Right, thank you. Good morning, everyone. My name is Yatin Suneja, one of the biotech analysts here at Guggenheim. It is my pleasure to welcome you all to our Emerging Outlook Biotech Summit 2026, our next presenting company at SAB Biotherapeutics. From the company, we have a few executives here, but I will be chatting here with Chairman and CEO Sam Reich. Sam, thank you for your time. We appreciate it. Why don't you make some opening comments? Tell us about the SABS story, what are some of the upcoming milestones, and then we'll go into some of the Q&A that I have prepared for you.
Sure. Great. So I'm Sam Reich. I'm CEO of SAB. Our mission at SAB is to transform what it means to get a Type 1 Diabetes diagnosis by developing new medicines that change the course of disease rather than just treat the symptoms. So we are currently in a pivotal trial, which is a Phase 2b with our lead, our lead asset, which is called SAB-142, which is an anti-thymocyte immunoglobulin, that's fully human. And the anti-thymocyte immunoglobulin mechanism of action has proven to be efficacious in Type 1 Diabetes, so we have high confidence in, in the drug's ability to be efficacious. The drug is made in a wholly-owned platform, which is called Tc Bovine, which gives SAB multilevel intellectual property protection, which creates exclusivity for SAB-142 and a very high for a long time, very long-term exclusivity.
Type 1 Diabetes is a major unmet medical need and a large multi-billion dollar market opportunity with no drug approved today. We're fully funded through turning data from a pivotal trial, with a significant runway with a great team and syndicate of investors, which include long-term, long-only biotech specialists as in addition to Sanofi.
Well, very good. Thank you. So you're going after Type 1 Diabetes. Could you articulate for us, like, what is the unmet need, which stage of patient you are targeting, why you are going with that stage? And then we'll go into 142, SAB-142, more on the mechanism after that.
Sure.
What is the goal? Like, what are you trying to achieve here on a high level?
So Type 1 Diabetes is an autoimmune disease characterized by a patient having autoantibodies that attack their pancreas, the beta cells of the pancreas, which is where insulin is made. There are 64,000 new patients diagnosed every year. Stage 3 T1D is the point at which the patients have lost so many beta cells that they need to use exogenous insulin, begin giving themselves insulin. Insulin treatment is just managing the day-to-day symptoms for survival. It does not treat the disease or change the course of disease. The unmet need, there is no drug approved today, is to treat the patient's autoimmune disease and preserve the organ. First-line therapy for a Type 1 Diabetes patient is to preserve the patient's beta cells, to preserve their ability to make insulin.
Our drug acts on a mechanism of action which induces tolerance to preserve beta cells, which is the goal in this patient population.
Got it. Could you elaborate a little bit more on the mechanism? Like, what exactly are you doing? How these ATG preserve beta cell function?
Our drug SAB-142 is anti-thymocyte immunoglobulin.
Yeah.
It is a T-cell engaging drug modality which binds T- cells upon administration, activates those T- cells, which leads to T- cell exhaustion. T- cell exhaustion is correlated with self-tolerance and efficacy. Something very special about SAB-142 and the anti-thymocyte immunoglobulin mechanism is that we can induce exhaustion in T- cells while preserving Tregs. Tregs are critical for self-tolerance, and monoclonal type therapies or more also have an impact on Tregs, where we can induce exhaustion while preserving Tregs.
Got it. So there is a lot of precedent with this, ATG or Thymoglobulin approach, right? But that, that has limitations. It's the rabbit. Could you maybe articulate what the limitations are and how do you address it, and then also put in perspective what we have seen? Because I think there are, like, three or four key studies: the START study, the TN19 study, the MELD study.
Yes, that's great. So why are we confident in our mechanism of action and how do we know that this is going to be efficacious? It is from a drug which is rabbit. That drug is called Thymoglobulin, and it is a rabbit anti-thymocyte immunoglobulin. There have been multiple studies testing that, proving efficacy. The drug Thymoglobulin is a Sanofi drug that is approved for organ transplant. It has been studied in Type 1 Diabetes in clinical trials. The first one, the START study, didn't work. It was too high of a dose. Then lower doses were studied, TN19 in 2018 and the MELD-ATG study which just got published in September in The Lancet.
