists.
AID407984	Antagonist activity at PAR1 in human platelets assessed as inhibition of ADP-induced platelet aggregation	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1217255	Drug metabolism in insect microsomes at 10 uM after 120 mins by LC-MS/MS analysis in presence of NADPH	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1217253	Drug metabolism assessed as human recombinant CYP2J2-mediated 2-hydroxyethyl (1R,3aR,4aR,6R,8aR,9S,9aS)-9-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-1-methyl-3-oxododecahydronaphtho[2,3-c]furan-6-ylcarbamate formation at 25 uM after 120 mins by LC-MS/M	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1217252	Drug metabolism assessed as human recombinant CYP3A4-mediated 2-hydroxyethyl (1R,3aR,4aR,6R,8aR,9S,9aS)-9-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-1-methyl-3-oxododecahydronaphtho[2,3-c]furan-6-ylcarbamate formation at 25 uM after 120 mins by LC-MS/M	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1458246	In vivo antagonist activity at PAR1 in guinea pig assessed as inhibition of TRAP-stimulated platelet aggregation at 10 mg/kg, po pretreated for 2 hrs followed by TRAP stimulation measured after 5 mins	2017	Journal of medicinal chemistry, 08-24, Volume: 60, Issue:16	Discovery of Potent Orally Active Protease-Activated Receptor 1 (PAR1) Antagonists Based on Andrographolide.
AID408000	Oral bioavailability in rat 10 mg/kg	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1217286	Drug metabolism assessed as human recombinant CYP3A4-mediated 2-hydroxyethyl (1R,3aR,4aR,6R,8aR,9S,9aS)-9-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-1-methyl-3-oxododecahydronaphtho[2,3-c]furan-6-ylcarbamate formation at 25 uM after 120 mins by LC-MS/M	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID408004	Oral bioavailability in monkey 1 mg/kg	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1217225	Activity of human recombinant CYP2C9 assessed as enzyme-mediated drug metabolism at 10 uM after 120 mins by LC-MS/MS analysis in presence of NADPH	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1056262	Metabolic stability in rat liver microsomes assessed as time when 50% of compound remains	2013	ACS medicinal chemistry letters, Nov-14, Volume: 4, Issue:11	Discovery of Octahydroindenes as PAR1 Antagonists.
AID407997	Antagonist activity at human PAR1 in HCASMC assessed as inhibition of thrombin-induced thymidine incorporation	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1217282	Drug metabolism in human liver microsomes overexpressing CYP3A4 assessed as (3R,3aS,4S,4aR,7R,8aR,9aR)-7-amino-4-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-3-methyldecahydronaphtho[2,3-c]furan-1(3H)-one formation at 25 uM after 120 mins by LC-MS/MS ana	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID527581	Displacement of high affinity TRAP form human platelet PAR1	2010	Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22	Discovery of a vorapaxar analog with increased aqueous solubility.
AID408027	Oral absorption in monkey 10 mg/kg, po	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1217287	Drug metabolism assessed as human recombinant CYP2J2-mediated 2-hydroxyethyl (1R,3aR,4aR,6R,8aR,9S,9aS)-9-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-1-methyl-3-oxododecahydronaphtho[2,3-c]furan-6-ylcarbamate formation at 25 uM after 120 mins by LC-MS/M	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID408014	Inhibition of CYP2C9 in human liver microsomes at 90 uM	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID408009	Anticoagulant activity in human plasma assessed as activated partial thromboplastin time	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID408025	Ex vivo inhibition of haTRAP-induced platelet aggregation in cynomolgus monkey at 0.1 mg/kg after >24 hrs by impedance aggregometry	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1217226	Activity of human recombinant CYP2C19 assessed as enzyme-mediated drug metabolism at 10 uM after 120 mins by LC-MS/MS analysis in presence of NADPH	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1667462	Ratio of drug concentration in brain to plasma in Sprague-Dawley rat at 5 mg/kg, po measured at 8 hrs	2020	Bioorganic & medicinal chemistry letters, 04-15, Volume: 30, Issue:8	Design and synthesis of potent PAR-1 antagonists based on vorapaxar.
AID408016	Inhibition of CYP2D16 in human liver microsomes at 90 uM	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID408005	Half life in monkey 1 mg/kg, iv	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1217258	Activity of human recombinant CYP3A4 assessed as enzyme-mediated ((4aR,6R)-9-{2-[(1R,4S)-5-((S)-3-Fluoro-phenyl)-pyridin-2-yl]-vinyl}-1-methyl-3-oxo-dodecahydro-naphtho[2,3-c]furan-6-yl)-carbamic acid(R)-2-hydroxy-ethyl ester formation at 10 uM after 120	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1458248	Toxicity in guinea pig assessed as inhibition of ADP-stimulated platelet aggregation at 10 mg/kg, po pretreated for 2 hrs followed by ADP stimulation measured after 5 mins	2017	Journal of medicinal chemistry, 08-24, Volume: 60, Issue:16	Discovery of Potent Orally Active Protease-Activated Receptor 1 (PAR1) Antagonists Based on Andrographolide.
AID407986	Antagonist activity at PAR1 in human platelets assessed as inhibition of GYPGKF-induced platelet aggregation	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1217284	Drug metabolism in human liver microsomes overexpressing CYP3A4 assessed as (3R,3aS,4S,4aR,7R,8aR,9aR)-7-amino-4-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-3-methyldecahydronaphtho[2,3-c]furan-1(3H)-one formation at 25 uM after 120 mins by LC-MS/MS ana	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID1217288	Drug metabolism in human liver microsomes assessed as 2-hydroxyethyl (1R,3aR,4aR,6R,8aR,9S,9aS)-9-((E)-2-(5-(3-fluorophenyl)pyridin-2-yl)vinyl)-1-methyl-3-oxododecahydronaphtho[2,3-c]furan-6-ylcarbamate formation at 25 uM after 120 mins by LC-MS/MS analys	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID407993	Ex vivo inhibition of haTRAP-induced platelet aggregation in cynomolgus monkey at 0.5 mg/kg, po after 24 hrs by impedance aggregometry	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID407985	Antagonist activity at PAR1 in human platelets assessed as inhibition of U46619-induced platelet aggregation	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1667461	Oral bioavailability in Sprague-Dawley rat at 5 mg/kg	2020	Bioorganic & medicinal chemistry letters, 04-15, Volume: 30, Issue:8	Design and synthesis of potent PAR-1 antagonists based on vorapaxar.
AID408028	Antagonist activity at PAR1 in human platelets assessed as inhibition of collagen-induced platelet aggregation	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID408003	Cmax in monkey 1 mg/kg, po	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID407995	Ex vivo inhibition of haTRAP-induced platelet aggregation in cynomolgus monkey at 0.05 mg/kg, po after 24 hrs by impedance aggregometry	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1217260	Drug metabolism in human intestine microsomes assessed as ((4aR,6R)-9-{2-[(1R,4S)-5-((S)-3-Fluoro-phenyl)-pyridin-2-yl]-vinyl}-1-methyl-3-oxo-dodecahydro-naphtho[2,3-c]furan-6-yl)-carbamic acid(R)-2-hydroxy-ethyl ester formation by LC-MS/MS analysis in pr	2011	Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1	Identification of human liver cytochrome P450 enzymes involved in the metabolism of SCH 530348 (Vorapaxar), a potent oral thrombin protease-activated receptor 1 antagonist.
AID408011	Binding affinity to PAR3	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
AID1458242	Antagonist activity at PAR1 in human platelet-rich plasma assessed as reduction in TRAP-stimulated platelet aggregation preincubated for 20 mins followed by TRAP stimulation measured after 5 mins by aggregometric analysis	2017	Journal of medicinal chemistry, 08-24, Volume: 60, Issue:16	Discovery of Potent Orally Active Protease-Activated Receptor 1 (PAR1) Antagonists Based on Andrographolide.
AID1346347	Human PAR1 (Proteinase-activated receptors)	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Discovery of a novel, orally active himbacine-based thrombin receptor antagonist (SCH 530348) with potent antiplatelet activity.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Timeframe	Studies, This Drug (%)	All Drugs %
pre-1990	0 (0.00)	18.7374
1990's	0 (0.00)	18.2507
2000's	18 (8.22)	29.6817
2010's	177 (80.82)	24.3611
2020's	24 (10.96)	2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Publication Type	This drug (%)	All Drugs (%)
Trials	57 (25.33%)	5.53%
Reviews	74 (32.89%)	6.00%
Case Studies	0 (0.00%)	4.05%
Observational	0 (0.00%)	0.25%
Other	94 (41.78%)	84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (15)

