US-based Neuropore Therapies has signed an agreement with Belgian biopharmaceutical firm UCB to develop and commercialise therapeutic products to slow progression of Parkinson’s disease (PD) and related disorders.
The deal includes the development of Neuropore’s small molecule, NPT200-11, which targets pathogenic alpha-synuclein.
NPT200-11 is said to block pathological protein misfolding, aggregation and deposition that contribute to synaptic dysfunction and cell death in PD and related disorders.
It is currently in preclinical development, while the clinical Phase I trial is expected to begin in 2015.
UCB new medicines president Ismail Kola said: "Parkinson’s disease is a debilitating neurodegenerative disorder that results in disruption of normal movement and motor function, as well as cognitive and other life-altering symptoms."
Under the agreement, Neuropore will secure an initial upfront payment of $20m, and is also eligible to receive a potential total of $460m, based on development, regulatory and sales-based milestones payments, in addition to royalties on net sales.
UCB will be eligible to receive the worldwide exclusive license to develop and commercialise NPT200-11 in all indications.
Both firms will work together to complete non-clinical trials and a first Phase I trial, which is expected to commence later this year.
Under the deal, UCB will also take responsibility for all further clinical development, regulatory activities and commercialisation.
Neuropore Therapies CEO Dieter Meier said: "By working together we wish to accelerate the development of new treatments that can halt or slow the progression of Parkinson’s disease and other neurodegenerative diseases for patients who suffer from such debilitating conditions.
"UCB’s commitment and expertise in this field offers the best opportunity to collaboratively develop orally available small molecules to treat diseases that affect large patient populations and possibly certain orphan diseases."
Image: Histological sample of Substantia nigra in Parkinson’s disease. Photo: courtesy of Werner CJ, Heyny-von Haussen R, Mall G, Wolf S.