NCT06330077: MODIF-MS

A Phase 2 Trial Assessing Ifenprodil as a ReMyelinating repurpOsed Drug in Multiple Sclerosis

Not yet recruiting Phase 2 Last updated 18 March 2024

What this trial tests

Phase 2 trial testing Ifenprodil in Multiple Sclerosis in 60 participants. Not yet recruiting.

Timeline

1 March 2024

Primary endpoint
1 March 2027

1 June 2027

Quick facts

Lead sponsor	Assistance Publique - Hôpitaux de Paris
Phase	Phase 2
Status	Not yet recruiting
Study type	INTERVENTIONAL
Allocation	randomized
Design	parallel
Masking	single
Primary purpose	treatment
Enrollment	60
Start date	1 March 2024
Primary completion	1 March 2027
Estimated completion	1 June 2027
Sites	2 locations across France

Drugs / interventions tested

• Ifenprodil — full drug profile →
• Placebo

Conditions studied

• Multiple Sclerosis — all drugs for Multiple Sclerosis →
• Remitting Relapsing Multiple Sclerosis — all drugs for Remitting Relapsing Multiple Sclerosis →

Sponsor

Assistance Publique - Hôpitaux de Paris — full company profile →

Who can join

Adults 18 to 55, any sex, with Multiple Sclerosis or Remitting Relapsing Multiple Sclerosis. Healthy volunteers can join.

What's being measured

Primary outcomes are the specific endpoints the trial is designed to prove or disprove.

• Change in P100 latency according to visual evoked potential.
  Time frame: Between months 6 and months 12
  Assess the efficacy of ifenprodil on the remyelination of the optic nerve measured as the improvement of P100 latency, assessed using full field visual evoked potentials.

Sponsor's own description

Multiple sclerosis (MS) is the most frequently acquired demyelinating disease and the first cause of non-traumatic chronic disability in young adults. Major progress has been achieved in the treatment of MS through the development of therapies targeting the adaptative immune system, which drastically reduce the relapse rate, with various efficiency and safety profiles (Ontaneda, 2015). However, these drugs generally fail to prevent disability worsening along the disease course, and we are now assisting to a shift in therapeutic objectives from the development of new immune drugs towards the identification of therapeutic strategies that could prevent neurodegeneration by promoting myelin regeneration (Stangel, 2017; Stankoff, 2016), in order to prevent neurological disability in MS (Irvine and Blakemore, 2008; Patrikios, 2006; Duncan I, 2017, Bodini, 2016).

Among the first candidate compounds developed to promote remyelination was the anti Lingo1 antibody, which enhance remyelination (Mi, 2009). Medium and large throughput screening of drug libraries subsequently identified several chemical classes of compounds with strong promyelinating properties, such as the antifongic drug miconazole (Najm, 2015) or the muscarinic antagonist clemastine (Wei, 2014). A recent innovative trial has investigated the effect of clemastine, compared to placebo, in a small sample of subjects (25 patients per group) and showed that clemastine could significantly improve the optic nerve conduction speed which reflecting myelin integrity and functionality (Green, 2017).

Our preclinical research has allowed us to identify ifenprodil as a powerful drug to promote myelin repair in vitro and in vivo across species. In parallel our team recently pioneered and optimized a PET imaging approach for quantifying remyelination in the whole brain, that allowed to enhance the sensitivity to detect the myelin repair process, and showed that patients are characterized by heterogeneous profiles of spontaneous remyelination profiles that are closely linked to disability accrual (Bodini, 2016).

Publications & conference data

8 peer-reviewed publications reference this trial (live from Europe PMC):

1. Identifying Biomarkers for Remyelination and Recovery in Multiple Sclerosis: A Measure of Progress.
   Ricigliano VAG, Marenna S, Borrelli S, Camera V, et al · · 2025 · cited 5× · PMID 40002770 · DOI 10.3390/biomedicines13020357
2. Neuroprotective strategies in multiple sclerosis: a status update and emerging paradigms.
   Coclitu CI, Constantinescu CS, Tanasescu R. · · 2025 · cited 4× · PMID 40440559 · DOI 10.1080/14737175.2025.2510405
3. Remyelinating Drugs at a Crossroad: How to Improve Clinical Efficacy and Drug Screenings.
   Al Jaf AIA, Peria S, Fabiano T, Ragnini-Wilson A. · · 2024 · cited 3× · PMID 39195216 · DOI 10.3390/cells13161326
4. Neuro-Immune Crosstalk: Molecular Mechanisms, Biological Functions, Diseases, and Therapeutic Targets.
   Guo X, Liu H, Song YJ, Wang JH, et al · · 2026 · cited 2× · PMID 41583906 · DOI 10.1002/mco2.70497
5. Gene Expression and Alternative Splicing Analysis in a Large-Scale Multiple Sclerosis Study.
   Sak M, Chariker JH, Park JW, Rouchka EC. · · 2024 · cited 2× · PMID 39596026 · DOI 10.3390/ijms252211957
6. Translational molecular imaging and drug development in multiple sclerosis.
   Tay D, Ahmed H, Dawoud A, Salam M, et al · · 2026 · PMID 41356192 · DOI 10.7150/thno.119559
7. Recent Advances in Interventions Targeting Remyelination and a Systematic Review of Remyelinating Effects of Approved Disease-Modifying Treatments for Multiple Sclerosis.
   De Keersmaecker AV, van Doninck E, Wens I, El Ouaamari Y, et al · · 2025 · PMID 41216863 · DOI 10.1111/ene.70397
8. The Road to Remyelination in Multiple Sclerosis: Breakthroughs, Challenges, and Considerations for Future Trial Design.
   Zuroff L, Farkhondeh V, Bove R, Green AJ. · · 2025 · PMID 40956548 · DOI 10.1007/s40265-025-02212-x