Trial Overview

Trial	Phase	Enrollment	Study Type	Start Date	Status
A Study to Determine the Bioequivalence of SCH 530348 2.5 mg Tablets Containing a High and Low Percentage of Drug as the Free Base Within the Range Used in the Pivotal Phase 3 Efficacy and Safety Trials. (Protocol No. P06558) [NCT01358344]	Phase 1	173 participants (Actual)	Interventional	2010-08-31	Completed
Influence of Vorapaxar on Thrombin Generation and Coagulability [NCT03207451]	Phase 4	81 participants (Actual)	Interventional	2016-01-01	Completed
Vorapaxar in the Human Endotoxemia Model A Randomized, Double-Blind, Crossover Study [NCT02875028]	Phase 4	16 participants (Actual)	Interventional	2016-06-30	Completed
A Double Blind Randomised Comparison of Vorapaxar Versus Placebo for the Treatment of HIV Associated Inflammation and Coagulopathy in Patients With Well Controlled HIV Replication [NCT02394730]	Phase 1/Phase 2	65 participants (Actual)	Interventional	2015-09-30	Completed
Phase II Study of SCH 530348 in Subjects With Cerebral Infarction [NCT00684515]	Phase 2	90 participants (Actual)	Interventional	2006-09-21	Completed
Phase II Study of SCH 530348 in Subjects With Acute Coronary Syndrome [NCT00684203]	Phase 2	120 participants (Actual)	Interventional	2006-12-01	Completed
A Randomized, Double-Blind, Placebo-Controlled Study to Evaluate the Ocular Safety of SCH 530348 in Subjects Participating in the Schering-Plough P04737 Study (TRA^SM-Secondary Prevention Ocular Safety Study) [NCT00617123]	Phase 3	258 participants (Actual)	Interventional	2008-07-01	Completed
Excellence In Peripheral Artery Disease Thrombin Receptor Antagonist Intervention In Claudication Evaluation (XLPAD-TRACE Trial) [NCT02660866]	Phase 4	200 participants (Anticipated)	Interventional	2016-07-31	Recruiting
A Double-blind, Randomized, Placebo Controlled Pilot Trial to Evaluate the Safety and Efficacy of Vorapaxar in Maturation of Arteriovenous Fistulae for Hemodialysis Access [NCT02475837]	Phase 2	17 participants (Actual)	Interventional	2015-08-26	Completed
A Multicenter, Randomized, Double-Blind, Placebo-Controlled Study to Evaluate the Safety of SCH 530348 in Subjects Undergoing Non-Emergent Percutaneous Coronary Intervention [NCT00132912]	Phase 2	1,030 participants (Actual)	Interventional	2005-08-30	Completed
A Double-blind, Randomized, Parallel Design Two Center Study to Compare the Effect of Vorapaxar vs. Placebo on Lower Extremity Vein Graft Maturation, Remodeling, and Function [NCT02975583]	Phase 4	0 participants (Actual)	Interventional	2017-10-01	Withdrawn(stopped due to We could not secure adequate medication)
A Multicenter, Randomized, Double-Blind, Placebo-Controlled Study to Evaluate the Safety and Efficacy of SCH 530348 in Addition to Standard of Care in Subjects With a History of Atherosclerotic Disease: Thrombin Receptor Antagonist in Secondary Prevention [NCT00526474]	Phase 3	26,449 participants (Actual)	Interventional	2007-09-01	Completed
Pharmacodynamic Effects of Vorapaxar as an Add-On Antiplatelet Therapy in Patients With and Without Diabetes Mellitus: The Optimizing Anti-Platelet Therapy In Diabetes MellitUS (OPTIMUS)-5 Study [NCT02548650]	Phase 4	66 participants (Actual)	Interventional	2016-03-25	Completed
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 4	130 participants (Actual)	Interventional	2016-02-29	Completed
A Multicenter, Randomized, Double-Blind, Placebo-Controlled Study to Evaluate the Safety and Efficacy of SCH 530348 in Addition to Standard of Care in Subjects With Acute Coronary Syndrome: Thrombin Receptor Antagonist for Clinical Event Reduction in Acut [NCT00527943]	Phase 3	12,944 participants (Actual)	Interventional	2007-12-01	Terminated(stopped due to The trial was terminated at the request of the Data and Safety Monitoring Board.)
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Trial	Outcome
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced an MI Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death, MI, or Stroke Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death or an MI Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death or an MI Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced Clinically Significant Bleeding Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced Clinically Significant Bleeding Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced Cardiovascular (CV) Death, Myocardial Infarction (MI), Stroke, or Urgent Coronary Revascularization (UCR) Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced a Stroke Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Died From Any Cause, or Experienced an MI, Stroke, or Any Revascularization Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Died From Any Cause Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Had a UH-VCIN Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced UCR Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced Death From Any Cause, MI, Stroke, or UCR Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced Death From Any Cause, MI, Stroke, or UCR Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death, MI, Stroke, UCR, or Urgent Hospitalization for Vascular Cause of Ischemic Nature (UH-VCIN) Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death, MI, Stroke, UCR, or UH-VCIN Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death, MI, Stroke, or UCR Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death, MI, Stroke, Any Revascularization, or UH-VCIN Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Met GUSTO Moderate or Severe Bleeding Criteria Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Met Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries (GUSTO) Moderate or Severe Bleeding Criteria Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Had Any Revascularization Performed Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Had Any Revascularization Performed Within 3 Years From Randomization
NCT00526474 (25) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Had a UH-VCIN Within 3 Years From Randomization
NCT00527943 (14) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced a Stroke Within 2 Years From Randomization
NCT00527943 (14) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Met Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries (GUSTO) Moderate or Severe Bleeding Criteria Within 2 Years From Randomization
NCT00527943 (14) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced UCR Within 2 Years From Randomization
NCT00527943 (14) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced RIR Within 2 Years From Randomization
NCT00527943 (14) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death, MI, Stroke, or UCR Within 2 Years From Randomization
NCT00527943 (14) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death Within 2 Years From Randomization
NCT00527943 (14) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death or MI Within 2 Years From Randomization
NCT00527943 (14) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced Cardiovascular Death, Myocardial Infarction, Stroke, Recurrent Ischemia With Re-hospitalization, and/or Urgent Coronary Revascularization Within 2 Years From Randomization
NCT00527943 (14) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced Cardiovascular Death, Myocardial Infarction, and/or Stroke Within 2 Years From Randomization
