Neuroregenerative peptide treatment for multiple sclerosis

Informacje na temat projektu

REGENERA MS

Identyfikator umowy o grant: 101158120

DOI

10.3030/101158120

Projekt został zamknięty

Data podpisania przez KE 12 Lutego 2024

Data rozpoczęcia 1 Lipca 2024

Data zakończenia 31 Grudnia 2025

Finansowanie w ramach

• European Research Council (ERC)

Koszt całkowity

Brak danych

Wkład UE

€ 150 000,00

Koordynowany przez

HELSINGIN YLIOPISTO
Finland

Periodic Reporting for period 1 - REGENERA MS (Neuroregenerative peptide treatment for multiple sclerosis)

Okres sprawozdawczy: 2024-07-01 do 2025-12-31

Podsumowanie kontekstu i ogólnych celów projektu

Multiple sclerosis (MS) is a chronic inflammatory, autoimmune, and neurological disease without a cure, affecting the lives of 1.2M Europeans and causing significant economic costs to patients and society. MS primarily affects young adults aged 20-30 and is characterized by demyelination and neuronal death, where the immune system mistakenly targets the protective myelin covering of nerve fibers. This results in neurological impairments such as tremors, stiffness, and bladder problems, significantly impacting patients’ daily lives, independence, mobility, and social interactions.

In the REGENERA MS project the technical and commercial potential of MANF fragment a groundbreaking therapy with neurorestorative potential for the treatment of multiple sclerosis (MS) was investigated
We validated the effect of MANF fragment in in vitro (Olineu cells, in vitro OPC cultures) and in vivo models of MS (EAE and LPC mouse models) and studied the IP strategy and business development including market research and engagement with industry.

Prace wykonane od początku projektu do końca okresu sprawozdawczego oraz najważniejsze dotychczasowe rezultaty

We were able to show that MANF fragment induced remyelination, improves motor coordintion and reduce symptoms in an animal model of MS. In more detailed,
we were able to show that C-MANF suppresses neuroinflammatory activation and facilitates the recovery of
oligodendrocytes after demyelination, while reducing long-term activation of the UPR. Furthermore, we showed that
C-MANF enhances myelination of primary OPCs in culture, that promotion of remyelination in cerebellar organotypic slice
cultures is dependent on UPR-modulation, and that exogenously applied C-MANF suppresses chronic activation of all
three UPR pathways in oligodendroglia. Finally, we showed that demyelination in MANF-deficient brains (analyzing MANF knock out mice)
leads to extensive neuroinflammation and CNS degeneration, implicating UPRmodulation by MANF as a key component in tissue responses
to demyelination. Altogether, we show that UPR modulation with C-MANF is a promising new therapeutic approach for
treating neuroinflammatory demyelination.

Regarding the business developent activities, during the REGENERA MS proect, we were able to file a new patent application, conduct a market study and make a thorough research on competitors in the MS market.

Innowacyjność oraz oczekiwany potencjalny wpływ (w tym dotychczasowe znaczenie społeczno-gospodarcze i szersze implikacje społeczne projektu)

As summary, C-terminal fragment of MANF (studied in the Regenera MS project)
significantly improved clinical recovery in EAE mice via improved remyelination and
suppression of neuroinflammation in the CNS. We also showed that
endogenous MANF is a key player in restoring tissue homeostasis
following demyelination. This is a result of a novel form of UPR
modulation, and presents a new therapeutic avenue for treating diseases featuring autoimmune demyelination, such as MS.
Based on these results we can say that MANF fragment has clear potential in the treatment of MS.
As there are no MS drugs that can induce remyelination, MANF fragment also has high commercial potential.