Sana Biotechnology Announces Publication of Preclinical Diabetes Data in Cell Stem Cell Demonstrating Insulin Independence Following Transplantation of Hypoimmune Allogeneic Primary Islet Cells Without Immunosuppression in a Diabetic NHP

"Sana Biotechnology's HIP-modified Pancreatic Islet Cells"

Sana Biotechnology, Inc. (NASDAQ: SANA), a company focused on changing the possible for patients through engineered cells, today announced that Cell Stem Cell has published a paper titled “Hypoimmune islets achieve insulin independence after allogeneic transplantation in a fully immunocompetent non-human primate.” The paper evaluated a transplant of Sana’s engineered allogeneic, hypoimmune (HIP)-modified pancreatic islet cells into a fully immunocompetent, diabetic non-human primate (NHP). These modified islet cells, which cluster into effective endocrine organoids, are termed “pseudo islet grafts” (p-islets). The results demonstrated that the HIP-modified p-islets engrafted following intramuscular injection and provided stable endocrine function, enabling insulin independence in the absence of immunosuppression.

“The results of this preclinical study are remarkable, and if they translate into the clinic, we have the potential to profoundly change the way that type 1 diabetes is addressed, potentially eliminating the need for insulin injections or immunosuppression,” said Sonja Schrepfer, MD, PhD, Sana’s Head of Hypoimmune Platform. “We look forward to insights from an investigator-sponsored trial (IST), a first-in-human study of HIP-modified, allogeneic primary islet cells later this year, which would serve as clinical proof-of-concept to assess the safety, cell survival, immune evasion, and C-peptide production of transplanted HIP-modified primary islet cells without immunosuppression into a patient with type 1 diabetes. This publication, along with the ongoing IST, will provide invaluable insights toward our stem cell derived product candidate, SC451. With more than 8 million patients with type 1 diabetes worldwide, there is an enormous need to cure – rather than simply manage – this disease.”

“JDRF is dedicated to harnessing the power of research, advocacy, and community engagement to advance life-changing breakthroughs for type 1 diabetes,” said Sanjoy Dutta, PhD, JDRF Chief Scientific Officer. “The development of cell therapies that replace the loss of insulin-producing cells could one day offer cures for type 1 diabetes. A key area of focus for JDRF is to develop strategies to protect these cells after transplantation that remove the use of broad immunosuppression. As a supporter and investor in Sana through the JDRF T1D Fund, we look forward to seeing if the results described in this paper translate into people, as they would represent a meaningful advance in the treatment of type 1 diabetes.”

The transplant setting was purposely designed to be a high immunological bar by maximizing the donor-to-recipient mismatch. Diabetes mellitus was chemically induced in the recipient as shown by the development of major blood glucose instability and the need for daily insulin injections to control blood sugar. Following stabilization of glucose with insulin treatment, the diabetic NHP underwent transplantation of the HIP p-islets without any induction or maintenance immunosuppression and the administration of insulin was tapered to zero over the course of nine days. Rapidly following HIP p-islet transplantation, the diabetic NHP recipient showed tightly controlled blood glucose levels, was completely insulin-independent, continuously healthy, and exhibited no physical or behavioral abnormalities for the six-month study duration. C-peptide levels, which are a marker for endogenous insulin production and release, reached the normal levels observed prior to induction of diabetes. Furthermore, there was no indication that the allogeneic HIP p-islet graft induced any immune recognition or any type of immune response at any time.

To demonstrate that there was no regeneration or recovery of an endogenous islet cell population in the diabetic NHP, HIP p-islets were eliminated using an anti-CD47 antibody. The antibody blocked the protective CD47 signal and triggered a “missing self” innate immune cell response that led to the rapid destruction of the HIP p-islet graft. Following the anti-CD47 treatment, blood glucose levels in the diabetic NHP began to fluctuate and increase markedly, and insulin injections needed to be resumed. It was thus demonstrated that the tightly controlled blood glucose levels and insulin independence was entirely due to well-functioning HIP p-islets.

The publication is available for online viewing at


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