NCT00527943 (14) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced an MI Within 2 Years From Randomization
NCT00527943 (14) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced All-cause Death, MI, Stroke, RIR, or UCR Within 2 Years From Randomization
NCT00527943 (14) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced All-cause Death, MI, Stroke, or UCR Within 2 Years From Randomization
NCT00527943 (14) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Died From Any Cause Within 2 Years From Randomization
NCT00527943 (14) [back to overview]	Kaplan-Meier Estimate of the Percentage of Participants Who Experienced Clinically Significant Bleeding Within 2 Years From Randomization
NCT00617123 (5) [back to overview]	Number of Participants Who Have a Decrease in Visual Acuity Score of at Least Seven Letters From Baseline
NCT00617123 (5) [back to overview]	Number of Participants With Change From Baseline of Center Foveal Thickness of Greater Than 15 Microns as Measured by OCT
NCT00617123 (5) [back to overview]	Change From Baseline in the Numerical Score of Graded Abnormalities as Measured by Fundus Photography
NCT00617123 (5) [back to overview]	Change From Baseline in the Numerical Score of Graded Abnormalities as Measured by OCT
NCT00617123 (5) [back to overview]	Number of Participants Who Develop Vacuolization in the Inner Nuclear Layer (INL) of the Retina as Measured by Ocular Coherence Tomography (OCT)
NCT00684203 (15) [back to overview]	Number of Participants Who Underwent PCI With Inhibition of Platelet Aggregation By Study Visit
NCT00684203 (15) [back to overview]	Number of Participants Experiencing Adverse Events (AEs) Who Underwent Percutaneous Coronary Interventions (PCI)
NCT00684203 (15) [back to overview]	Number of Participants Experiencing Non-Major Adverse Cardiac Events (MACE) Who Underwent PCI
NCT00684203 (15) [back to overview]	Number of Participants With Major, Minor, and Non-TIMI Bleeding Events Among Participants Who Did Not Undergo PCI
NCT00684203 (15) [back to overview]	Number of Participants With Major, Minor, and Non-Thrombolysis in Myocardial Infarction Cooperative Group (TIMI) Bleeding Events Among Participants Who Underwent PCI
NCT00684203 (15) [back to overview]	Number of Participants Experiencing Non-MACE AEs Among Participants Who Did Not Undergo PCI
NCT00684203 (15) [back to overview]	Mean CD40 Ligand Levels Among Participants Who Did Not Undergo PCI
NCT00684203 (15) [back to overview]	Number of Participants Who Did Not Undergo PCI But Had Bleeding Events That Required Transfusion
NCT00684203 (15) [back to overview]	Number of Participants Who Did Not Undergo PCI But Had Bleeding Events That Required Subsequent Hospitalization
NCT00684203 (15) [back to overview]	Number of Participants Who Underwent PCI With Clinically Important Bleeding Events During Treatment and After Hospital Discharge
NCT00684203 (15) [back to overview]	Number of Participants Who Did Not Undergo PCI That Had Clinically Important Bleeding Events
NCT00684203 (15) [back to overview]	Median Hs-CRP Levels Among Participants Who Did Not Undergo PCI
NCT00684203 (15) [back to overview]	Median High-Sensitivity C-Reactive Protein (Hs-CRP) Levels Among Participants Who Underwent PCI By Study Visit
NCT00684203 (15) [back to overview]	Mean Membrane-Bound P-Selectin Levels Among Participants Who Underwent PCI
NCT00684203 (15) [back to overview]	Mean CD40 Ligand Levels Among Participants Who Underwent PCI
NCT00684515 (6) [back to overview]	Number of Participants Experiencing Non-Major Adverse Cardiac Events (Non-MACE)
NCT00684515 (6) [back to overview]	Mean CD40 Ligand Levels By Study Visit
NCT00684515 (6) [back to overview]	Mean Membrane-Bound P-Selectin Levels By Study Visit
NCT00684515 (6) [back to overview]	Median High-Sensitivity C-Reactive Protein (Hs-CRP) Levels By Study Visit
NCT00684515 (6) [back to overview]	Number of Participants With MACE or Death
NCT00684515 (6) [back to overview]	Number of Paticipants Experiencing Thrombolysis in Myocardial Infarction (TIMI) Major, Minor, and Non-TIMI Bleeding Events
NCT02394730 (15) [back to overview]	Total Number of Participants With Any SAE Between Baseline and Week 18
NCT02394730 (15) [back to overview]	Total Number of Participants With BARC Type 1, 2, 3, 4, or 5 Bleeding Episodes
NCT02394730 (15) [back to overview]	Number of Patients in Each Treatment Group With D-dimer <165ng/mL at Week 12
NCT02394730 (15) [back to overview]	Percent Change From Baseline Hs-CRP (ug/mL) to the Average of Week 8 and Week 12
NCT02394730 (15) [back to overview]	Total Number of Participants With Any AE Between Baseline to Week 18
NCT02394730 (15) [back to overview]	Mean Change From Baseline to Week 12 in CD8+ Cell Counts
NCT02394730 (15) [back to overview]	Number of Patients in Each Treatment Group With D-dimer > or Equal to 165ng/mL at Week 18
NCT02394730 (15) [back to overview]	Number of Participants in Each Treatment Group With Plasma HIV-1 RNA <50 Copies/mL
NCT02394730 (15) [back to overview]	Mean Percent Change From Baseline IL-6 (pg/mL) to the Average of Week 8 and Week 12
NCT02394730 (15) [back to overview]	Mean Percent Change From Baseline for D-dimer (ng/mL) to the Average of Weeks 8 and 12
NCT02394730 (15) [back to overview]	Mean Change From Baseline to Week 12 in CD4+ Cell Counts
NCT02394730 (15) [back to overview]	Mean Change From Baseline in log10 Hs-CRP at Week 18
NCT02394730 (15) [back to overview]	Mean Change From Baseline in log10 D-Dimer
NCT02394730 (15) [back to overview]	Differences Between Treatment Groups in Mean Change From Baseline log10 IL-6
NCT02394730 (15) [back to overview]	Changes From Baseline in Renal Function Measured by the CKD-EPI Estimate of Creatinine Clearance at Week 12
NCT02475837 (4) [back to overview]	Time to AV Fistula Functional Maturation
NCT02475837 (4) [back to overview]	Count Participants With AV Fistula Patency
NCT02475837 (4) [back to overview]	Count of All Participants With Bleeding Events
NCT02475837 (4) [back to overview]	Count of Participants With AV Fistula Use
NCT02545933 (1) [back to overview]	Maximal Platelet Aggregation
NCT02548650 (2) [back to overview]	Maximal Platelet Aggregation in DM
NCT02548650 (2) [back to overview]	Maximal Platelet Aggregation in Non-DM
NCT02875028 (12) [back to overview]	P-Selectin
NCT02875028 (12) [back to overview]	Thrombin-Antithrombin Complexes
NCT02875028 (12) [back to overview]	Thrombomodulin
NCT02875028 (12) [back to overview]	Protease Activated Receptor (PAR)-1 Expression on Platelets
NCT02875028 (12) [back to overview]	Platelet Factor 4
NCT02875028 (12) [back to overview]	Plasmin-Antiplasmin Complexes
NCT02875028 (12) [back to overview]	Interleukin 6
NCT02875028 (12) [back to overview]	E-Selectin
NCT02875028 (12) [back to overview]	Changes in Prothrombin Fragments F1+2
NCT02875028 (12) [back to overview]	C-reactive Protein
NCT02875028 (12) [back to overview]	Von Willebrand Factor
NCT02875028 (12) [back to overview]	Tumor Necrosis Factor Alpha
NCT03207451 (3) [back to overview]	Effects of Vorapaxar on Thrombin Induced Platelet-fibrin Clot Strength (TIP-FCS)
NCT03207451 (3) [back to overview]	Effects of Vorapaxar on 15 μmol/L SFLLRN (PAR-1 Activating Peptide) Induced Platelet Aggregation
NCT03207451 (3) [back to overview]	Effects of Vorapaxar on Von Willebrand Factor (vWF).

