Blood
Glanzmann Thrombasthenia
Also known as GT, thrombasthenia of Glanzmann and Naegeli, ITGA2B/ITGB3 deficiency
Glanzmann thrombasthenia is a rare inherited platelet function disorder caused by biallelic mutations in ITGA2B or ITGB3 encoding the platelet integrin alphaIIbbeta3 (glycoprotein IIb/IIIa), the principal platelet surface receptor for fibri
4
studies recruiting now
as of 7 Sept 2026
19
studies registered in total
as of 7 Sept 2026
2
countries with a recruiting site
as of 7 Sept 2026
22 Aug 2025
most recent study posted
among recruiting studies
Recruiting trials
ATHNdataset Registry
Eptacog Beta in Glanzmann's (HeT_LFB-Strength-Study_FID531)
The Genetics and Functional Basis of Inherited Platelet, White Blood Cell, Red Blood Cell, and Blood Clotting Disorders.
Showing the 4 most recently updated recruiting studies, as recorded 7 Sept 2026. Live status on each study page.
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About Glanzmann Thrombasthenia
Glanzmann thrombasthenia is a rare inherited platelet function disorder caused by biallelic mutations in ITGA2B or ITGB3 encoding the platelet integrin alphaIIbbeta3 (glycoprotein IIb/IIIa), the principal platelet surface receptor for fibrinogen, which is essential for platelet aggregation and primary hemostasis. Three types are recognized: type I (less than 5% alphaIIbbeta3 expression), type II (10-20% expression), and type III (variant with dysfunctional receptor), all resulting in severely impaired platelet aggregation with all physiological agonists despite a normal platelet count. The condition causes lifelong mucocutaneous bleeding with particularly severe implications for surgical procedures, trauma, and childbirth.
Common clinical features
From Orphanet’s phenotype annotations (CC BY 4.0). Not a complete list.
Treatments being studied
1 in clinical development, from Open Targets (CC BY 4.0). Not medical advice.
Before you apply
Things trial teams commonly ask about for Glanzmann Thrombasthenia. Not eligibility rules; those are set by each study.
- Platelet aggregometry showing absent aggregation with ADP, collagen, epinephrine, and thrombin receptor activating peptide (TRAP) but normal ristocetin-induced agglutination is diagnostic and required for trial enrollment.
- Alloantibody status against alphaIIbbeta3 from platelet transfusions is critical; patients with anti-alphaIIbbeta3 antibodies may be excluded from some trials but are specifically targeted in others testing novel hemostatic agents.
- Bleeding Assessment Tool (BAT) scores and surgical or obstetric bleeding history should be documented; trials evaluating recombinant activated factor VII or thrombopoietin agents require detailed baseline bleeding phenotype.
Related conditions
Information, not medical advice. Trial listings are shown as recorded on ClinicalTrials.gov; whether any study is right for you is a decision for you and your clinicians, and eligibility is decided by each research team. Disease information from Orphanet (CC BY 4.0).