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NCT06373926: MONOCYTAN
Evaluation of Cell Membrane Expression of Annexin A2 on Monocytes by Flow Cytometry in Primary Antiphospholipid Syndrome
NA trial testing blood withdrawal in Antiphospholipid Syndrome in 60 participants. Currently enrolling.
1 March 2026
Quick facts
| Lead sponsor | Centre Hospitalier Universitaire, Amiens |
|---|---|
| Phase | NA |
| Status | Recruiting now |
| Study type | INTERVENTIONAL |
| Allocation | non randomized |
| Design | parallel |
| Masking | none |
| Primary purpose | diagnostic |
| Enrollment | 60 |
| Start date | 5 February 2025 |
| Primary completion | 1 March 2026 |
| Estimated completion | 1 March 2026 |
| Sites | 1 location across France |
Drugs / interventions tested
- blood withdrawal — full drug profile →
Conditions studied
- Antiphospholipid Syndrome — all drugs for Antiphospholipid Syndrome →
Sponsor
Centre Hospitalier Universitaire, Amiens
Who can join
18 and older, any sex, with Antiphospholipid Syndrome. Healthy volunteers can join.
What's being measured
Primary outcomes are the specific endpoints the trial is designed to prove or disprove.
-
Cell membrane expression rate of ANXA2 on circulating monocytes in APS
Time frame: 1 hour
Sponsor's own description
Annexin A2 (ANXA2), an endothelial cell receptor for plasminogen and tissue plasminogen activator, plays a pivotal role in regulation of fibrinolysis in vitro and in vivo and has been identified as a new autoantigen in antiphospholipid syndrome (APS). ANXA2 can exist as a monomer or a heterotetrameric complex with S100A10 protein. The aim of this study was to evaluate the cell membrane expression of ANXA2 on circulating monocytes in APS by flow cytometry. Several pathogenic mechanisms are involved in APS such as activation of endothelial cells, platelets and monocytes, inhibition of the natural anticoagulant protein C/protein S pathway, activation of the complement system and also impairment of fibrinolysis. Annexin A2 which hits binding partner S100A10, ANXA2 forms a cell surface complex that regulates generation of plasmin. ANXA2 is involved in the pathogenesis of APS-associated through several possible mechanisms. Human peripheral blood monocytes represent the major circulating ANXA2-expressing cell and ANXA2-mediated assembly of plasminogen and tissue activator of plasminogen (tPA) on monocyte/macrophages contributes to plasmin generation. Thus the investigators could suppose that decrease of cell membrane expression of ANXA2 on circulating monocytes represent a new pathogenic mechanism in APS.
Publications & conference data
No peer-reviewed publications indexed yet for this trial.
Verify or expand the search:
- PubMed search for NCT06373926
- Europe PMC full search
- ASCO Meeting Library
- ESMO Meeting Library
- bioRxiv preprints
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Verify against primary sources
- ClinicalTrials.gov — authoritative US registry record
- WHO ICTRP — international registry index
- EU Clinical Trials Register
- Sponsor press releases (Google)
- Trial protocol + status: ClinicalTrials.gov NCT06373926 (US National Library of Medicine, public domain)
- Drug + disease cross-links: matched in real time against Drug Landscape's normalised drug + company + condition tables
- Sponsor: as reported to ClinicalTrials.gov by Centre Hospitalier Universitaire, Amiens
- Last refreshed: 17 November 2025
Drug Landscape aggregates and links these public records for informational use only. Always verify against the primary source before clinical or regulatory decisions. Canonical URL: https://druglandscape.com/trial/NCT06373926.
Primary sources · FDA · ClinicalTrials.gov · EMA · SEC EDGAR · ChEMBL · Wikidata · full sourcing