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced an MI Within 3 Years From Randomization

The time (in days) from study start to the first occurrence of an MI was recorded. A CEC reviewed and adjudicated each suspected efficacy endpoint event while blinded to treatment. Participants who did not have any endpoint event until last visit or participants who were lost to follow-up and had no event were censored at the time of last available information (last study visit). If a participant had a fatal event that was not part of a specific endpoint for analysis, they were censored at the time of death. The Kaplan-Meier estimate reports the percentage of participants who experienced an MI within 3 years from randomization. (NCT00526474)
Timeframe: up to 3 years

Intervention	Percentage of Participants (Number)
Placebo	6.4
Vorapaxar	5.4
Placebo	6.1
Vorapaxar	5.2

Intervention	participants (Number)
	4 months (n=90, n=86)	8 months (n=86, n=80)	12 months (n=78, n=78)
Placebo	8	8	9
Vorapaxar	10	10	7

Intervention	participants (Number)
	4 months (n=91, n=86)	8 months (n=86, n=80)	12 months (n=77, n=78)
Placebo	28	26	29
Vorapaxar	27	23	19

Intervention	score on a scale (Mean)
	Baseline score (n=91, n=87)	4 months change (n=90, n=86)	8 months change (n=86, n=80)	12 months change (n=76, n=77)
Placebo	3.9	-0.4	-0.6	-0.3
Vorapaxar	4.1	-0.2	-0.4	-0.6

Intervention	score on a scale (Mean)
	Baseline score (n=92, n=87)	4 months change (n=91, n=86)	8 months change (n=86, n=80)	12 months change (n=77, n=78)
Placebo	3.4	0.7	0.9	0.0
Vorapaxar	3.1	0.2	0.6	0.2

Intervention	Participants (Number)
	Baseline	Day 30	Day 60	Day 74 (follow-up period)	Day 90 (follow-up period)	Day 121 (follow-up period)
Placebo/Placebo PCI	3	3	1	3	3	3
Vorapaxar 1 mg Maintenance Dose PCI	5	5	3	5	5	5
Vorapaxar 2.5 mg Maintenance Dose PCI	4	4	3	4	4	4

Intervention	Participants (Number)
Vorapaxar 20 mg Loading Dose PCI	40
Vorapaxar 40 mg Loading Dose PCI	30
Placebo/Placebo PCI	21

