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Related Concept Videos

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Activation of Integrins01:15

Activation of Integrins

Integrins bind ligands and transmit information from outside the cell to inside or vice-versa through an "outside-in signaling" or "inside-out signaling."
In "outside-in signaling," external factors in the extracellular space bind to exposed ligand binding sites on integrins. This causes the inactive protein to undergo a conformational change to become active. Integrins are often clustered on the cell membrane. Repetitive and regularly spaced ligand binding events provide an effective stimulus.
Integrins01:10

Integrins

Animal and protozoan cells do not have cell walls to help maintain shape and provide structural stability. Instead, these eukaryotic cells secrete a sticky mass of carbohydrates and proteins into the spaces between adjacent cells. This network of proteins and molecules is called an extracellular matrix or ECM.
Some ECM proteins assemble into a basement membrane to which the remaining components adhere. Proteoglycans typically form the bulk of the ECM while fibrous proteins, like collagen,...
GPI Anchoring of Proteins in the ER Membrane01:29

GPI Anchoring of Proteins in the ER Membrane

GPI-anchoring is a post-translational, reversible protein modification that is ubiquitous in eukaryotes. Such proteins are primarily present on the exoplasmic leaflet of the plasma membrane.
GPI-anchor structure
A sequence of 11 enzymatic reactions results in the synthesis of the complete GPI anchor consisting of a hydrophobic and a hydrophilic portion. The hydrophobic portion comprises phosphatidylinositol, while the hydrophilic part comprises polar groups like phosphoethanolamine,...

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Related Experiment Video

Updated: Jun 5, 2026

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
04:32

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry

Published on: June 5, 2019

Targeting the platelet integrin GPIIb/IIIa.

Christoph E Hagemeyer1, Karlheinz Peter

  • 1Atherothrombosis and Vascular Biology, Baker IDI Heart and Diabetes Institute, PO Box 6492 St Kilda Road Central, Melbourne, Victoria 8008, Australia. christoph.hagemeyer@bakeridi.edu.au

Current Pharmaceutical Design
|January 21, 2011
PubMed
Summary

Platelet GPIIb/IIIa inhibitors are vital anti-thrombotic agents, but oral versions and reduced bleeding remain challenges. Future drug development aims to improve upon current GPIIb/IIIa blockers.

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Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
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Last Updated: Jun 5, 2026

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
04:32

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry

Published on: June 5, 2019

An In Vitro Assay to Study Platelet Migration Using RGD-Functionalized Avidin-Biotin Tethers
05:43

An In Vitro Assay to Study Platelet Migration Using RGD-Functionalized Avidin-Biotin Tethers

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Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
10:10

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Published on: October 27, 2009

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology
  • Structural Biology

Background:

  • The platelet integrin GPIIb/IIIa is crucial for thrombus formation and a key target for anti-thrombotic therapies.
  • Structural biology has elucidated the ligand binding site, validating GPIIb/IIIa blockade for cardiovascular medicine.

Purpose of the Study:

  • To review current knowledge on GPIIb/IIIa structure, function, and signaling.
  • To discuss the benefits and limitations of existing GPIIb/IIIa inhibitors.
  • To explore future directions for developing improved oral GPIIb/IIIa blockers with reduced bleeding risks.

Main Methods:

  • Literature review of structural biology, pharmacology, and clinical data on GPIIb/IIIa inhibitors.
  • Analysis of current therapeutic strategies and unmet needs in anti-platelet therapy.

Main Results:

  • GPIIb/IIIa inhibitors have been successful in various cardiovascular conditions, with three licensed agents (abciximab, eptifibatide, tirofiban).
  • Oral GPIIb/IIIa antagonists have faced challenges, highlighting a need for better oral agents with improved safety profiles.

Conclusions:

  • Despite successes, there is an unmet need for orally available GPIIb/IIIa inhibitors with reduced bleeding complications.
  • Lessons from past development failures can guide the creation of next-generation GPIIb/IIIa blockers.