Probiodrug AG, a biopharmaceutical company developing novel therapeutic solutions to treat Alzheimer’s disease (AD), has inked an agreement to license the TBA2.1 mouse to QPS Austria Neuropharmacology, a leading CRO for CNS drug development.

This mouse model has been developed, characterised and patented by Probiodrug. It has been used within the efforts to establish a new therapeutic concept of reducing brain pyroglutamate-modified Abeta (pGlu-Abeta) for the treatment of Alzheimer disease. Licensing this model to QPS Austria Neuropharmacology makes it accessible to a wider community of academic and industry research groups.

Commenting on the announcement, Hans-Ulrich Demuth, co-founder and former CSO of Probiodrug, said, “Characterisation and use of this model has been extremely useful for our understanding of the involvement of pGlu-Abeta in the initiation and progression of AD. This model is only one of a set of new AD-like models developed by Probiodrug to establish a comprehensive validation of pGlu-Abeta as a potential target to treat Alzheimer’s disease and to extensively profile potential drug candidates. I’m very pleased about the collaboration of Probiodrug with QPS to thereby offer our TBA2.1 mouse model to the wider AD and neurodegeneration research.”

Birgit Hutter-Paier, director-neuropharmacology at QPS Austria added, “We are optimistic about this model being perfectly complementary to QPS’ current range of animal models for AD drug research. Transgenic animals are still among the most crucial tools to investigate drug candidates for the treatment of AD. The TBA2.1 mouse model will be a valuable addition to our portfolio of mouse models addressing the increasingly multifaceted APP pathology, which still has a prominent and highly relevant position in the field.”

As of today, Probiodrug has progressed two complementary strategies for tackling pGlu-Abeta with two medicine candidates in development: PQ912, a small molecule inhibitor of Glutaminyl Cyclase, now in phase 2, and PBD C06, a pGlu-Abeta-specific mAB in preclinical stage.

The TBA2.1 transgenic mouse model over-expresses pGlu-Abeta in neurons and is suitable to model neuronal loss and neurodegeneration, characteristics typical for disease progression. These mice represent the most rapid murine model of Abeta induced cognitive impairment, demonstrating the highly toxic nature of pGlu-Abeta.

Selective hippocampal neurodegeneration in transgenic mice expressing small amounts of truncated Aß is induced by pyroglutamate-Aß formation.