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20-F
AC IMMUNE SA filed this Form 20-F on 03/21/2019
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These applications of alpha-synuclein PET imaging agents have the potential to fundamentally change the approach of treating PD and other similar diseases and we are planning to conduct a first-in-human study in H1 2019 with our most advanced lead molecule.

 

The PD market size is estimated to grow from USD 3.6 billion in 2012 to approximately USD 5.3 billion in 2022.

 

To complement our pipeline of PET imaging tracers, we selected Tar DNA-binding Protein (TDP-43) as a third target. TDP-43 in its physiological function is a protein participating in nucleic acid transport. As Abeta, Tau and alpha-synuclein, TDP-43 misfolds in TDP-43 proteinopathies into insoluble, beta-sheet rich aggregates in the cytoplasm of neurons leading to cellular dysfunction and eventually clinical symptoms. TDP-43 pathology often appears in other neurodegenerative diseases (e.g. AD) as a part of mixed pathologies and it has been proposed that misfolded TDP-43 contributes to the observed clinical phenotype in addition to the primary pathology. The precise molecular diagnosis and differentiation of early stages of such diseases is of critical importance.

 

There are no imaging products in the market today targeting TDP-43. This provides us with a unique opportunity to become the first company providing TDP-43-PET imaging to the market. We believe the ability to image TDP-43 deposits in the brain will enable:

 

·The diagnosis of primary TDP-43 proteinopathies such as FTD-TDP-43, AD and ALS and separation from other proteinopathies for targeted, early therapeutic intervention;

 

·The use of TDP-43 quantification as a biomarker in TDP-43 proteinopathies in clinical studies of novel therapeutic regimens designed to slow or halt disease progression; and

 

·The direct diagnosis of TDP-43 co-pathologies in other neurodegenerative diseases for patient segmentation.

 

The application of TDP-43 imaging agents has the potential to fundamentally change the approach of treating primary and secondary TDP-43 based proteinopathies to provide the best outcome for patients.

 

License Agreements and Collaborations

 

Our SupraAntigen and Morphomer platforms have generated large numbers of clinical assets that address diseases related to protein misfolding, such as AD, PD and Down syndrome. Select key assets in the product pipeline have been licensed for upfront payments, milestones and royalties to help offset the cost of our research and internal product development. Discussions with other companies are ongoing. We have signed a number of licensing agreements with leading pharmaceutical companies to assist and accelerate the development of our product pipeline, including:

 

·A worldwide licensing agreement with Genentech signed in November 2006 (and amended in May 2015) for crenezumab for AD, under which we may become eligible to receive payments potentially greater than USD 340 (CHF 339) million, excluding royalties.

 

·A worldwide licensing agreement with Genentech signed in June 2012 for anti-Tau antibodies for AD, under which we may become eligible to receive payments potentially greater than CHF 400 million, excluding royalties.

 

·A worldwide licensing agreement with Janssen signed in December 2014 (and amended in April 2016 and July 2017) for therapeutic anti-Tau vaccines for AD, and potentially other Tauopathies, under which we may become eligible to receive payments totaling up to CHF 500 million, excluding royalties.

 

·A worldwide licensing and collaboration agreement (“LCA”) with Life Molecular Imaging SA (formerly Piramal Imaging SA) signed in May 2014 for small molecule Tau ligands for use as PET tracers under which we may become eligible to receive payments totaling up to EUR 157 (CHF 179) million, excluding royalties.

 

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