Glycoprotein IIb/IIIa inhibitors

In medicine, glycoprotein IIb/IIIa inhibitors, also GpIIb/IIIa inhibitors, is a class of antiplatelet agents.

Several GpIIb/IIIa inhibitors exist:

Use

Glycoprotein IIb/IIIa inhibitors are frequently used during percutaneous coronary intervention (PCI) (angioplasty with or without intracoronary stent placement). Their benefit comes from preventing thrombosis, when typically clear blood vessels are blocked by blood clot formation.[1] Preventing platelet adhesion and thus, thrombus formation is achieved through inhibition of the GpIIb/IIIa receptor on the surface of individual platelets. They have also assisted with other blood-clot-related treatment procedures outside of the heart.[1]

Glycoprotein IIb/IIIa inhibitors may also be used to treat acute coronary syndromes (ACS), without percutaneous coronary intervention, depending on Thrombolysis In Myocardial Infarction (TIMI) risk.[1][2]

History

Glycoprotein IIb/IIIa inhibitors development arose from the understanding of Glanzmann's thrombasthenia, a condition in which the GpIIb/IIIa receptor is deficient or dysfunctional.[3] The dysfunction in the receptor impairs the ability to form blood clots in wound repair (hemostasis), causing chronic bleeding, especially in the soft tissue membranes that line body cavities. [4] Sample platelets from these patients exhibited a similar, but abnormal, glycoprotein pattern, which, along with a patient's body developing an antibody, lead scientist to explore targeting the receptor as a treatment option for patients.[1]

Aspirin had been used to inhibit platelet formation, but in the 1980s, scientists created an antibody Fab fragment that performed better.[1] Abciximab, a monoclonal antibody, was then clinically approved to reduce blood clot formation during PCI to help the procedure go more smoothly. [1] Over the next ten years, improvements were made to develop other glycoprotein inhibitors, such as eptifibatide and tirofiban, by shortening their half-lives to make them more suitable for treatments.[1]


Molecular Mechanisms

The glycoprotein IIb/IIIa cellular receptor ultimately facilitates the joining of individual platelets to form clots by attaching and chaining together adhesive ligands.[1]

References

  1. ^ a b c d e f g h Ortega-Paz, Luis; Durukan, Selina; Farahmandsadr, Maryam (2025), Gresele, Paolo; López, José A.; Angiolillo, Dominick J.; Page, Clive P. (eds.), "Glycoprotein IIb/IIIa Antagonists", Platelet Pharmacology and Therapy: Volume 5, Cham: Springer Nature Switzerland, pp. 1983–1995, doi:10.1007/978-3-031-96360-5_3#DOI, ISBN 978-3-031-96360-5, retrieved 2026-03-10{{citation}}: CS1 maint: work parameter with ISBN (link)
  2. ^ Tricoci, Pierluigi; Newby, L. Kristin; Hasselblad, Vic; Kong, David F.; Giugliano, Robert P.; White, Harvey D.; Théroux, Pierre; Stone, Gregg W.; Moliterno, David J.; Van de Werf, Frans; Armstrong, Paul W.; Prabhakaran, Dorairaj; Rasoul, Saman; Bolognese, Leonardo; Durand, Eric (June 2011). "Upstream Use of Small-Molecule Glycoprotein IIb/IIIa Inhibitors in Patients With Non–ST-Segment Elevation Acute Coronary Syndromes: A Systematic Overview of Randomized Clinical Trials". Circulation: Cardiovascular Quality and Outcomes. 4 (4): 448–458. doi:10.1161/CIRCOUTCOMES.110.960294. ISSN 1941-7713.
  3. ^ Seligsohn, U (2002). "Glanzmann thrombasthenia: a model disease which paved the way to powerful therapeutic agents". Pathophysiol Haemost Thromb. 32 (5–6): 216–7. doi:10.1159/000073569. PMID 13679645.
  4. ^ Krause, Katherine A.; Graham, Brendan C. (2023-08-28), "Glanzmann Thrombasthenia", StatPearls [Internet], StatPearls Publishing, PMID 30855858, retrieved 2026-03-10
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