Greywolf and Genomics partner to develop first-in-class ERAP autoimmune disease treatments

UK-based Greywolf Therapeutics and Genomics have announced a strategic research collaboration to apply large-scale human genetic data to the development of ERAP autoimmune disease treatments, with Genomics deploying its proprietary genotype-phenotype platform to validate ERAP1 and ERAP2 as therapeutic targets across multiple autoimmune indications and guide Greywolf’s pipeline expansion strategy.

Under the agreement, Genomics will curate and analyze multiple independent genetic association studies drawn from what the company describes as the world’s largest harmonized genotype-phenotype data resource, with the objective of identifying which specific ERAP1 ERAP2 genetic variants drive disease susceptibility across conditions including inflammatory bowel disease, ankylosing spondylitis, and psoriasis. The resulting insights will inform Greywolf’s indication selection and patient stratification strategy for its ERAP-targeting small molecule pipeline, with GRWD0715 currently progressing in a Phase I/II trial in axial spondyloarthritis. Financial terms were not disclosed.

Greywolf’s development program centers on antigen modulation — specifically the control of T cell activation through modulation of antigen presentation via the MHC class I pathway. ERAP1 and ERAP2 are aminopeptidases responsible for trimming peptides prior to loading onto MHC class I molecules; genetic variants in both enzymes alter the antigenic peptide repertoire presented to the immune system, and have been shown through genome-wide association studies to increase susceptibility to a range of autoimmune conditions. Greywolf’s first-in-class autoimmune treatment approach targets this mechanism directly, with GRWD0715 designed to correct aberrant antigen presentation rather than broadly suppress immune function.

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The collaboration addresses a specific technical challenge in ERAP-focused immunotherapy drug development: ERAP1 and ERAP2 are highly polymorphic, with multiple functionally distinct haplotypes that produce different enzymatic activities across human populations. Standard preclinical models cannot capture this complexity, making human genetic evidence the most reliable basis for both target validation and indication prioritization. Genomics’ platform applies statistical genetics methods including Mendelian randomization and colocalization analysis to biobank-scale datasets, enabling causal inference at the variant level rather than relying on aggregate association signals.

Genomics, spun out of the University of Oxford in 2014, has built its platform over a decade of statistical and human genetics research. The company’s CEO and co-founder, Professor Sir Peter Donnelly, previously directed the Wellcome Centre for Human Genetics at Oxford, where his group conducted genome-wide association studies that identified ERAP1 and ERAP2 as autoimmune disease risk genes. That scientific history positions Genomics as a particularly direct fit for this program, given that the foundational genetic evidence underpinning Greywolf’s target selection originated in part from the same institution.


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