Evidence map›Paper›PMID 29269513›Full record

Trial reportArteriosclerosis, thrombosis, and vascular biology2018

PAR4 (Protease-Activated Receptor 4) Antagonism With BMS-986120 Inhibits Human Ex Vivo Thrombus Formation.

Simon J Wilson, Fraz A Ismat, Zhaoqing Wang, Michael Cerra, Hafid Narayan, Jennifer Raftis, Timothy J Gray, Shea Connell, Samira Garonzik, Xuewen Ma and 2 more

Registry-linked trialOpen access · bronzeAbstract readClinical Trial, Phase IComparative StudyRandomized Controlled Trial
In one paragraph

Trial report in Arteriosclerosis, thrombosis, and vascular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02439190 (A Single Dose Study to Evaluate the Effect of BMS-986120 on Thrombus Formation in an Ex Vivo Thrombosis Chamber Model in Healthy Subjects), which is not on this map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
8.4field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT02439190 phase1completednot on this map

A Single Dose Study to Evaluate the Effect of BMS-986120 on Thrombus Formation in an Ex Vivo Thrombosis Chamber Model in Healthy Subjects

TypeinterventionalSponsorBristol-Myers SquibbRan2015 to 2016Enrolled42ConditionsThrombosisArmsBMS-986120, Aspirin, Clopidogrel
3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 105 citations in OpenAlex.

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  18. Article
  19. Species Differences in Platelet Protease-Activated Receptors.International journal of molecular sciences · 2023
    Review
  20. PARs in the inflammation-cancer transformation of CRC.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

Simon J WilsonFrom the British Heart Foundation Centre for Cardiovascular Science (S.J.W., D.E.N.), Medical Research Council Centre for Inflammation Research (J.R., S.C.), and Edinburgh College of Medicine (T.J.G.), University of Edinburgh, United Kingdom; Bristol Myers Squibb, Princeton, NJ (F.A.I., Z.W., M.C., S.G., X.M., J.Y.); and Royal Infirmary of Edinburgh, United Kingdom (H.N.). simonwilson3@nhs.net.
Fraz A IsmatFrom the British Heart Foundation Centre for Cardiovascular Science (S.J.W., D.E.N.), Medical Research Council Centre for Inflammation Research (J.R., S.C.), and Edinburgh College of Medicine (T.J.G.), University of Edinburgh, United Kingdom; Bristol Myers Squibb, Princeton, NJ (F.A.I., Z.W., M.C., S.G., X.M., J.Y.); and Royal Infirmary of Edinburgh, United Kingdom (H.N.).
Zhaoqing WangFrom the British Heart Foundation Centre for Cardiovascular Science (S.J.W., D.E.N.), Medical Research Council Centre for Inflammation Research (J.R., S.C.), and Edinburgh College of Medicine (T.J.G.), University of Edinburgh, United Kingdom; Bristol Myers Squibb, Princeton, NJ (F.A.I., Z.W., M.C., S.G., X.M., J.Y.); and Royal Infirmary of Edinburgh, United Kingdom (H.N.).
Michael CerraFrom the British Heart Foundation Centre for Cardiovascular Science (S.J.W., D.E.N.), Medical Research Council Centre for Inflammation Research (J.R., S.C.), and Edinburgh College of Medicine (T.J.G.), University of Edinburgh, United Kingdom; Bristol Myers Squibb, Princeton, NJ (F.A.I., Z.W., M.C., S.G., X.M., J.Y.); and Royal Infirmary of Edinburgh, United Kingdom (H.N.).
Hafid NarayanFrom the British Heart Foundation Centre for Cardiovascular Science (S.J.W., D.E.N.), Medical Research Council Centre for Inflammation Research (J.R., S.C.), and Edinburgh College of Medicine (T.J.G.), University of Edinburgh, United Kingdom; Bristol Myers Squibb, Princeton, NJ (F.A.I., Z.W., M.C., S.G., X.M., J.Y.); and Royal Infirmary of Edinburgh, United Kingdom (H.N.).
Jennifer RaftisFrom the British Heart Foundation Centre for Cardiovascular Science (S.J.W., D.E.N.), Medical Research Council Centre for Inflammation Research (J.R., S.C.), and Edinburgh College of Medicine (T.J.G.), University of Edinburgh, United Kingdom; Bristol Myers Squibb, Princeton, NJ (F.A.I., Z.W., M.C., S.G., X.M., J.Y.); and Royal Infirmary of Edinburgh, United Kingdom (H.N.).
Timothy J GrayFrom the British Heart Foundation Centre for Cardiovascular Science (S.J.W., D.E.N.), Medical Research Council Centre for Inflammation Research (J.R., S.C.), and Edinburgh College of Medicine (T.J.G.), University of Edinburgh, United Kingdom; Bristol Myers Squibb, Princeton, NJ (F.A.I., Z.W., M.C., S.G., X.M., J.Y.); and Royal Infirmary of Edinburgh, United Kingdom (H.N.).
Shea ConnellFrom the British Heart Foundation Centre for Cardiovascular Science (S.J.W., D.E.N.), Medical Research Council Centre for Inflammation Research (J.R., S.C.), and Edinburgh College of Medicine (T.J.G.), University of Edinburgh, United Kingdom; Bristol Myers Squibb, Princeton, NJ (F.A.I., Z.W., M.C., S.G., X.M., J.Y.); and Royal Infirmary of Edinburgh, United Kingdom (H.N.).
Samira GaronzikFrom the British Heart Foundation Centre for Cardiovascular Science (S.J.W., D.E.N.), Medical Research Council Centre for Inflammation Research (J.R., S.C.), and Edinburgh College of Medicine (T.J.G.), University of Edinburgh, United Kingdom; Bristol Myers Squibb, Princeton, NJ (F.A.I., Z.W., M.C., S.G., X.M., J.Y.); and Royal Infirmary of Edinburgh, United Kingdom (H.N.).
Xuewen MaFrom the British Heart Foundation Centre for Cardiovascular Science (S.J.W., D.E.N.), Medical Research Council Centre for Inflammation Research (J.R., S.C.), and Edinburgh College of Medicine (T.J.G.), University of Edinburgh, United Kingdom; Bristol Myers Squibb, Princeton, NJ (F.A.I., Z.W., M.C., S.G., X.M., J.Y.); and Royal Infirmary of Edinburgh, United Kingdom (H.N.).
Jing YangFrom the British Heart Foundation Centre for Cardiovascular Science (S.J.W., D.E.N.), Medical Research Council Centre for Inflammation Research (J.R., S.C.), and Edinburgh College of Medicine (T.J.G.), University of Edinburgh, United Kingdom; Bristol Myers Squibb, Princeton, NJ (F.A.I., Z.W., M.C., S.G., X.M., J.Y.); and Royal Infirmary of Edinburgh, United Kingdom (H.N.).
David E NewbyFrom the British Heart Foundation Centre for Cardiovascular Science (S.J.W., D.E.N.), Medical Research Council Centre for Inflammation Research (J.R., S.C.), and Edinburgh College of Medicine (T.J.G.), University of Edinburgh, United Kingdom; Bristol Myers Squibb, Princeton, NJ (F.A.I., Z.W., M.C., S.G., X.M., J.Y.); and Royal Infirmary of Edinburgh, United Kingdom (H.N.).
Bristol-Myers Squibb (United States) · US

