Address
1 Avenue d'Ester - 87280 LIMOGES
Email
info@curlim.eu
Revolutionizing Neuropathy Treatment
Through Cutting-Edge Nanodrug Innovation
- About Curlim
Driven by unmet medical needs.
Empowered by breakthrough science.
Founded in 2024 as a spin-off from the University of Limoges, Curlim brings together three PhD scientists and a C-level Business person to tackle one of the biggest unmet needs in neurology: effective treatment for hereditary peripheral neuropathies.
Our first mission: to develop a breakthrough therapy for Charcot-Marie-Tooth disease type 1A (CMT1A) — the most common hereditary neuropathy.
CLM001
A Breakthrough Nanodrug Targeting the Root Causes of CMT1A
CLM001 is intended for the treatment of Charcot-Marie-Tooth disease type 1A(CMT1A), the most common inherited peripheral neuropathy, caused by progressive demyelination and axonal damage. Over time, it leads to muscle weakness, sensory loss, and impaired motor coordination.
- Our technology
Developed through nanotechnology, CLM001 is an innovative and efficient drug assembled from three components that work together to ensure optimal protection, delivery, and action.
Our technology offers multiple synergistic benefits :
- Solubilization and protection of the API (Active Pharmaceutical Ingredient)
- Extended bioavailability
- Targeted action on key pathological mechanisms of CMT1A : oxidative stress, endoplasmic reticulum stress, and inflammation
This next-generation nanodrug not only improves the API’s stability and absorption, but also ensures it reaches the target cells and acts directly on the root causes of the disease.
BIOAVAILABILITY
Measured blood concentration of curcumin (ng/mL) over time. CLM001 provides sustained release compared to free API
- Proof of concept
Increase in motor nerve conduction
0
%
On the most severely affected models
0
%
Comparison between a healthy myelinated nerve fiber (left) and a demyelinated nerve fiber in CMT1A (right).
Healthy myelin
Ensures rapid and efficient signal transmission.
Demyelinated nerve
Signal conduction is slowed or disrupted due to damaged myelin.
CLM001 has demonstrated robust and multi-dimensional therapeutic effects across 3 preclinical studies in animal models of CMT1A.
The treatment resulted in a 120% increase in motor nerve conduction, improved coordination, and clear biological impacts on oxidative stress, inflammation, and remyelination — all without observed toxicity.
Notably, the most severely affected models showed the greatest functional recovery, with conduction speed increasing by up to 218%.
With no treatment currently available for CMT1A, these conclusive findings represent a major breakthrough — and a clear path toward full clinical development and human trials.
- Our partners