Intervention	Participants (Number)
Vorapaxar 20 mg/1 mg PCI	21
Vorapaxar 20 mg/2.5 mg PCI	19
Vorapaxar 40 mg/1 mg PCI	16
Vorapaxar 40 mg/2.5 mg PCI	14
Placebo/Placebo PCI	21

Intervention	Participants (Number)
	Major TIMI Events	Minor TIMI Events	Non-TIMI Bleeding Events
Placebo/Placebo Non-PCI	0	0	1
Vorapaxar 20 mg Loading Dose Non-PCI	1	0	1
Vorapaxar 40 mg Loading Dose Non-PCI	2	0	8

Intervention	Participants (Number)
	Major TIMI Bleeding Events	Minor TIMI Bleeding Events	Non-TIMI Bleeding Events
Placebo/Placebo PCI	0	2	11
Vorapaxar 1 mg Maintenance Dose PCI	2	5	22
Vorapaxar 2.5 mg Maintenance Dose PCI	0	3	17

Intervention	ng/mL (Mean)
	Baseline	Time of Hospital Discharge
Placebo/Placebo Non-PCI	11.1	12.9
Vorapaxar 20 mg Loading Dose Non-PCI	8.4	10.1
Vorapaxar 40 mg Loading Dose Non-PCI	4.6	7.1

Intervention	Participants (Number)
	Treatment Phase	Post-Hospital Discharge
Placebo/Placebo PCI	0	0
Vorapaxar 20 mg/1 mg PCI	3	1
Vorapaxar 20 mg/2.5 mg PCI	0	0
Vorapaxar 40 mg/1 mg PCI	2	2
Vorapaxar 40 mg/2.5 mg PCI	0	0

Intervention	Participants (Number)
	Intracranial hemorrhage	Bleeding requiring transfusion	Bleeding requiring hospitalization	Major TIMI bleeding
Placebo/Placebo Non-PCI	0	0	0	0
Vorapaxar 20 mg Loading Dose Non-PCI	0	1	0	1
Vorapaxar 40 mg Loading Dose Non-PCI	1	2	1	2

Intervention	mg/L (Median)
	Baseline (n=37, 34, 21)	Day 30 (n=35, 34, 21)	Day 60 (n=30, 25, 13)
Placebo/Placebo PCI	1.78	2.99	1.27
Vorapaxar 1 mg Maintenance Dose PCI	1.30	1.28	1.20
Vorapaxar 2.5 mg Maintenance Dose PCI	2.00	1.01	0.79

Intervention	Arbitrary Units (Mean)
	Baseline (n=4, 4, 3)	Day 30 (n=3, 4, 3)	Day 60 (n=2, 3, 1)
Placebo/Placebo PCI	15.9	18.8	19.4
Vorapaxar 1 mg Maintenance Dose PCI	24.8	20.6	25.0
Vorapaxar 2.5 mg Maintenance Dose PCI	16.5	16.4	14.9

Intervention	ng/mL (Mean)
	Baseline (n=37, 34, 21)	Day 30 (n=35, 34, 31)	Day 60 (n=30, 25, 13)
Placebo/Placebo PCI	4.8	6.2	5.7
Vorapaxar 1 mg Maintenance Dose PCI	5.6	5.9	5.6
Vorapaxar 2.5 mg Maintenance Dose PCI	6.9	5.9	5.4

Intervention	mg/L (Mean)
	Baseline (n=33, 29, 28)	Day 7 (n=32, 28, 27)	Day 14 (n=32, 29, 28)	Day 30 (n=31, 28, 28)	Day 45 (n=29, 27, 28)	Day 60 (n=29, 26, 27)
Placebo	5.9	5.6	6.6	5.9	6.2	6.0
Vorapaxar 1 mg	6.5	7.2	6.3	6.7	5.9	6.2
Vorapaxar 2.5 mg	8.3	5.8	6.5	7.1	5.7	5.3

Intervention	Arbitrary Units (Mean)
	Baseline (n=2, 1, 3)	Day 30 (n=2, 1, 3)	Day 60 (n=2, 1, 3)
Placebo	17.4	17.1	18.0
Vorapaxar 1 mg	15.7	19.9	17.8
Vorapaxar 2.5 mg	19.5	16.6	18.3

Intervention	mg/L (Median)
	Baseline (n=33, 29, 28)	Day 7 (n=32, 28, 27)	Day 14 (32, 29, 28)	Day 30 (n=31, 28, 28)	Day 45 (n=29, 27, 28)	Day 60 (n=29, 26, 27)
Placebo	0.56	0.41	0.44	0.56	0.59	0.61
Vorapaxar 1 mg	0.65	0.77	0.93	0.96	0.70	0.59
Vorapaxar 2.5 mg	0.67	0.49	0.62	0.55	0.48	0.53

Intervention	Participants (Number)
	Major TIMI Bleeding	Minor TIMI Bleeding	Non-TIMI Bleeding
Placebo	0	1	6
Vorapaxar 1 mg	0	0	5
Vorapaxar 2.5 mg	0	0	10

Intervention	percent aggregation (Mean)
DAPT Plus Vorapaxar	52
Prasugrel/Ticagrelor Plus Vorapaxar	64
DAPT	74

vorapaxar

Description

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Synonyms (68)

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Studies (219)

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Research Demand Index: 54.82

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Clinical Trials (15)

Trial Overview

Trial Outcomes

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced an MI Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death, MI, or Stroke Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death or an MI Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death or an MI Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced Clinically Significant Bleeding Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced Clinically Significant Bleeding Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced Cardiovascular (CV) Death, Myocardial Infarction (MI), Stroke, or Urgent Coronary Revascularization (UCR) Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced a Stroke Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Died From Any Cause, or Experienced an MI, Stroke, or Any Revascularization Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Died From Any Cause Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Had a UH-VCIN Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced UCR Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced Death From Any Cause, MI, Stroke, or UCR Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced Death From Any Cause, MI, Stroke, or UCR Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death, MI, Stroke, UCR, or Urgent Hospitalization for Vascular Cause of Ischemic Nature (UH-VCIN) Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death, MI, Stroke, UCR, or UH-VCIN Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death, MI, Stroke, or UCR Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death, MI, Stroke, Any Revascularization, or UH-VCIN Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Met GUSTO Moderate or Severe Bleeding Criteria Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Met Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries (GUSTO) Moderate or Severe Bleeding Criteria Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Had Any Revascularization Performed Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Had Any Revascularization Performed Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Had a UH-VCIN Within 3 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced a Stroke Within 2 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Met Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries (GUSTO) Moderate or Severe Bleeding Criteria Within 2 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced UCR Within 2 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced RIR Within 2 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death, MI, Stroke, or UCR Within 2 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death Within 2 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced CV Death or MI Within 2 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced Cardiovascular Death, Myocardial Infarction, Stroke, Recurrent Ischemia With Re-hospitalization, and/or Urgent Coronary Revascularization Within 2 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced Cardiovascular Death, Myocardial Infarction, and/or Stroke Within 2 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced an MI Within 2 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced All-cause Death, MI, Stroke, RIR, or UCR Within 2 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced All-cause Death, MI, Stroke, or UCR Within 2 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Died From Any Cause Within 2 Years From Randomization

