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Parkinson’s Disease: AC Immune Receives a Grant from The Michael J. Fox Foundation

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A new USD 0.5 million grant brings up to USD 3.7 million the total amount The Michael J. Fox Foundation awarded the Swiss company.

AC Immune SA, a Lausanne-based clinical-stage biopharmaceutical company pioneering precision medicine for neurodegenerative diseases, today announced that The Michael J. Fox Foundation for Parkinson’s Research (MJFF) awarded the Company a new grant to continue development of its Morphomer®-based alpha-synuclein (a-syn) positron emission tomography (PET) tracer, ACI-12589.

AC Immune has received continuous grant support from MJFF since 2015 to develop a-syn PET tracers. This new grant brings the total MJFF funding for this program up to USD 3.7 million. If successful, AC Immune’s a-syn PET tracer program could deliver the world’s first imaging agent capable of accurately detecting and monitoring progression of Parkinson’s disease (PD). This would potentially enable and accelerate the development of novel PD therapies by providing a powerful tool for measuring the effect of novel drugs on a-syn pathology in the brain.

Earlier this year, AC Immune and its collaborators reported clinical proof-of-concept data on ACI-12589, with the PET tracer generating the first live images of a-syn in the human brain. PET images from multiple system atrophy (MSA) patients dosed with ACI-12589 showed enhanced contrast and a-syn target specificity, as well as increased tracer retention in brain areas affected by MSA disease processes. ACI-12589 also displayed pharmacokinetic and safety profiles suitable for further development as a human brain PET imaging agent.

AC Immune’s portfolio in PD covers the full spectrum of treatment modalities addressing a-syn, a well-characterized target in PD. In addition to ACI-12589, the portfolio includes the Phase 2 ready anti-a-syn vaccine, ACI-7104, as well as an anti-a-syn antibody and a Morphomer® a-syn aggregation inhibitor, both in pre-clinical development. Together, these assets have the potential to enable a precision medicine approach to treating PD and other a-synucleinopathies, detecting the disease early and treating the right patient, with the most appropriate treatment modality, at the most effective time.

Prof. Andrea Pfeifer, CEO of AC Immune SA, commented: “We are delighted to receive this additional grant from MJFF and further expand our long-standing and highly productive relationship. The grant recognizes the exciting potential of ACI-12589 to play a key role in developing precision medicines to treat PD and other neurodegenerative diseases. Imaging agents, capable of earlier detection and disease monitoring, are a vital element in effective treatment of these conditions. The data generated so far demonstrate ACI-12589’s potential to be the first non-invasive diagnostic for alpha-synucleinopathies and underline the productivity of AC Immune’s proprietary small molecule Morphomer® discovery platform.”

Jamie Eberling, PhD, Senior Vice President of Research Programs at MJFF, said: “The Foundation is pleased to continue its support of the development of AC Immune’s a-syn PET tracer, ACI-12589. The clinical results reported to date hold promise that a key element in the diagnosis of a-synucleinopathies like PD and other neurodegenerative diseases is now within reach.”

The USD 0.5 million provided by the new MJFF award will support ACI-12589 dosimetry studies in healthy individuals and GMP manufacturing, thus paving the way for expanded clinical development in-house and with third parties. The grant will also support ACI-12589 PET scans in additional human subjects to further evaluate disease and target specificity, with the aim of assessing potential PET signal retention in a-syn-positive PD/dementia with Lewy Body (DLB) subjects versus expected a-syn-negative Alzheimer’s disease (AD), progressive supranuclear palsy (PSP) and spinocerebellar ataxia (SCA) subjects.

AC Immune also received MJFF grants for the development of first-in-class brain penetrant small molecules targeting a-syn and the (NOD)-like receptor protein 3 (NLRP3) inflammasome pathway in PD.