Related Experiment Video
Updated: Jun 21, 2026

Ferric Chloride-induced Murine Thrombosis Models
Published on: September 5, 2016
The evolution of platelet-directed pharmacotherapy
1Division of Hematology, Duke University School of Medicine, Duke Clinical Research Institute, Durham, NC 27705, USA. becke021@mc.duke.edu
The evolution of platelet directed pharmacotherapy in the prevention and treatment of patients with thrombotic disorders is based soundly on a rapidly expanding knowledge of platelet biology. Traditionally viewed, throughout most of its relatively brief history in medicine, as an anucleate, passive contributor to hemostasis, a more contemporary perspective acknowledges platelets as complex, multidimensional cells that participate actively in coagulation, vascular repair, angiogenesis and thrombosis within the micro and the macro-circulatory systems. Herein, we consider platelet-directed pharmacotherapy from these fundamental, biology-based exemplars--megakaryocytes, signal transduction and the platelet--coagulation protease interface. We also highlight the emerging biopharmacology platform of oligonucleotide platelet adhesion antagonists and their complementary antidotes.
The evolution of platelet directed pharmacotherapy in the prevention and treatment of patients with thrombotic disorders is based soundly on a rapidly expanding knowledge of platelet biology. Traditionally viewed, throughout most of its relatively brief history in medicine, as an anucleate, passive contributor to hemostasis, a more contemporary perspective acknowledges platelets as complex, multidimensional cells that participate actively in coagulation, vascular repair, angiogenesis and thrombosis within the micro and the macro-circulatory systems. Herein, we consider platelet-directed pharmacotherapy from these fundamental, biology-based exemplars--megakaryocytes, signal transduction and the platelet--coagulation protease interface. We also highlight the emerging biopharmacology platform of oligonucleotide platelet adhesion antagonists and their complementary antidotes.
Related Concept Videos
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Formation of the Platelet Plug
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...
Structure and Function of Platelets
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...
Anticoagulant Drugs: Low-Molecular-Weight Heparins
Clot Retraction and Fibrinolysis
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...

