Summary
Karim Ghoufiri
Business developper
Technology
- COUM’ACTIV2 introduces a paradigm shift: rather than preventing only aggregation, it aims to actively eliminate pathological alpha-synuclein aggregates by selective activation of KLK6 (neurosin), a naturally occurring serine protease in the central nervous system. In synucleinopathies, KLK6 activity is reduced, impairing the brain’s natural clearance mechanisms. Targeted pharmacological activation of KLK6 restores this clearance pathway.
Market
- Synucleinopathies are a group of severe neurodegenerative diseases characterized by the pathological aggregation of alpha-synuclein, including Parkinson’s disease (PD), Dementia with Lewy Bodies (DLB), and Multiple System Atrophy (MSA)
- Parkinson’s disease is the second most prevalent neurodegenerative disorder worldwide, with incidence increasing due to population ageing and environmental risk factors
- All available treatments are symptomatic only
Development status
In vitro proof of concept
Why is this approach revolutionary?
- KLK6 activity increases to about 300% of the baseline level (3× activation)
- Other proteases (KLK1, KLK5, KLK8, KLK13, KLK14, Plasmin) show minimal or no activation, demonstrating high selectivity
- Highly potent and well-tolerated neuroprotective effects
- No toxicity observed at the tested concentrations
IP
- Patent application filed
Valorisation strategy
- SATT Lutech offers a co-development strategy by combining its support in resources and IP management with the partner’s R&D expertise, or through a direct licensing agreement to integrate innovations into their portfolio.