Kaplan-Meier Estimate of the Percentage of Participants Who Experienced Clinically Significant Bleeding Within 2 Years From Randomization

Number of Participants Who Have a Decrease in Visual Acuity Score of at Least Seven Letters From Baseline

Number of Participants With Change From Baseline of Center Foveal Thickness of Greater Than 15 Microns as Measured by OCT

Change From Baseline in the Numerical Score of Graded Abnormalities as Measured by Fundus Photography

Change From Baseline in the Numerical Score of Graded Abnormalities as Measured by OCT

Number of Participants Who Develop Vacuolization in the Inner Nuclear Layer (INL) of the Retina as Measured by Ocular Coherence Tomography (OCT)

Number of Participants Who Underwent PCI With Inhibition of Platelet Aggregation By Study Visit

Number of Participants Experiencing Adverse Events (AEs) Who Underwent Percutaneous Coronary Interventions (PCI)

Number of Participants Experiencing Non-Major Adverse Cardiac Events (MACE) Who Underwent PCI

Number of Participants With Major, Minor, and Non-TIMI Bleeding Events Among Participants Who Did Not Undergo PCI

Number of Participants With Major, Minor, and Non-Thrombolysis in Myocardial Infarction Cooperative Group (TIMI) Bleeding Events Among Participants Who Underwent PCI

Number of Participants Experiencing Non-MACE AEs Among Participants Who Did Not Undergo PCI

Mean CD40 Ligand Levels Among Participants Who Did Not Undergo PCI

Number of Participants Who Did Not Undergo PCI But Had Bleeding Events That Required Transfusion

Intervention	mm (Mean)
Vorapaxar	62.8
Vorapaxar and Clopidogrel	61.0
Vorapaxar and Aspirin	61.6
Vorapaxar, Aspirin, and Clopidogrel	62.2

