ReviewDrugs2010
Thrombin receptor antagonists for the treatment of atherothrombosis: therapeutic potential of vorapaxar and E-5555.
Review in Drugs, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 30 citations in OpenAlex.
- Novel Function for Endothelial Protease-Activated Receptors in Modulating Insulin Receptor Activity With Implications for Diabetes.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Protease-activated receptor-mediated platelet aggregation in acute coronary syndrome patients on potent P2YResearch and practice in thrombosis and haemostasis · 2019Article
- Vein graft failure: from pathophysiology to clinical outcomes.Nature reviews. Cardiology · 2016Review
- Vorapaxar: a review of its use in the long-term secondary prevention of atherothrombotic events.Drugs · 2015Review
- Vorapaxar: first global approval.Drugs · 2014Review
- Novel anti-platelet agents: focus on thrombin receptor antagonists.Journal of cardiovascular translational research · 2013Review
- Thrombin induced connective tissue growth factor expression in rat vascular smooth muscle cells via the PAR-1/JNK/AP-1 pathway.Acta pharmacologica Sinica · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Platelet activation, achieved through a variety of surface receptors and biochemical mediators, represents a key event in the pathogenesis of atherothrombosis and its clinical manifestations. The major pathways involved in platelet activation are triggered by thromboxane A(2), adenosine diphosphate and thrombin, with the latter being the most potent of these agonists. Despite the effective inhibition of the first two pathways with aspirin and several generations of P2Y(12) receptor antagonists, respectively, the recurrence of ischaemic events in patients with atherothrombosis remains high. In addition, there is a growing concern over the safety profile of increasingly powerful antiplatelet drugs in terms of bleeding, which has tempered expectations of newly developed compounds. Thrombin receptor antagonists are a novel class of antiplatelet agents that inhibit thrombin-mediated platelet activation. Preliminary data indicate that these compounds may have the potential to improve ischaemic outcomes without significantly increasing the bleeding liability. Currently, two agents of this class are under clinical development: vorapaxar (previously known as SCH 530348) and E-5555. In this review we discuss this novel class of antiplatelet agents, focusing in particular on their therapeutic potential.
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What OpenQuestion holds
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.