Thryv Therapeutics licences a new class of SGK1 inhibitors from Spain’s CSIC and Universidad Autónoma de Madrid, extending its platform into neurodegenerative disease

Thryv Therapeutics has entered into an exclusive, worldwide, royalty-bearing patent and know-how license agreement with the Spanish National Research Council (Consejo Superior de Investigaciones Científicas, the Autonomous University of Madrid (Universidad Autónoma de Madrid) and Fundación de la Universidad Autónoma de Madrid).

The agreement became effective on 1 July 2026. 

Thryv holds rights across all fields of use and in all territories, with the right to sublicense.

Thryv’s existing clinical SGK1 inhibitor candidates were built through independent medicinal chemistry on a single in-licensed scaffold, supported by a library of more than 500 synthesised analogues and a granted selection patent estate.

The CSIC/UAM series is a distinct chemotype arising from an entirely separate discovery programme, a genuinely new starting point rather than an extension of the existing series. Adding a second independent series gives Thryv the ability to match chemistry to indication, continuing to optimize its current molecules for cardiac and cardiometabolic diseases while developing compounds designed from the outset to reach the brain.

The licenced invention was developed by research groups with complementary expertise directly relevant to that ambition: the medicinal chemistry group led by Dr Ana Martínez and Dr Carmen Gil and the cardiovascular group led by Dr Eduardo Oliver Pérez at CSIC’s Centro de Investigaciones Biológicas Margarita Salas, together with the neurobiology group led by Dr Isabel Lastres-Becker at UAM’s Institute for Biomedical Research and the vascular pharmacology group led by Dr Ana Briones Alonso at UAM’s Department of Pharmacology.

Activated SGK1 sits at the intersection of several pathways central to neurodegeneration. Published work has implicated the kinase in tau phosphorylation, in the handling of misfolded and aggregating proteins, in neuroinflammatory signalling, and in FOXO- and NRF2-dependent cellular stress responses. This disease biology is directly relevant to Parkinson’s disease, Alzheimer’s disease and related tauopathies.