OutSee Selected for Discovery Award from Longitude Prize on ALS to Accelerate AI-Based Target Discovery

• Funding to identify novel targets for ALS treatment using OutSee’s ‘genomics first’ target discovery platform, Nomaly
• Provides access to world’s largest and most comprehensive ALS patient dataset
• Part of £7.5M global challenge prize to leverage innovations in AI-based discovery

CAMBRIDGE, England--(BUSINESS WIRE)--OutSee, a genomics and drug discovery company pioneering a unique AI-based predictive genomics approach to target discovery, today announced it has been selected to receive a Discovery Award from the Longitude Prize on ALS. The award grants OutSee access to genomic data from 9,000 amyotrophic lateral sclerosis (ALS) patients, in addition to £100k in funding, supporting a research project to uncover novel therapeutic targets for ALS using OutSee’s proprietary ‘genomics first’ platform, Nomaly.

The Longitude Prize provides access to the world’s largest ALS patient dataset, combining biological information from a large array of global sources, available together for the first time. This includes whole genome sequence data from 9,000 ALS patients, combined with epigenomic, transcriptomic, and proteomic data for over 2,000 cases, and supported by extensive neuroimaging and clinical data. The dataset will help to deepen our understanding of the mechanisms that underpin the disease, and provide new insights into therapeutic targets.

The Discovery Award funding will enable OutSee to initiate a nine-month discovery project, using the Company’s AI-driven platform, Nomaly, to analyse the ALS dataset. In contrast to other approaches, Nomaly uses hypothesis-free, predictive modelling to generate conclusions from the fundamental molecular and cellular biology of the genome, enabling it to predict disease and phenotype ab initio directly from a single genome. Uniquely, this enables Nomaly to uncover new insights from datasets that have been previously analysed using other approaches, or from regions of the genome that are otherwise inaccessible. Once identified, OutSee will work with partners, including Dr Martin Turner’s group at the University of Oxford’s Department of Clinical Neurosciences, to provide disease-specific expertise and advance promising disease targets to the next stage of development.

Inspired by the historic Longitude Act of 1714, the modern Longitude Prize was created to drive innovation in areas of high unmet need, and has supported breakthrough research in areas including antimicrobial resistance and dementia. The Longitude Prize on ALS is a competitive £7.5 million global challenge prize, aiming to leverage recent advances in AI-based discovery to uncover new therapeutic targets and effectively treat ALS – a fatal, progressive neurodegenerative disease that affects around 1 in 300 people throughout their lifetimes. ALS currently has no cure and is increasing in prevalence, with studies estimating cases will rise 25% by 2040 due to an aging global population¹.

Dr Chang Lu, Chief Scientific Officer, OutSee, commented: “We are excited to have been selected for a Discovery Award, which will enable us to access genomic data from ALS patients on an unprecedented scale. We have already built a strong internal pipeline of targets in CNS diseases, and are confident that our breakthrough genomics platform and expertise in AI-driven target identification uniquely place OutSee to unlock new insights into the mechanisms that underpin ALS, and to translate those insights into valuable new therapeutic targets.”

The Longitude Prize on ALS is principally funded by the MND Association and designed and delivered by Challenge Works, home of the Longitude Prize. Additional funders include Nesta, the Alan Davidson Foundation, My Name’5 Doddie Foundation, LifeArc, FightMND, The 10,000 Brains Project, Answer ALS and The Packard Center at Johns Hopkins.

1. Vasta R, Callegaro S, Canosa A, et al. Amyotrophic Lateral Sclerosis Prevalence Projection in 2040: A Less Rare Disease. Ann Clin Transl Neurol. 2026;13(2):379-386. doi:10.1002/acn3.70226