Merck Serono, the biopharmaceutical division of Merck, has signed a license agreement has been signed with the Spanish National Cancer Research Centre (CNIO) in Madrid in the area of cancer drug development. The global agreement will build upon CNIO research discoveries to encourage the development and commercialisation of new compounds in the field of oncology. Under the terms of the license agreement, CNIO has granted to Merck exclusive rights to develop and commercialise their new inhibitors of the ataxia telangiectasia and Rad3-related (ATR) kinase.
In exchange, Merck will make an initial payment along with other potential income of up to nearly € 19 million, as well as royalties on net sales. The agreement encompasses the licensing of two series of ATR inhibitors, as well as a screening platform to validate the compounds, which have currently reached an advanced preclinical stage.
“Part of Merck’s commitment to oncology includes the focus on strategic agreements that allow us to foster a constant flow of innovations,” said Andree Blaukat, Head of Translational Innovation Platform Oncology for Merck Serono. “We are convinced that working with like-minded organisations, like the CNIO, will further strengthen our efforts towards finding the next generation of breakthrough therapies.”
“As a research organisation, the CNIO is committed to fostering and promoting innovation. Among other initiatives, the CNIO’s Experimental Therapeutics Program carries out early drug discovery projects. The CNIO is delighted to be working with Merck to hopefully translate this research into potential new treatment options for patients with cancer,” said María Blasco, Director, CNIO. “It is through collaborations with industry oncology leaders that we can bring CNIO discoveries, such as those made by the group led by Oscar Fernández-Capetillo, to patients, and contribute new improved products to the battle against cancer.”
ATR kinase has an important role in the response to DNA damage and in facilitating cell survival. Due to the fact that tumour cells accumulate more DNA damage than healthy cells, blocking ATR kinase activity with selective inhibitors appears to be a strategy worth investigating further for specific tumour types.
EP News Bureau– Mumbai