Sana Biotechnology, Inc. (Nasdaq: SANA), a Seattle-based cell engineering company, announced a strategic collaboration with Mayo Clinic to accelerate development of SC451, an investigational hypoimmune-modified pancreatic islet cell therapy for type 1 diabetes. Under the agreement, Mayo Clinic will contribute multidisciplinary clinical and operational expertise across protocol development, surgical technique refinement, clinical trial design, and biomarker identification, while also making an equity investment in Sana, with an option to make an additional equity investment under the terms of the agreement. Financial terms were not disclosed.
SC451 is a gene-modified, stem cell-derived pancreatic islet cell therapy engineered using Sana’s proprietary hypoimmune platform to evade immune rejection without requiring ongoing immunosuppression. Sana expects to file an Investigational New Drug application and initiate a Phase I clinical study of SC451 as early as 2026.
The collaboration covers multiple operational domains. Mayo Clinic will provide end-to-end clinical and operational insight to optimize workflows including product handling, delivery, and post-treatment care; refine surgical procedural techniques; standardize handling and post-treatment management protocols; and lead clinical trial design efforts including biomarker identification to guide patient selection and longitudinal monitoring. The resulting protocols and processes are intended to support deployment across Mayo Clinic facilities and other sites globally.
SC451 is designed to allow a single administration of pancreatic islet cells to support long-term glucose control without the need for exogenous insulin or immunosuppression. The therapy leverages Sana’s hypoimmune platform, which applies multiplex genetic engineering — including knockout of MHC Class I and Class II molecules to reduce adaptive immune recognition, overexpression of CD47 to block innate immune destruction via NK cells and macrophages, and expression of HLA-E to further inhibit NK cell activation. The combination is intended to resolve the immune evasion paradox that has historically limited allogeneic cell therapy: removing MHC expression to prevent T cell rejection while simultaneously blocking the innate “missing self” response triggered by that absence.
An investigator-sponsored clinical study evaluating donor-derived, HIP-modified pancreatic islet cells in a patient with type 1 diabetes showed the cells were well-tolerated, survived, evaded immune detection, and continued to produce insulin through 14 months of follow-up. Sana cited these data in framing its IND filing timeline.
The collaboration positions SC451 within a competitive field that includes Vertex Pharmaceuticals’ VX-880 and VX-264 programs, which are also stem cell-derived islet cell therapies in clinical development for type 1 diabetes. Vertex’s VX-264 uses a physical encapsulation device as its immune-evasion strategy, in contrast to Sana’s genetic engineering approach, which produces unencapsulated cells intended to engraft naturally and receive vascularization. The comparative durability and function of encapsulated versus hypoimmune-engineered islet cells in humans remains an open clinical question.