Can We Cure Diabetes?

A conversation with Katy Digovich, CEO, Minutia

Roughly 589 million adults, aged 20 to 79, are living with diabetes, and it’s estimated that number will rise to 853 million by 2050. Management is often cumbersome for those with the disease.

Minutia CEO Katy Digovich has type 1 diabetes, so the mission for a cure is personal. We caught up with her to discuss engineered iPSC-derived islets intended for transplantation into the forearm, which could make a functional cure for insulin-dependent diabetes broadly accessible.

Why does insulin-dependent diabetes remain one of medicine's greatest unsolved challenges despite a century of insulin therapy?

The discovery of insulin was one of the most important breakthroughs in medical history. It transformed type 1 diabetes from a fatal disease into a manageable chronic condition and has saved millions of lives. But despite a century of innovation, insulin remains a treatment, not a cure.

As someone who has lived with type 1 diabetes for more than 30 years, I know firsthand that diabetes is a full-time job and even with some of the amazing continuous glucose monitors, insulin pumps, and algorithms that we have today, devices still fail and can put you in a life-threatening situation. Every meal, every workout, every poor night of sleep, every illness, and every stressful event impact blood sugar levels. People living with diabetes are either constantly making decisions about insulin dosing and glucose management or are incredibly dependent on devices. The reality is that insulin therapy and the best devices on the market do not replace the biology that has been lost. That's why we believe the future of diabetes treatment lies in replacing insulin-producing cells themselves.

At Minutia, we're working toward what we call a broadly accessible functional cure for type 1 diabetes that could also be relevant for some people living with type 2 diabetes who take insulin. Our goal is to not only restore the body's natural ability to sense glucose and secrete insulin by transplanting stem cell-derived islets that function like the islets that have been lost but also to develop the exact transplant that those of us at the company living with type 1 diabetes want in our bodies.

What's unique about our approach is that we're not only developing immune-evasive cells and improving their ability to engraft but we are also leveraging a platform that allows us to get real-time data from transplanted cells. In cell therapy development we spend a lot of time and money creating cells and modifying them, and then we put the cells in vivo and cross our fingers. We need more visibility into what happens in vivo and how different modifications to cells perform head-to-head. At Minutia, we’re building a platform needed to make cell therapy practical and scalable. That includes looking to drop the cost of manufacturing clinical-grade stem cell-derived islets as much as possible, developing a minimally invasive transplant procedure in the forearm, and creating a tracker that allows us to monitor transplanted cells in real time after they're implanted.

Ultimately, our mission is simple: reduce the burden of diabetes and create a future where people living with diabetes have the option to spend less time on diabetes and more time living their lives.

Can you tell me what your preclinical research looked like? What models were used? What outcomes did you see?

Our preclinical work was designed to answer several critical questions:

• Can we manufacture high-quality stem cell-derived islets from a clinically compatible human iPSC line?
• Can those cells function like native islets?
• Can they survive transplantation and control blood glucose?
• Can we monitor them after transplantation? The encouraging answer so far has been yes.

At the recent American Diabetes Association Scientific Sessions, we presented data demonstrating that our stem cell-derived islets can regulate blood glucose levels in animal models. In one study, animals received stem cell-derived islets before diabetes was induced. Those transplanted animals remained normoglycemic for more than 100 days after administration of streptozotocin, while control animals developed severe hyperglycemia.

In a second study, we asked an even more important question: can these cells survive under conditions of extreme hyperglycemia and reverse established diabetes? The answer was yes. Animals with streptozotocin-induced diabetes received the stem cell-derived islets and subsequently returned to normal glucose control without any exogenous insulin, while the controls remained hyperglycemic.

Our preclinical studies show that our stem cell-derived islets engraft very successfully within muscle tissue. The stem cell-derived islets express both insulin and glucagon, control blood glucose effectively, and remain functional for extended periods following transplantation.

We also demonstrated that transplanted cells produced circulating human C-peptide levels that were comparable to donor islets, providing further evidence that the cells were functioning appropriately after transplantation. Another important finding was that our cells functioned across multiple transplant locations, including intramuscular transplantation, which is central to our clinical strategy.

Together, these studies give us confidence that the combination of our manufacturing process, cell product, and delivery strategy can support durable function after transplantation.

Can you walk me through what happens over the three-week period where human pluripotent stem cells form islets that express and secrete insulin?

This is really where developmental biology meets engineering.

We begin with human induced pluripotent stem cells, which have the ability to become virtually any cell type in the body. Over approximately three weeks, we guide those cells through a carefully controlled differentiation process that mirrors the developmental stages of pancreatic formation.

The cells first become definitive endoderm, which is the tissue that ultimately gives rise to the pancreas. They then progress through posterior foregut and pancreatic progenitor stages before becoming endocrine precursor cells and ultimately mature endocrine cells capable of producing insulin.

At every stage, we perform quality control assessments to ensure the cells are progressing appropriately and expressing the markers we expect to see. This is incredibly important because consistency is everything in cell therapy manufacturing.

Our goal is not simply to make insulin-producing cells; it is to create a reproducible process capable of producing high-quality clinical-grade islets at scale.

By the end of the differentiation process, we generate islet-like clusters that not only express insulin but also reverse hyperglycemia, which is ultimately what is needed to be relevant for people living with diabetes.

How is this delivery an improvement from current practice? How did you ensure effective delivery of the stem cell-derived islets? How can this inform diabetes treatment?

Along with the challenge of making enough cells, one of the biggest difficulties in the field is figuring out where and how to put them into the body. Historically, donor islets and emerging stem cell-derived islet approaches have relied on transplantation into the liver through the portal vein.

That procedure is invasive, requires specialized transplant centers, and can result in significant variability in outcomes. The liver can be a challenging environment for engraftment.

One of the biggest obstacles in cell therapy today is that physicians often have limited visibility into what is happening after transplantation. If cells begin to fail or come under immune attack, there is often no early warning system. We created a tracker that is incorporated directly into the stem cell-derived islets. These sensors allow us to visualize and monitor transplanted cells non-invasively after implantation.

At ADA, we presented data showing that these signals remained stable for up to six months and comparing how the same cells survive across different animal models that test different elements. Importantly, the imaging signal closely correlated with actual cell survival.

That means we may eventually be able to monitor graft health quantitatively and in real time without invasive procedures. We believe that's a significant advance not only for diabetes but potentially for the broader field of cell therapy.

Ultimately, what excites me most is that we're bringing together several innovations that have historically been developed independently: stem cell biology, transplantation science, immune protection, and real-time monitoring.

Our goal is to create a broadly accessible functional cure that can restore natural insulin production and fundamentally change the lives of people living with type 1 diabetes.

As someone who has spent more than three decades living with type 1, that's a future I am humbled to be building.

About The Expert

Katy Digovich is cofounder and chief executive officer of Minutia, a biotechnology company developing next-generation cell therapies for type 1 diabetes. Living with type 1 diabetes herself, she leads the company's efforts to engineer stem cell-derived islets integrated with nanosensor technology, with the goal of restoring natural insulin production while enabling real-time monitoring and improving long-term graft function. Under her leadership, the company has secured funding from the California Institute for Regenerative Medicine (CIRM) to advance novel approaches, including immune-evasive stem cell-derived beta cells, bioengineered islet organoids, and integrated biosensing technologies designed to improve the safety, durability, and effectiveness of cell replacement therapies. Katy earned a bachelor's degree in biology from Princeton University.