GAITHERSBURG, Md. & MUNICH—With an Aug. 21 announcement, the clock began ticking on a five-year strategic research collaboration between AstraZeneca and its global biologics research and development arm, MedImmune, with Ethris GmbH (Ethris), a company with a focus on mRNA-based therapeutics and specific expertise in pulmonary disease.
At the heart of the deal is Ethris’ proprietary mRNA technology, SNIM RNA, which can be targeted to the lungs to assist in replacing, inhibiting or augmenting proteins that play roles in initiating or worsening respiratory disease. The companies aim to develop new stabilized non-immunogenic modified RNA therapies in pulmonological applications
“This collaboration validates Ethris’ leading position in development and delivery of mRNA therapies for the treatment of pulmonary diseases,” said Dr. Carsten Rudolph, president and CEO of Ethris. “This collaboration pairs our proprietary technology with the world-class expertise of AstraZeneca and MedImmune in respiratory diseases, biologics development and commercialization, and positions us to bring forward new options for patients.”
Ethris will give AstraZeneca exclusive access to the SNIM RNA technology through its MedImmune and Innovative Medicines (IMED) biotech units, building on AstraZeneca’s expertise in respiratory diseases and inhaled delivery technologies. The goal is to develop multiple new targets to investigate for treatment of asthma, chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis.
In return, Ethris will receive €25 million up front plus research funding, and it will be eligible for future research and development milestones, including sales-related royalties upon commercialization. AstraZeneca and MedImmune will have the option to take exclusive worldwide licenses upon completion of the research plan for each target within the collaboration.
“Rapid advances over the last decade have made mRNA a very promising tool for clinical application, and we are excited to collaborate with Ethris, whose advanced platform is leading in RNA delivery to the lung,” said Bahija Jallal, executive vice president of MedImmune. “This collaboration complements our respiratory science focused on early intervention and disease modification by adding novel ways to target disease mechanisms that cannot be addressed by other approaches currently in our pipeline.”
In other recent news involving respiratory disease—but also oncology, inflammation and autoimmunity—MedImmune renewed for the second time a collaboration with Inserm Transfert, the private subsidiary of the French National Institute of Health and Medical Research (Inserm), that was first launched in 2011. The new three-year term is intended to build upon key ongoing research in translational biology and new disease mechanisms.
The collaboration has already led to 18 scientific publications in peer-reviewed journals, as well as eight patent applications, including several important advances and publications on immuno-oncology and the tumor microenvironment.
“This alliance is part of our long-term strategic vision, and—leveraging our collaborative relationship with MedImmune—we are excited to continue advancing cutting-edge science from our laboratories,” said Pascale Augé, chairman of the executive management board of Inserm Transfert. "The strength of our projects, where academic and industrial excellence meet, enables us to allow for the best innovation at the highest international standards.”
Furthermore, on the oncology front, MedImmune and Washington University School of Medicine in St. Louis have entered an oncology research and clinical alliance aimed at developing neoantigen vaccines for use in combination with checkpoint inhibitors and other cancer immunotherapy agents. Working collaboratively, the teams will advance both preclinical and clinical research to develop personalized neoantigen vaccines that may be delivered in combination with immunotherapies in MedImmune and AstraZeneca’s oncology portfolio, including durvalumab, a human monoclonal antibody directed against PD-L1, which blocks the interaction of PD-L1 with PD-1 and CD80.
