The TAK1 mechanism is a central biological switch for several central inflammatory processes. By dampening its activity, there is potential to block and delay progression in severe and chronic diseases. The target has been identified as a key mechanism by academia and industry, and there is widespread interest in its potential in a number of indications.

 

Aqilion's internal drug development has led to unique small molecule inhibitors and the collaboration with Merck KGaA further added new molecular assets. The new project strategy for the TAK1 program is based on proprietary data in combination with data and knowledge generated in collaboration with Merck KGaA during 2023 -2024.

 

Sarah Fredriksson, CEO of Aqilion, comments:

“We are pleased and excited to continue our preclinical TAK1 program, since it is a highly interesting drug target in several chronic inflammation and autoimmune diseases. The analysis of all data, generated internally and externally, encouraged us to resume the development. We are looking forward to presenting the program during partnering meetings later this year.”
 

About TAK1

TAK1 (Transforming growth factor-β-activated kinase 1) is a ”master regulator” of both     NF-κB and JNK signaling. It is a key kinase in innate immunity that integrates and controls signaling and production of key pathological cytokines. TAK1 integrates clinically and genetically validated pathways in human disease. Aqilion has discovered highly selective and potent TAK1 inhibitors with excellent drug-like properties within a unique chemical space.

Kinases are a very succesful drug target class. Immune kinases including, JAK1, JAK2, JAK3, TYK2 and BTK have shown clinical effects in many autoimmune and and inflammatory diseases. However, innate immunity kinase targets that are hypothesized to affect e.g. NF-kB or JNK signaling have failed to provide sufficient or sustained efficacy. These include p38⍺, SYK, TPL2 and IRAK4. Due to the central upstream node function of TAK1, inhibiting this kinase has the potential to provide a higher degree of efficacy by modulating the key cytokines IL-1β, IL-6 and TNF⍺.

About the collaboration with Merck KGaA

The TAK1 program began in the fall of 2019 and in early 2023, Aqilion signed a pre-clinical licensing- and collaboration deal with Merck KGaA Darmstadt, Germany (10 M€ upfront and 950 M€ in potential milestones) to discover, develop and commercialize small-molecule inhibitors of TAK1. June 20, 2024 Aqilion announced that Aqilion and Merck have decided to terminate the joint development of the TAK1 program. Data generated in the course of the collaboration have altered the risk-benefit profile within the intended indications. Merck has returned all rights according to the licensing and collaboration agreement.

For further information, please contact:
Sarah Fredriksson, CEO, AQILION AB, + 46 (0)70 261 4575, sarah.fredriksson@aqilion.com