QurAlis Corp. has entered into an exclusive license agreement with Eli Lilly and Co. in which QurAlis is granting Lilly global rights to develop and commercialize QRL-204, a potentially best-in-class splice-switching antisense oligonucleotide (ASO) designed to restore UNC13A function in amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and other neurodegenerative diseases.
 
Under the agreement, QurAlis granted Lilly an exclusive, worldwide license to develop and commercialize QRL-204 and other UNC13A-targeting compounds in exchange for an upfront payment of $45 million to QurAlis, plus an additional equity investment. QurAlis is also eligible for future milestone payments of up to $577 million and royalties on sales.
 
The agreement includes a R&D collaboration to identify and develop additional candidates targeting UNC13A, leveraging QurAlis’ FlexASO Splice Modulator Platform. The QurAlis FlexASO Splice Modulator Platform was developed to generate splice-switching ASOs with improved potency and increased therapeutic index. QurAlis’ ASOs correct UNC13A mis-splicing, restore UNC13A protein production and reduce cryptic exons that may contribute to disease progression.
 
“We are determined at Lilly to uncover the next great idea, the next collaboration, the next advancement in technology that will drive us toward meaningful treatments for ALS and FTD patients. It’s all for one reason – to make life better for even more people,” said Andrew Adams, senior vice president, neurodegeneration research, and director, Lilly Institute for Genetic Medicine. “Genetic precision medicines like QRL-204 that target specific causal components of disease pathology hold great promise for delivering meaningful advances against a range of neurodegenerative diseases like ALS and FTD.”
 
Kasper Roet, chief executive officer and co-founder of QurAlis, said, “At QurAlis, we are driven to explore the deepest aspects of human neurology to find the treatments patients urgently need. This partnership enables QRL-204 to rapidly move toward the clinic, while we continue to advance our other lead programs. We look forward to combining our complementary strengths to uncover additional candidates that target UNC13A that have the potential to transform the treatment of neurodegenerative diseases like ALS and FTD and beyond.”