ReviewCirculation research2013
Integrin αIIbβ3: from discovery to efficacious therapeutic target.
Review in Circulation research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
What it found
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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
78 citing papers in PubMed, 154 citations in OpenAlex.
- A murine stable thrombosis model enabling therapeutic evaluation of antithrombotic drugs.Blood vessels, thrombosis & hemostasis · 2026Article
- Snake Venom Protease Detection and Inhibition in Serum.ChemMedChem · 2026Article
- Identification of an αvβ3-targeting bicyclic peptide with atypical norArg-Gly-Asp sequence.Communications chemistry · 2026Article
- The emerging role of human transmembrane RGD-based counter-receptors of integrins in health and disease.Cellular & molecular biology letters · 2025Review
- A Novel KGD-Based αIIbβ3 Antagonist Prevents Arterial Thrombosis While Preserving Hemostasis and Avoiding Thrombocytopenia.International journal of molecular sciences · 2025Article
- Influence of the Immune Checkpoint Inhibitors on the Hemostatic Potential of Blood Plasma.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2025Article
- Epidemiological and clinical characteristics of children and young adults with Glanzmann's thrombasthenia in upper Egypt: a multicenter cross-sectional study.Annals of hematology · 2025Observational
- Recent advances in vascular thiol isomerases: insights into structures, functions in thrombosis and antithrombotic inhibitor development.Thrombosis journal · 2025Review
- The Impact of Single Nucleotide Polymorphisms and Other Mechanisms on Aspirin Resistance.Cardiovascular & hematological disorders drug targets · 2025Review
- Full-length αIIbβ3 cryo-EM structure reveals intact integrin initiate-activation intrinsic architecture.Structure (London, England : 1993) · 2024Article
- Identifications of novel host cell factors that interact with the receptor-binding domain of the SARS-CoV-2 spike protein.The Journal of biological chemistry · 2024Article
- Review
- Review
- Venom-derived peptides for breaking through the glass ceiling of drug development.Frontiers in chemistry · 2024Review
- Antiplatelet and Antithrombotic Activities ofEvidence-based complementary and alternative medicine : eCAM · 2024Article
- Article
- GDF-15 Inhibits ADP-Induced Human Platelet Aggregation through the GFRAL/RET Signaling Complex.Biomolecules · 2023Article
- Antiplatelet strategies: past, present, and future.Journal of thrombosis and haemostasis : JTH · 2023Review
- The Cellular and Protein Arms of Coagulation in Diabetes: Established and Potential Targets for the Reduction of Thrombotic Risk.International journal of molecular sciences · 2023Review
- Integrin signaling in cancer: bidirectional mechanisms and therapeutic opportunities.Cell communication and signaling : CCS · 2023Review
18 more citing papers are in PubMed but not listed here.
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 1 institution in 2 countries.
Funding
Abstract
From the initial description of platelets in 1882, their propensity to aggregate and to contribute to thrombosis was apparent. Indeed, excessive platelet aggregation is associated with myocardial infarction and other thrombotic diseases whereas Glanzmann thrombasthenia, in which platelet aggregation is reduced, is a bleeding syndrome. Over the last half of the 20th century, many investigators have provided insights into the cellular and molecular basis for platelet aggregation. The major membrane protein on platelets, integrin αIIbβ3, mediates this response by rapidly transiting from its resting to an activated state in which it serves as a receptor for ligands that can bridge platelets together. Monoclonal antibodies, natural products, and small peptides were all shown to inhibit αIIbβ3 dependent platelet aggregation, and these inhibitors became the forerunners of antagonists that proceeded through preclinical testing and into large patient trials to treat acute coronary syndromes, particularly in the context of percutaneous coronary interventions. Three such αIIbβ3 antagonists, abciximab, eptifibatide, and tirofiban, received Food and Drug Administration approval. Over the past 15 years, millions of patients have been treated with these αIIbβ3 antagonists and many lives have been saved by their administration. With the side effect of increased bleeding and the development of new antithrombotic drugs, the use of αIIbβ3 antagonists is waning. Nevertheless, they are still widely used for the prevention of periprocedural thrombosis during percutaneous coronary interventions. This review focuses on the biology of αIIbβ3, the development of its antagonists, and some of the triumphs and shortcomings of αIIbβ3 antagonism.
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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.