Servier and Treventis Teaming Up to Develop Therapies That Can Circumvent Protein Misfolding

Servier and Treventis will work together on therapies that can circumvent the misfolded proteins involved in Alzheimer’s and other neurodegenerative diseases.

The goal is to develop compounds that prevent the brain’s accumulation of two faulty proteins associated with the disorders — amyloid beta and tau.

Servier is an international pharmaceutical concern led by a non-profit foundation based in France. Treventis is a U.S. company that specializes in developing small molecules that can circumvent the misfolded proteins in the harmful versions of tau and amyloid beta.

Under their agreement, Servier will cover the research costs and have worldwide rights to commercialize any compounds the partners develop.

“We very much hope that this new collaboration will allow us to answer the huge unmet patient need for disease-modifying treatment of Alzheimer’s disease, thanks to Treventis’ unique and innovative technology,” Christian de Bodinat, director of Servier’s Center of Therapeutic Innovation in Neuropsychiatry, said in a press release. “We are very excited to be part of one of the first programs employing a dual approach in this field.”

Developing small molecules that can prevent the production of faulty versions of both tau and amyloid beta is a major challenge because the two proteins misfold in different ways.Treventis scientists are dealing with the challenge by zeroing in on a binding site that the proteins have in common.

“We are very excited to work with Servier to progress new therapies for neurodegenerative diseases,” said L. William McIntosh, the chairman of Traventis’ board. “We believe that the combination of Treventis’ innovative platforms and technologies with Servier’s deep expertise in central nervous system drug development has significant potential to rapidly advance new treatments for patients in need.”

Last year, for the first time ever, researchers were able to track how tau spreads in Alzheimer’s patients’ brains. Their discovery suggested that memory problems stem from tau accumulation. At the same time, the team discovered that changes in brain glucose metabolism, rather than tau, is what appears to cause a decline in overall cognition.

The study, “Longitudinal changes of tau PET imaging in relation to hypometabolism in prodromal and Alzheimer’s disease dementia,” appeared in the journal Molecular Psychiatry.

A study in 2016 had shown that the plasma levels of two types of amybloid beta peptides affect cognitive function and brain volume, both of which are diminished in Alzheimer’s. The findings suggested that blood plasma levels of the peptides, which are an easy to collect, are a good way to predict the risk of someone developing the disease.

The study, “The Relationship Between Plasma Aβ Levels, Cognitive Function and Brain Volumetrics: Sydney Memory and Ageing Study,” was published in Current Alzheimer Research.