Vision and Mission
We are a pioneering biopharmaceutical company developing novel, effective therapeutics addressing the root cause of Alzheimer’s disease and other neurodegenerative disorders.
Our breakthrough discovery on the gene regulatory function of the key genetic variants has uncovered the “true disease-causing factors” and provided new, unexploited molecular targets for small molecules discovery programs.
The Selonterra Value Proposition
Rooted in human genetics
De-risking translation to humans
Differentiated, competitive advantage
Targeted patient population
Rational selection of trial participants
Small molecule drugs
Patient convenience, Market advantage
Our groundbreaking research addresses the root cause of neurodegenerative diseases.
- Genetic variants cause neurodegeneration
- The DNA change in its genomic environment causes disease
- This in turn changes gene expression nearby
- True disease genes – entirely unexploited targets
Single nucleotide polymorphism
Nucleotide repeat expansion
The Selonterra Platform
Development of orally available, disease modifying therapies
Small molecule discovery program
Identification of molecular route from target to disease
Strong, compelling genetic links to neurodegenerative diseases
Genetic variants control the expression of genes nearby
Those genes are the true disease-causing factors
Our Platform creates a rich Pipeline across Neurodegenerative Disorders
In Vivo POC
- Alzheimer’s Disease (APOE4)
- Parkinson’s Disease (SNCA A53T, LRRK2 G2019S)
- ALS / FTD (C9orf72 Repeat Expansion)
- Alzheimer’s Disease (Familial mutations)
We have developed small molecule modulators of our novel, unexploited, highly druggable target. Our lead compounds restore APOE4-induced gene expression dysfunction and synaptic deficits. We are poised to rapidly move through lead optimization to IND-enabling studies.
Important genetic contributors to Parkinson’s disease are variants of the SNCA and LRRK2 genes. We have identified novel drug targets with dysregulated expression levels in human neurons carrying PD associated gene variants.
We pursue complementary programs for the therapy of ALS caused by nucleotide repeat expansions in C9orf72 and single nucleotide variants in familial AD (APP mutations). Orphan indications offer an additional regulatory protection for a development compound.