Roche gains rights to preclinical-stage neurotoxicity-targeting products.
Roche is teaming up with Belgian firm reMynd to develop the latter’s preclinical-stage small molecule drug candidates targeting the α-synuclein and tau-related toxicities involved in Parkinson and Alzheimer diseases. reMynd claims the deal could be worth up to Euro 500,000 (about $636,000) in milestone payments from Roche, even before sales royalties.
The collaboration will involve the two firms establishing joint research teams, with Roche providing chemistry, lead-optimization, and preclinical development expertise, and reMynd carrying out nonclinical pharmacology studies and further research to unpick the underlying molecular mechanisms. Roche will take on all clinical development and worldwide commercialization of relevant products.
ReMynd claims its candidates are designed to inhibit the mechanisms of neurotoxicity involved in both these diseases, rather than just address the resulting symptoms. “Our most advanced compound in Parkinson’s disease has demonstrated full inhibition of disease progression in preclinical models and could be the first treatment in clinical development for Parkinson’s disease targeting α-synuclein-induced toxicity,” claims Gerard Griffioen, reMynd’s CSO. “Our Alzheimer’s tau program represents perhaps a greater potential as it addresses one of the most fundamental aspects of the disease,” adds Koen De Wite.
ReMynd is centered on the development of disease-modifying treatments against protein misfolding disorders, with a particular focus on Parkinson and Alzheimer diseases. The firm is exploiting its expertise both through the development of an in-house drug pipeline and through the provision of contract research services for evaluating the in vivo efficacy of experimental Alzheimer treatments using validated transgenic mouse models.
ReMynd’s preclinical pipeline includes four Alzheimer disease candidates that target tau toxicity, two Parkinson disease candidates against α-synuclein toxicity, and two type 2 diabetes candidates designed to counteract islet amyloid polypeptide toxicity.