Biotech
CRES101 and CRES102 are novel and specific biotechologies for treatment of neurodegenerative disorders.
Precursor CRES101 (EFG) induces positive response in Experimentals models of Multiple Sclerosis and Chronic Inflammatory Demyelinating Polyneuropathy (CIDP).
Background
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EGF is a human peptide widespread in many tissues and it participates to specific developmental processes
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EGF stimulates oligodendrocyte and Schwann cells differentiation and maturation in vitro, necessary for remyelination
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EGF-driven oligodendrocyte differentiation and maturation are evident after CNS injury
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EGF gene is strongly activated in the repair phase, following demyelination induced by Theiler virus in mice
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EGF mRNA synthesis is significantly increased in the corpus callosum during remyelination, after cuprizone-induced demyelination
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EGF is the effector of the myelinotropic action of cobalamin (Cbl)
- EGF positively regulate myelinotropic PrPC protein synthesis, essential for myelin maintenance
technology
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Most patients with necrotizing enterocolitis have low salivary EGF levels, in line with a decrease in EGF in the spinal cord of multiple sclerosis
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EGF prevents macrophage M1 polarization and promotes M2 polarization in experimental necrotizing enterocolitis
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M2 macrophages polarization drives oligodendrocyte and Schwann cells differentiation during CNS remyelination
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M2 cell polarization is essential for efficient remyelination
- These findings support CRES101 and CRES201 as treatments for neurodegenerative disorders such as Multiple Sclerosis, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) or Guillain-Barre Syndrome (GBS)
Scientific evidence
versus a reference corticoid derived treatment.
(luxol fast blue stained sections of spinal cord).
indications
chronic inflammatory demyelinating polyneuropathy (CIDP) - Orphan disease
From a pathological and clinical standpoint, CIDP has numerous analogies with MS: progressive and relapsing forms of CIDP are also observed.
Guillain Barré Syndrome (GBS) - orphan disease
GBS is an acute form of CIDP and an immune condition, often following an infection.
Nerve lesions marked by demyelination are the pathological hallmarks.
Multiple Sclerosis progressive forms (ms) - rare disease
Myelin continually degrades leading to axon degeneration and neuronal death.
Neurodegeneration is responsible for the chronic disability and progression of MS.
Current treatments for MS rely on immunosuppression with little action, if not on neuroprotection: progressive forms are hardly treated.
Alzheimer disease
Alzheimer’s is a neurodegenerative disease in which protein deposits form amyloid plaques and tau tangles in the brain: neurons stop functioning, lose connections and die; the brain shrinks dramatically.
The disease begins with memory impairment; evolution progressively leads to communication problems, addiction and eventually death.
There is no disease-modifying treatment. Only symptomatic treatments somehow delay progression.
pipeline
