RecruitingPhase 3NCT05334368
Immune
Hypereosinophilic Syndrome
Also known as HES, idiopathic hypereosinophilia, FIP1L1-PDGFRA HES
Hypereosinophilic Syndrome is defined by persistent blood eosinophilia exceeding 1,500 cells per microliter with evidence of eosinophil-mediated organ damage, encompassing heterogeneous subtypes including the FIP1L1-PDGFRA fusion-driven mye
ORPHA:168956 ↗Gene FIP1L1-PDGFRA (subset)Prevalence 0.5-1 in 100,000Onset Any age; myeloid/neoplastic HES peaks in 4th-5th decade; lymphocytic HES variableEosinophilic disorder (myeloproliferative or lymphocytic variant)
16
studies recruiting now
as of 7 Sept 2026
141
studies registered in total
as of 7 Sept 2026
21
countries with a recruiting site
as of 7 Sept 2026
26 Jun 2026
most recent study posted
among recruiting studies
Recruiting trials
RecruitingNCT00091871
A Longitudinal Study of Familial Hypereosinophilia (FE): Natural History and Markers of Disease Progression
RecruitingNCT06422078
A Non-interventional, Prospective Study With Benralizumab
RecruitingNCT07214753
A Real-life Observational Study in Severe Eosinophilic Asthma Adult Participant Treated With Benralizumab in Italy
RecruitingPhase 3NCT07671001
A Study of Depemokimab in Participants of 6 to 11 Years of Age
Showing the 5 most recently updated recruiting studies, as recorded 7 Sept 2026. Live status on each study page.
See all 16 recruiting studiesWhere recruiting studies are running
Countries with at least one recruiting site among the studies above, 7 Sept 2026. Tap a country to search trials there.
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About Hypereosinophilic Syndrome
Hypereosinophilic Syndrome is defined by persistent blood eosinophilia exceeding 1,500 cells per microliter with evidence of eosinophil-mediated organ damage, encompassing heterogeneous subtypes including the FIP1L1-PDGFRA fusion-driven myeloid variant (highly responsive to imatinib), lymphocyte-variant HES (driven by aberrant IL-5-secreting T-cell clones), and idiopathic HES where no underlying cause is identified. End-organ damage from eosinophilic infiltration and granule protein deposition can affect the heart (Loeffler endocarditis), nervous system, skin, and lungs. Mepolizumab (anti-IL-5) has demonstrated efficacy and is approved for HES in patients without FIP1L1-PDGFRA.
Common clinical features
Persistent eosinophilia >1,500/µL on two occasionsLoeffler endocarditis with endomyocardial fibrosisPeripheral neuropathy and CNS thromboemboliChronic urticaria, angioedema, and pruritusPulmonary infiltrates and pleural effusionsSplenomegaly (particularly in myeloid variant)Constitutional symptoms (fatigue, fever, weight loss)
From Orphanet’s phenotype annotations (CC BY 4.0). Not a complete list.
Treatments being studied
2 approved treatments and 9 in clinical development, from Open Targets (CC BY 4.0). Not medical advice.
Approved: ImatinibApproved: Mepolizumab (Bosatria)
Phase 3Depemokimab
Phase 3Prednisone (Cortan)
Phase 3Prednisolone (Cortalone)
Phase 3Benralizumab (Fasenra)
Phase 2Dexpramipexole
Phase 2Reslizumab (Cinqaero)
Phase 2Ruxolitinib (Jakavi)
Phase 2Dupilumab (Dupixent)
+ 1 more in development
Before you apply
Things trial teams commonly ask about for Hypereosinophilic Syndrome. Not eligibility rules; those are set by each study.
- HES subtype classification (myeloid/FIP1L1-PDGFRA, lymphocytic, idiopathic) determines trial eligibility; FIP1L1-PDGFRA FISH or RT-PCR testing and T-cell clonality studies are required before applying
- Anti-IL-5 therapy trials (mepolizumab, benralizumab) typically exclude FIP1L1-PDGFRA positive patients who should instead be on imatinib; confirm and document fusion gene status
- Cardiac screening with echocardiography is mandatory in most trials given risk of Loeffler endocarditis; provide most recent echo with ejection fraction and valvular assessment
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).