Condition	Indicated	Relationship Strength	Studies	Trials
Intermittent Claudication A symptom complex characterized by pain and weakness in SKELETAL MUSCLE group associated with exercise, such as leg pain and weakness brought on by walking. Such muscle limpness disappears after a brief rest and is often relates to arterial STENOSIS; muscle ISCHEMIA; and accumulation of LACTATE.	0	9.72	1	1
Apoplexy [description not available]	0	16.26	48	28
Peripheral Arterial Diseases [description not available]	0	14.27	30	14
Ischemia A hypoperfusion of the BLOOD through an organ or tissue caused by a PATHOLOGIC CONSTRICTION or obstruction of its BLOOD VESSELS, or an absence of BLOOD CIRCULATION.	0	15.12	10	7
Stroke A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)	0	16.26	48	28
Peripheral Arterial Disease Lack of perfusion in the EXTREMITIES resulting from atherosclerosis. It is characterized by INTERMITTENT CLAUDICATION, and an ANKLE BRACHIAL INDEX of 0.9 or less.	0	14.27	30	14
Cardiovascular Stroke [description not available]	0	17.08	62	34
Myocardial Infarction NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).	0	17.08	62	34
Acute Coronary Syndrome An episode of MYOCARDIAL ISCHEMIA that generally lasts longer than a transient anginal episode that ultimately may lead to MYOCARDIAL INFARCTION.	0	17.02	61	27
Diabetic Glomerulosclerosis [description not available]	0	2.41	1	0
Diabetic Nephropathies KIDNEY injuries associated with diabetes mellitus and affecting KIDNEY GLOMERULUS; ARTERIOLES; KIDNEY TUBULES; and the interstitium. Clinical signs include persistent PROTEINURIA, from microalbuminuria progressing to ALBUMINURIA of greater than 300 mg/24 h, leading to reduced GLOMERULAR FILTRATION RATE and END-STAGE RENAL DISEASE.	0	2.41	1	0
Atherogenesis [description not available]	0	13.17	21	9
Innate Inflammatory Response [description not available]	0	8.31	12	2
Inflammation A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.	0	8.31	12	2
Vascular Diseases Pathological processes involving any of the BLOOD VESSELS in the cardiac or peripheral circulation. They include diseases of ARTERIES; VEINS; and rest of the vasculature system in the body.	0	2.31	1	0
Atherosclerosis A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.	0	13.17	21	9
Cryptogenic Fibrosing Alveolitis [description not available]	0	3.57	2	0
Idiopathic Pulmonary Fibrosis A common interstitial lung disease of unknown etiology, usually occurring between 50-70 years of age. Clinically, it is characterized by an insidious onset of breathlessness with exertion and a nonproductive cough, leading to progressive DYSPNEA. Pathological features show scant interstitial inflammation, patchy collagen fibrosis, prominent fibroblast proliferation foci, and microscopic honeycomb change.	0	3.57	2	0
Chronic Kidney Diseases [description not available]	0	2.6	1	0
Vascular Injuries [description not available]	0	2.6	1	0
Acute Kidney Failure [description not available]	0	2.6	1	0
Anoxemia [description not available]	0	2.6	1	0
Cirrhosis [description not available]	0	4.25	5	0
Injury, Ischemia-Reperfusion [description not available]	0	3.01	3	0
Hypoxia Sub-optimal OXYGEN levels in the ambient air of living organisms.	0	2.6	1	0
Fibrosis Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.	0	9.25	5	0
Reperfusion Injury Adverse functional, metabolic, or structural changes in tissues that result from the restoration of blood flow to the tissue (REPERFUSION) following ISCHEMIA.	0	3.01	3	0
Renal Insufficiency, Chronic Conditions in which the KIDNEYS perform below the normal level for more than three months. Chronic kidney insufficiency is classified by five stages according to the decline in GLOMERULAR FILTRATION RATE and the degree of kidney damage (as measured by the level of PROTEINURIA). The most severe form is the end-stage renal disease (CHRONIC KIDNEY FAILURE). (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002)	0	2.6	1	0
Acute Kidney Injury Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.	0	2.6	1	0
Fatty Liver, Nonalcoholic [description not available]	0	2.6	1	0
Disease Models, Animal Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases.	0	3.98	4	0
Non-alcoholic Fatty Liver Disease Fatty liver finding without excessive ALCOHOL CONSUMPTION.	0	2.6	1	0
Blood Clot [description not available]	0	13.45	44	5
Thrombosis Formation and development of a thrombus or blood clot in the blood vessel.	1	15.45	44	5
Bleeding [description not available]	0	22.76	71	35
Chronic Kidney Failure [description not available]	0	5.4	2	2
Hemorrhage Bleeding or escape of blood from a vessel.	0	17.76	71	35
Kidney Failure, Chronic The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.	0	5.4	2	2
Arteriosclerosis, Coronary [description not available]	0	8.79	11	1
Coronary Artery Disease Pathological processes of CORONARY ARTERIES that may derive from a congenital abnormality, atherosclerotic, or non-atherosclerotic cause.	0	13.79	11	1
Cardiovascular Diseases Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.	0	18.53	24	12
Anti-Phospholipid Antibody Syndrome [description not available]	0	2.25	1	0
Antiphospholipid Syndrome The presence of antibodies directed against phospholipids (ANTIBODIES, ANTIPHOSPHOLIPID). The condition is associated with a variety of diseases, notably systemic lupus erythematosus and other connective tissue diseases, thrombopenia, and arterial or venous thromboses. In pregnancy it can cause abortion. Of the phospholipids, the cardiolipins show markedly elevated levels of anticardiolipin antibodies (ANTIBODIES, ANTICARDIOLIPIN). Present also are high levels of lupus anticoagulant (LUPUS COAGULATION INHIBITOR).	0	2.25	1	0
Infections, Coronavirus [description not available]	0	2.25	1	0
2019 Novel Coronavirus Disease [description not available]	0	2.25	1	0
Pneumonia, Viral Inflammation of the lung parenchyma that is caused by a viral infection.	0	2.25	1	0
Coronavirus Infections Virus diseases caused by the CORONAVIRUS genus. Some specifics include transmissible enteritis of turkeys (ENTERITIS, TRANSMISSIBLE, OF TURKEYS); FELINE INFECTIOUS PERITONITIS; and transmissible gastroenteritis of swine (GASTROENTERITIS, TRANSMISSIBLE, OF SWINE).	0	2.25	1	0
Ureteral Obstruction Blockage in any part of the URETER causing obstruction of urine flow from the kidney to the URINARY BLADDER. The obstruction may be congenital, acquired, unilateral, bilateral, complete, partial, acute, or chronic. Depending on the degree and duration of the obstruction, clinical features vary greatly such as HYDRONEPHROSIS and obstructive nephropathy.	0	2.25	1	0
Colitis, Granulomatous [description not available]	0	2.31	1	0
Crohn Disease A chronic transmural inflammation that may involve any part of the DIGESTIVE TRACT from MOUTH to ANUS, mostly found in the ILEUM, the CECUM, and the COLON. In Crohn disease, the inflammation, extending through the intestinal wall from the MUCOSA to the serosa, is characteristically asymmetric and segmental. Epithelioid GRANULOMAS may be seen in some patients.	0	2.31	1	0
Infections, Pneumococcal [description not available]	0	3.06	1	0
Pneumococcal Infections Infections with bacteria of the species STREPTOCOCCUS PNEUMONIAE.	0	3.06	1	0
Pneumonia, Pneumococcal A febrile disease caused by STREPTOCOCCUS PNEUMONIAE.	0	3.06	1	0
Non-ST-Elevation Myocardial Infarction [description not available]	0	3.53	1	1
Non-ST Elevated Myocardial Infarction A myocardial infarction that does not produce elevations in the ST segments of the ELECTROCARDIOGRAM. ST segment elevation of the ECG is often used in determining the treatment protocol (see also ST Elevation Myocardial Infarction).	0	3.53	1	1
Heart Disease, Ischemic [description not available]	0	10.87	10	5
Myocardial Ischemia A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION).	0	10.87	10	5
Afibrinogenemia, Congenital [description not available]	0	2.17	1	0
Afibrinogenemia A deficiency or absence of FIBRINOGEN in the blood.	0	7.17	1	0
