Treventis Partners its Preclinical Program in Alzheimer’s Disease with Takeda

Treventis Corporation, a privately held biotechnology company, announced today that it has entered an option, collaboration, and license agreement with Takeda for the further research, development, and commercialization of small molecules that target tau, a key protein in Alzheimer’s Disease (AD). This therapeutic strategy aims to markedly reduce tau misfolding and is a potential disease-modifying mechanism in AD as well as in other tauopathies.

Under the terms of the agreement, Takeda will have an option to exclusively license the program worldwide for the development and commercialization of the tau program. Subject to the terms of the agreement, Treventis will receive research funding as well as an upfront payment, option exercise and future clinical and commercial milestones of up to $372.5 million if all milestones are achieved over the course of the partnership plus tiered royalties on potential net sales of any commercial product resulting from the license.

“We are very excited to work with Takeda to progress new therapies for neurodegenerative diseases,” said Christopher Barden, CEO of Treventis. “We believe that the Treventis tau program synergizes well with Takeda’s significant expertise and commercial reach in central nervous system drug development. This partnership is a validating milestone for our Common Conformational Morphology platform as well as a major potential step forward in Alzheimer’s Disease therapeutics.”

Targeting tau using a small molecule has proven difficult because it is an “intrinsically disordered protein”, a class of proteins that have many conformations and resist attempts to experimentally document their three-dimensional structure. Treventis scientists have developed a methodology for targeting misfolding proteins using epitope commonality between multiple misfolded proteins. This information was used to create Common Conformational Morphology (CCM), a patented Treventis methodology for constructing models of the earliest stages of protein misfolding. CCM in silico prediction, coupled with special assays to evaluate speed of misfolding, allows for the identification and optimization of potent, drug-like compounds against targets such as tau.