News + Font Resize -

AC Immune, Biogen enter R&D collaboration in neurodegenerative diseases
Lausanne, Switzerland | Wednesday, April 20, 2016, 09:00 Hrs  [IST]

AC Immune, a leading Swiss-based biopharmaceutical company, announced it has entered into a research and development collaboration with Biogen comprising two radiopharmaceutical diagnostic programmes in neurodegenerative diseases. The companies will further research, develop and clinically validate an alpha-synuclein PET radioligand that will be used as an imaging biomarker for Parkinson’s disease and related synucleinopathies to enable the clinical development of new disease-modifying therapies. In parallel, the partners will pursue a new research programme to identify and develop novel PET radioligands for TDP-43, a recently identified target of growing interest in the pathogenesis of neurodegenerative diseases such as amyotrophic lateral sclerosis (Lou Gehrig’s Disease).

Prof. Andrea Pfeifer, CEO of AC Immune said, “We are very pleased to be working with a global leader such as Biogen in this joint diagnostic collaboration to accelerate the clinical development of novel therapeutics for neurodegenerative diseases where currently no disease modifying treatment is available.”

Martin Velasco, chairman of the Board added, “This new partnership adds to our existing collaborations, further validates our leadership in the science of neurodegeneration and reinforces our goal of revenue generation in the field of diagnostics.”

The collaboration will last for an initial three years and is funded primarily by Biogen. Both companies will share responsibilities for the research and development programme while AC Immune retains intellectual property and commercialisation rights from the collaboration. AC Immune continues to benefit from a 2015 grant from The Michael J. Fox Foundation for the alpha-synuclein PET programme.

“An alpha-synuclein PET tracer is a high priority for the Parkinson’s research field, and a collaborative approach can move us forward faster,” said Jamie Eberling, PhD, director of The Michael J. Fox Foundation Research Programmes.

AC Immune will lead the chemistry and biology research for both the alpha-synuclein PET tracer and the TDP-43 PET tracer program. Biogen will lead the scientific assessment and the radiopharmaceutical development of the AC Immune compounds. The two companies will share the clinical programme design.

Using its proprietary Morphomer chemistry technology platform, designed to interact with the basic process of protein misfolding, AC Immune has identified promising small molecule compounds with good selectivity for alpha-synuclein and suitable properties as neuro-radiopharmaceutical PET ligands. The primary goal of this collaboration with Biogen aims to develop a clinically validated alpha-synuclein PET tracer and generate longitudinal data in Parkinson’s disease patients. Such an alpha-synuclein PET tracer will assist the diagnosis of neurodegenerative diseases with alpha-synuclein pathology earlier and more accurately, and enable the tracking of disease pathology over time alongside symptomatic endpoints. In parallel the partners will seek to identifiy and develop a TDP-43-PET tracer which shall be of significant importance for future therapeutic programs targeting neurodegenerative diseases such as amyotrophic lateral sclerosis.

A brain positron emission tomography (PET) scan is an imaging test of the brain involving an imaging device and an imaging agent called a PET tracer. No alpha-synuclein PET tracer has received regulatory approval for commercial distribution, which represents a huge medical need, not only in Parkinson’s disease but also in other synucleinopathies such as multiple system atrophy and dementia with Lewy bodies. Once the alpha-synuclein PET tracer is introduced to the body, it transiently enters the brain, binds to abnormal alpha-synuclein protein structures (Lewy bodies). Through the radio-tracer on the tracer molecule, the imaging device detects the bound alpha-synuclein imaging agent and creates pictures reflecting the amount and distribution of pathological alpha-synuclein in the brain.

TDP-43 is an interesting new target in the area of neurodegenerative diseases. Misfolded, aggregated TDP-43 protein leads to a broad pathology that occurs in multiple neurodegenerative diseases like Alzheimer’s disease, in particular complementing Tau-related pathology. Pathologic TDP-43 also is the major disease protein in diseases as frontotemporal dementia (FTLD-TDP), amyotrophic lateral sclerosis (ALS), chronic traumatic encephalopathy and Huntington’s disease.

Parkinson’s disease is the second most common neurodegenerative disorder after Alzheimer’s disease. Parkinson’s disease affects approximately one percent of individuals older than 60 years and causes progressive disability (motor and non-motor symptoms). Current therapies only treat the symptoms of Parkinson’s; there is no available treatment that can slow or halt disease progression. The two major neuropathological findings in Parkinson’s disease are loss of dopaminergic neurons of the substantia nigra pars compacta and the presence of Lewy bodies and Lewy neurites in which the major constituent is alpha-synuclein. The abnormal accumulations of fibrillary alpha-synuclein in Lewy bodies, and the mutations in the gene for alpha-synuclein in familial forms of Parkinson's disease, have led to the belief that this protein has a central role in Parkinson’s disease. The development of alpha-synuclein pathology appears to correlate with the loss of dopaminergic neurons and subsequent decline in motor performance, making it a highly relevant molecular target for diagnostic approaches.

Post Your Comment

 

Enquiry Form