Endotoxemia A condition characterized by the presence of ENDOTOXINS in the blood. On lysis, the outer cell wall of gram-negative bacteria enters the systemic circulation and initiates a pathophysiologic cascade of pro-inflammatory mediators.	0	3.98	2	1
HIV Coinfection [description not available]	0	4.88	2	1
HIV Human immunodeficiency virus. A non-taxonomic and historical term referring to any of two species, specifically HIV-1 and/or HIV-2. Prior to 1986, this was called human T-lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV). From 1986-1990, it was an official species called HIV. Since 1991, HIV was no longer considered an official species name; the two species were designated HIV-1 and HIV-2.	0	2.17	1	0
HIV Infections Includes the spectrum of human immunodeficiency virus infections that range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS).	1	6.88	2	1
Hypercoagulability [description not available]	0	4.48	1	1
Thrombophilia A disorder of HEMOSTASIS in which there is a tendency for the occurrence of THROMBOSIS.	0	4.48	1	1
Kidney Diseases Pathological processes of the KIDNEY or its component tissues.	0	3.59	1	1
Recrudescence [description not available]	0	11.23	13	8
Brain Hemorrhage [description not available]	0	11.05	13	10
Intracranial Hemorrhages Bleeding within the SKULL, including hemorrhages in the brain and the three membranes of MENINGES. The escape of blood often leads to the formation of HEMATOMA in the cranial epidural, subdural, and subarachnoid spaces.	0	11.05	13	10
Disease Exacerbation [description not available]	0	3.43	2	0
Blood Loss, Postoperative [description not available]	0	4.82	2	1
Complication, Postoperative [description not available]	0	6.81	3	3
Postoperative Complications Pathologic processes that affect patients after a surgical procedure. They may or may not be related to the disease for which the surgery was done, and they may or may not be direct results of the surgery.	0	6.81	3	3
Coronary Thrombosis Coagulation of blood in any of the CORONARY VESSELS. The presence of a blood clot (THROMBUS) often leads to MYOCARDIAL INFARCTION.	0	6.86	5	1
Coronary Heart Disease [description not available]	0	7.22	4	2
Coronary Disease An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.	0	12.22	4	2
Pulmonary Hypertension [description not available]	0	3.01	1	0
Hypertension, Pulmonary Increased VASCULAR RESISTANCE in the PULMONARY CIRCULATION, usually secondary to HEART DISEASES or LUNG DISEASES.	0	3.01	1	0
Atheroma [description not available]	0	4.18	3	0
Cicatrization The formation of fibrous tissue in the place of normal tissue during the process of WOUND HEALING. It includes scar tissue formation occurring in healing internal organs as well as in the skin after surface injuries.	0	2.11	1	0
Cicatrix The fibrous tissue that replaces normal tissue during the process of WOUND HEALING.	0	2.11	1	0
Cerebral Ischemia [description not available]	0	8.71	7	6
Brain Ischemia Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.	0	8.71	7	6
Diabetes Mellitus A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.	0	9.82	2	1
Cardiac Death [description not available]	0	4.41	1	1
Anterior Circulation Transient Ischemic Attack [description not available]	0	5.85	2	2
Ischemic Attack, Transient Brief reversible episodes of focal, nonconvulsive ischemic dysfunction of the brain having a duration of less than 24 hours, and usually less than one hour, caused by transient thrombotic or embolic blood vessel occlusion or stenosis. Events may be classified by arterial distribution, temporal pattern, or etiology (e.g., embolic vs. thrombotic). (From Adams et al., Principles of Neurology, 6th ed, pp814-6)	0	5.85	2	2
Benign Neoplasms [description not available]	0	3.43	2	0
Neoplasms New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.	0	3.43	2	0
Allergic Encephalomyelitis [description not available]	0	2.11	1	0
Body Weight The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.	0	8.51	1	1
Leanness [description not available]	0	3.51	1	1
Kidney Failure A severe irreversible decline in the ability of kidneys to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism.	0	3.03	1	0
Renal Insufficiency Conditions in which the KIDNEYS perform below the normal level in the ability to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism. Renal insufficiency can be classified by the degree of kidney damage (as measured by the level of PROTEINURIA) and reduction in GLOMERULAR FILTRATION RATE.	0	3.03	1	0
Cancer of Colon [description not available]	0	3.03	1	0
Cells, Neoplasm Circulating [description not available]	0	3.03	1	0
Metastase [description not available]	0	3.03	1	0
Experimental Neoplasms [description not available]	0	3.03	1	0
Colonic Neoplasms Tumors or cancer of the COLON.	0	3.03	1	0
Neoplasm Metastasis The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.	0	3.03	1	0
Acute Disease Disease having a short and relatively severe course.	0	4.43	1	1
Diplopia A visual symptom in which a single object is perceived by the visual cortex as two objects rather than one. Disorders associated with this condition include REFRACTIVE ERRORS; STRABISMUS; OCULOMOTOR NERVE DISEASES; TROCHLEAR NERVE DISEASES; ABDUCENS NERVE DISEASES; and diseases of the BRAIN STEM and OCCIPITAL LOBE.	0	3.45	2	0
Cardiac Diseases [description not available]	0	3.53	1	1
Heart Diseases Pathological conditions involving the HEART including its structural and functional abnormalities.	0	3.53	1	1
Angina at Rest [description not available]	0	2.96	1	0
Angina, Unstable Precordial pain at rest, which may precede a MYOCARDIAL INFARCTION.	0	2.96	1	0
Adverse Drug Event [description not available]	0	4.75	2	1
Drug-Related Side Effects and Adverse Reactions Disorders that result from the intended use of PHARMACEUTICAL PREPARATIONS. Included in this heading are a broad variety of chemically-induced adverse conditions due to toxicity, DRUG INTERACTIONS, and metabolic effects of pharmaceuticals.	0	4.75	2	1
Thromboembolism Obstruction of a blood vessel (embolism) by a blood clot (THROMBUS) in the blood stream.	0	2.96	1	0
Obesity A status with BODY WEIGHT that is grossly above the recommended standards, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).	0	2.05	1	0
Ileus A condition caused by the lack of intestinal PERISTALSIS or INTESTINAL MOTILITY without any mechanical obstruction. This interference of the flow of INTESTINAL CONTENTS often leads to INTESTINAL OBSTRUCTION. Ileus may be classified into postoperative, inflammatory, metabolic, neurogenic, and drug-induced.	0	2.05	1	0
Thromboembolism, Venous [description not available]	0	2.07	1	0
Auricular Fibrillation [description not available]	0	2.07	1	0
Atrial Fibrillation Abnormal cardiac rhythm that is characterized by rapid, uncoordinated firing of electrical impulses in the upper chambers of the heart (HEART ATRIA). In such case, blood cannot be effectively pumped into the lower chambers of the heart (HEART VENTRICLES). It is caused by abnormal impulse generation.	0	2.07	1	0
Venous Thromboembolism Obstruction of a vein or VEINS (embolism) by a blood clot (THROMBUS) in the blood stream.	0	2.07	1	0
Hepatic Insufficiency Conditions in which the LIVER functions fall below the normal ranges. Severe hepatic insufficiency may cause LIVER FAILURE or DEATH. Treatment may include LIVER TRANSPLANTATION.	0	3.46	1	1
Hematochezia The passage of bright red blood from the rectum. The blood may or may not be mixed with formed stool in the form of blood, blood clots, bloody stool or diarrhea.	0	3.46	1	1
Hepatic Failure [description not available]	0	3.46	1	1
Gastrointestinal Hemorrhage Bleeding in any segment of the GASTROINTESTINAL TRACT from ESOPHAGUS to RECTUM.	0	3.46	1	1
Liver Failure Severe inability of the LIVER to perform its normal metabolic functions, as evidenced by severe JAUNDICE and abnormal serum levels of AMMONIA; BILIRUBIN; ALKALINE PHOSPHATASE; ASPARTATE AMINOTRANSFERASE; LACTATE DEHYDROGENASES; and albumin/globulin ratio. (Blakiston's Gould Medical Dictionary, 4th ed)	0	3.46	1	1