So Sana Biotechnology is trying to change the possible for patients by developing engineered cells as medicines. Today, I'm going to focus on our platform that is aiming to overcome allogeneic rejection, and it's called the Hypoimmune platform. The Hypoimmune platform is in four clinical programs, treating seven different indications in three broad therapeutic areas: oncology, B-cell-mediated autoimmune diseases, and Type 1 diabetes. Behind these programs, we also have a pipeline that are working on other areas of medicine, including CNS disorders. Here's a view of our pipeline, and today I'm going to be focusing on the four clinical trials I just mentioned. SC291, a Hypoimmune or HIP-modified CD19-directed allogeneic CAR T in blood cancers for the ARDENT trial. It is also being tested in the GLEAM trial for autoimmune disorders.
SC262, a HIP-modified CD22 allogeneic CAR T, also for blood cancers, and UP421, a HIP-modified primary islet cell therapy for Type 1 diabetes. So let's talk about the problem we aim to address. Since the advent of transplant medicine, the rejection of allogeneic cells has limited the broad implementation of cell therapy. So if I give my cells to you, your immune system will recognize them as foreign and kill them. The industry has approached this problem in two main ways. One is profound immunosuppression. The second is to use autologous, or your own cells. Both approaches have had limitations with the ability to scale. So you see here Sana's proprietary Hypoimmune approach, and this approach aims to address both parts of the immune system, the adaptive and the innate.
You can see that the adaptive immune system, which is your B and T cells, if you disrupt MHC class I and class II, cells are able to evade this part of the immune system. But we've evolved over time and developed an innate immune system, mostly your NK cells and macrophages, which will recognize those cells and attack them. So to address the innate immune system, we have applied a third gene edit, which is overexpression of CD47. With these three edits, disruption of MHC class I and class II, and the overexpression of CD47, we've created Hypoimmune cells that have the ability to evade both arms of the immune system. The team has been pioneering the Hypoimmune technology for many years, and we have applied this in preclinical models, including mice, humanized mice, and non-human primates.
Results from these preclinical studies have been published in peer-reviewed journals, including Nature and Cell. First, I'll start with blood cancer, where there continues to be a high unmet need. There have been many approved autologous CAR T therapies that have shown the possibility of curative intent and many allogeneic CAR T companies working on scaling. Our first data in clinical testing is SC291 in oncology. As we move through clinical development, we are collecting data to understand levels of evidence as the data mature, and we're addressing these four questions. One, does SC291 evade allogeneic immune rejection, as I just described in the slide before? Two, are we making great T cells that can function in the body? Three, do the early responses translate into durable, complete responses?
Four, over time, can we make the drug from multiple donors with a consistent and predictable safety and efficacy profile? Early data suggests the ability to dose safely and early clinical efficacy, and this is early data that we shared in January of this year. As you can see, some of the safety highlights that we've written as no dose-limiting toxicity, no graft-versus-host disease, no SC291-related SAEs, no CRS or ICANS. You can see some of the early clinical data, where three of four evaluable patients had at least a partial response, with two ongoing complete responses. I won't go into the details today, but the immune response data provide important early insights that we are seeing the desired immune evasion profile. The ARDENT trial continues with enrollment, and more data is expected in 2024.
Next, I'll discuss SC262, CD22-directed allogeneic CAR T with a Hypoimmune platform. Unfortunately, CD19 CAR T relapse patients represent a large and growing unmet need, with a median survival of approximately five months post CD19 CAR T therapy failure. We are using the same Hypoimmune platform to insert a CD22 CAR T construct. We're using the same CAR construct that has already been studied in a number of academic studies at Stanford and the NCI. We have the VIVID phase I trial, where we're testing this in CD19 CAR T failures. It's a dose escalation study starting at the starting cell dose of 90 million cells. Moving on to the next broad therapeutic area, B-cell-mediated autoimmune diseases.
Over the last few years, the field has really begun to understand the potential of CAR Ts in this space, and in fact, companies have been targeting B cells with a number of different drugs. There are approximately seventy different indications, where at some level, there's evidence that depleting B cells or knocking down B cells can have a clinical impact. You can also see that the depth of B-cell depletion with treatment predicts efficacy in early trials, and getting to the germinal center for B cells is really critical, where we believe CAR T therapies may have an advantage. The SC291 trial is across three different indications: lupus nephritis, extrarenal lupus, and ANCA-associated vasculitis, or AAV, where you see that there are over five hundred thousand patients in the U.S. and the E.U.
We believe there are many benefits versus autologous therapies, including no patient apheresis and the already scaled manufacturing process. The GLEAM trial is ongoing, with a starting dose of 90 million CAR T cells in the three indications that I mentioned before. It also has the potential to expand beyond these indications over time. We expect to share initial data in 2024. And the third broad therapeutic area I'm going to discuss today is Type 1 diabetes. Type 1 diabetes is caused by autoimmune destruction of insulin-producing pancreatic beta cells, resulting in no insulin production, and there's a large unmet need, with over 8 million patients worldwide. Our goal is to develop a therapy that has euglycemia without any immunosuppression or exogenous insulin. And emerging data suggests that a cure is possible. At Sana, we're combining a number of disciplines to work on this problem.
Number one, we know that cadaveric islet transplants offer long-term glucose control if you have heavy immunosuppression. Unfortunately, for many patients, having this deep immunosuppression is not beneficial over having lifelong insulin. Number two, we know from competitors that stem cell-derived islets can create an efficacious and potential scalable supply. However, it still requires this deep immunosuppression. So what we're working on in Sana is the third point: Can we eliminate the need for immunosuppression so that we can give a single treatment with long-term normal blood glucose without immunosuppression or insulin? Earlier this year, we published data from an NHP model of Type 1 diabetes, where we chemically induced diabetes with STZ, which knocks out the pancreatic beta cells.
You can see that the goals of the study are to demonstrate survival and function of these HIP-modified allogeneic islet cells, demonstrate long-term glucose normalization without exogenous insulin or immunosuppression, and to demonstrate the principle of a potential safety switch with an anti-CD47 antibody. Here's the data. We'll be looking at a graph of fasting glucose over time, and the data points in red and blue show the different time points throughout the day. You can see once you give the STZ administration, you've induced diabetes, and the data is all over the place. It is not in the green band, which is normalized glucose. We stabilize the NHP with insulin over a period of time, and once you see that the data is within that green band, we were able to give the cell transplantation, where we gave allogeneic NHP islet cells to the monkey.
You can see for a period of six months that glucose was normalized. This is no immunosuppression and no exogenous insulin. We then gave an anti-CD47 antibody as a kill switch to test the CD47 mechanism of action, and as expected, the diabetes returned. You can also see stable C-peptides through that six-month time period, and that is a measurement of islet cell function for the six months. Now we are basically replicating the experiment in humans with an investigator-sponsored trial. This trial is authorized at Uppsala University Hospital in Sweden. The goal of the IST is to understand immune evasion, islet cell survival, and cell function as measured by C-peptide, without immunosuppression.
We expect to share initial data in 2024, and you can see from the design, we'll be taking the cadaveric islet cells, applying the three HIP edits, and then transplanting into the arm of a Type 1 diabetic patient. So in summary, we continue to advance the Hypoimmune technology in four trials across seven indications in oncology, autoimmune diseases, and Type 1 diabetes. Reporting clinical data in 2024 in each therapeutic area to have an initial understanding of the safety and efficacy profile. Thank you for your time and attention.
Thank you, Nikki, and thanks, everyone, for joining us today.
Thank you.