Exelixis has entered into an exclusive collaboration and license agreement with StemSynergy Therapeutics for the discovery and development of novel oncology compounds targeting Casein Kinase 1 alpha (CK1α), a component of the Wnt signaling pathway implicated in key oncogenic processes. The agreement is part of Exelixis’ ongoing strategy beyond its two internally-discovered, commercially available compounds, cabozantinib and cobimetinib.
Under the terms of the agreement, Exelixis will partner with StemSynergy to conduct preclinical and clinical studies with compounds from StemSynergy’s CK1α Activator Program. Exelixis will pay StemSynergy an upfront payment of $3M and up to $3.5M in initial research and development funding. StemSynergy will be eligible for a variety of milestones for the first product to emerge from the collaboration, including preclinical and clinical development and regulatory milestone payments, commercial milestones, as well as single-digit royalties on worldwide sales. Exelixis will be solely responsible for the commercialization of products that arise from the collaboration.
“Supported by revenues from its commercial products and collaborations, Exelixis is on a growth trajectory and now actively focused on augmenting our pipeline both through targeted business development and internal drug discovery activities,” said Peter Lamb, Ph.D., Executive Vice President, Discovery Research and Chief Scientific Officer of Exelixis. “CK1α activation is an underexplored and intriguing mechanism for addressing the Wnt/β-catenin axis, a major pathway deregulated in multiple cancers. We look forward to working with StemSynergy to advance this compelling program as we build the next generation of Exelixis medicines.”
The CK1α Activator Program is representative of StemSynergy’s focus on treating cancer by targeting developmental processes that are reactivated in cancer cells. The Wnt signaling pathway is a prominent example of this process: the pathway plays an important role in embryonic development, but can support oncogenic processes when deregulated in adult tissues. Activation of β-catenin, a key downstream component of the pathway, is increased in multiple tumors, including a majority of colorectal cancers, where mutations in the APC gene that result in beta-catenin stabilization are prevalent. CK1α Activator Program compounds have been shown to induce degradation of β-catenin and pygopus, another member of the pathway, in preclinical CRC models, and to inhibit the growth of tumors. Importantly, their GI-sparing qualities may help overcome limitations of other approaches targeting the Wnt pathway.