New Therapeutic Strategy Against Preeclampsia

NCT06464159 · Status: RECRUITING · Type: OBSERVATIONAL · Enrollment: 100

Last updated 2026-05-06

No results posted yet for this study

Summary

Preeclampsia is a hypertensive disorder of pregnancy associated with important maternal and perinatal mortality. It complicates 2 to 5% of pregnancies and causes more than 70 000 maternal deaths each year worldwide. Although symptomatic management has improved there is currently no curative treatment, and only childbirth and delivery of the placenta, usually prematurely, alleviate the mother's symptoms. The management of extremely preterm infants is a major societal challenge in medical, ethical and economic terms.

Placental insufficiency plays a central role in the pathophysiology of preeclampsia. Abnormal placentation during the first trimester leads to placental hypoperfusion, which induces trophoblast dysfunction and the release in maternal circulation of trophoblastic factors leading to the maternal symptoms. Among molecules that participate to the pathophysiology of preeclampsia, one of the most important players is soluble fms-like tyrosine kinase 1 (sFlt-1), which is a soluble form of the vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF) receptor. sFlt-1 binds to free VEGF and PlGF in the maternal circulation, thus reducing their bioavailability for their membrane receptors. Targeting the sFlt-1 pathway is one of the most promising strategies for the development of new treatments for preeclampsia. As sFlt-1 results from alternative splicing, its peptide sequence is identical to that of the extracellular part of the membrane receptor. The development of drugs that act specifically on the soluble form and not on the membrane form is therefore particularly complex.

The general objective of this research is to restore the angiogenic balance that maintains the physiological concentrations of free angiogenic factors in order to significantly prolong the pregnancy and diminish the consequences of the great prematurity. The precise objectives of the APHERESE 2 project are:

1. To transpose the proof of concept of the APHERESE1 project to the scale of a real apheresis column
2. To develop an innovative assay technology to determine the global circulating angiogenic balance for each patient

Conditions

Interventions

BIOLOGICAL

Biological collection

A collection of maternal plasma, serum and urine

Sponsors & Collaborators

  • URC-CIC Paris Descartes Necker Cochin

    collaborator OTHER
  • Assistance Publique - Hôpitaux de Paris

    lead OTHER

Principal Investigators

  • Vassilis TSASARIS, MD, PhD · Assistance Publique - Hôpitaux de Paris

  • Edouard LECARPENTIER, MD, PhD · Institut National de la Santé Et de la Recherche Médicale, France

  • Jean GUIBOURDENCHE, MD, PhD · Assistance Publique - Hôpitaux de Paris

Eligibility

Min Age
18 Years
Max Age
50 Years
Sex
FEMALE
Healthy Volunteers
No

Timeline & Regulatory

Start
2026-02-10
Primary Completion
2028-02-29
Completion
2028-11-30

Countries

  • France

Study Locations

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Entities

Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT06464159 on ClinicalTrials.gov