Funding

British Heart Foundation CH/09/002/26360British Heart Foundation RE/13/3/30183British Heart Foundation RM/13/2/30158Wellcome Trust 103782
6 · The paper itself

Abstract

objectiveBMS-986120 is a novel first-in-class oral PAR4 (protease-activated receptor 4) antagonist with potent and selective antiplatelet effects. We sought to determine for the first time, the effect of BMS-986120 on human ex vivo thrombus formation. APPROACH AND

resultsForty healthy volunteers completed a phase 1 parallel-group PROBE trial (Prospective Randomized Open-Label Blinded End Point). Ex vivo platelet activation, platelet aggregation, and thrombus formation were measured at 0, 2, and 24 hours after (1) oral BMS-986120 (60 mg) or (2) oral aspirin (600 mg) followed at 18 hours with oral aspirin (600 mg) and oral clopidogrel (600 mg). BMS-986120 demonstrated highly selective and reversible inhibition of PAR4 agonist peptide (100 μM)-stimulated P-selectin expression, platelet-monocyte aggregates, and platelet aggregation (

conclusionsBMS-986120 is a highly selective and reversible oral PAR4 antagonist that substantially reduces platelet-rich thrombus formation under conditions of high shear stress. Our results suggest PAR4 antagonism has major potential as a therapeutic antiplatelet strategy. CLINICAL

trial registrationURL: http://www.clinicaltrials.gov. Unique identifier: NCT02439190.

Indexed as

Administration, OralAdultAspirinBenzofuransBlood PlateletsClopidogrelFemaleFibrinolytic AgentsHealthy VolunteersHumansImidazolesMaleMorpholinesPlatelet AggregationPlatelet Aggregation InhibitorsProspective StudiesAspirinBenzofuransBMS-986120ClopidogrelFibrinolytic AgentsImidazolesMorpholinesPlatelet Aggregation Inhibitorsprotease-activated receptor 4Receptors, ThrombinThiazolesantiplatelethumannovelprotease-activated receptor 4thrombosis

Identifiers

PMID29269513
PMCPMC5779320
OpenAlexW2778741366

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.