In both of those studies, the drug proved that, it could preserve beta cells, which showed by preservation of C-peptide and improved glycemic control, which was shown by, statistically significant reduction in HbA1c compared to placebo. So why isn't that drug going to market? Why isn't it sufficient? Because it is rabbit, it is foreign protein, it gives the patient something called serum sickness, which is a really miserable AE, and that is rashes all over the body, fever, flu-like symptoms that, that lasts multiple days. That is not great. It may be okay, but it's not great. And but in addition to that, because it's rabbit and inducing serum sickness, it cannot be redosed. So for multiple reasons, the drug cannot be redosed. One is the serum sickness, and another is the immunogenicity leading to anti-drug antibodies. And we really need to redose these patients.
This is a chronic therapy where patients need chronic dosing. One dose that leads to serum sickness that can't be redosed is not an acceptable commercial profile. Where SAB-142 and SAB come in is we have made an anti-thymocyte globulin, SAB-142, which is fully human, doesn't cause serum sickness, and can be redosed. We're able to rely on that efficacy outcome because it's the same drug modality with the same mechanism of action, but it doesn't cause serum sickness, it doesn't lead to the generation of anti-drug antibodies, and it can be redosed.
Got it. So you have completed a Phase 1 study in healthy volunteers, and I think there was a cohort in T1D patients. We have seen data on the Phase 1 healthy volunteers. Could you talk about some of the key takeaways from that? Talk about how did you come up with the dosing, what exactly did you see on the relative dose that you are moving into the SAFEGUARD or the pivotal study?
So the Phase 1 study was a first-in-man study, conducted and finished in 2024, where we announced data in early 2025. The majority of the subjects were adult healthy volunteers with a patient cohort, so we have data in patients. We dose escalated in the patients from a very low first dose in man all the way up to 4.5 mg per kg, which is higher than where we are dosing in Phase 2. So multiple doses were tested. We had a cohort that was redosed, so we have a redosing cohort, and we had a patient cohort, so we have data in patients. The objective of the Phase 1 was to show that the drug didn't cause serum sickness, did not lead to anti-drug antibodies, and had the same mechanism of action as Thymoglobulin. And we showed all that.
In terms of doses and how we select doses for the next trial, we were looking for doses that initiated durable T- cell exhaustion, and we selected two doses from the trial to put into SAFEGUARD that both initiated durable T- cell exhaustion.
Got it. What are those doses? And then, like, let's say if we have to compare to our ATG doses, like, how would you compare?
So the doses in SAFEGUARD are 2.5 mg per kg and 1.5 mg per kg. With rabbit Thymoglobulin, 2.5 mg per kg has been shown to be efficacious in two trials, but in the MELD trial, they dosed lower and showed lower doses all the way down to 0.5 mg per kg were efficacious. Now, one, it's not a one-to-one dose. It's a different drug. So 2.5 in rabbit is not necessarily exactly the same as 2.5 with SAB-142. And two, the objective of MELD, where they showed that 0.5 mg per kg worked, was to find the lowest efficacious dose, where that's not our objective. Our objective is to try is to find the best dose, the optimal dose.
So we have 2.5 mg per kg, and our other dose is 1.5 mg per kg, which is lower, consistent with MELD and the pattern of efficacy in Thymoglobulin, which is that lower doses can be good. But we don't need to match one-for-one to Thymoglobulin because, one, it's not perfect one-to-one dosing. It's a different drug. And two, our objective is different than the objective in the MELD study.
Got it. So, you are able to redose?
We are redosing. We are able to redose. We do not have immunogenicity. We do not cause serum sickness. We are indeed redosing, in SAFEGUARD. We did have a redosing cohort in the Phase 1.
That was in December. Okay. On the Type 1 Diabetes, I think there are six patients. How you are thinking about data disclosure? I mean, two of those six patients, I think four are on the drug, two are on the placebo. Do you think four patients is enough for us to see some sort of a stabilization or sort of a lower decline in C-peptide over time?
Yeah. So that's a good question, and, and of course, people are very interested in that. The primary objective, what we've, you know, told, told the public for the reason we did the patients, was to show safety in patients so that in the SAFEGUARD study, the investigators know and have the confidence and the comfort that patients have been dosed and they and they do okay. Because there's a difference between someone with Type 1 Diabetes and adult healthy volunteers. We wanted to make sure that we had safety from those patients for starting the SAFEGUARD study, which has gotten off to a great start, and that is thanks in part to the fact that we've already enrolled some patients. Now, we announced safety data. The safety is consistent with adult healthies.
It's a very small sample size, but people are interested in, you know, other things that we looked at in that study. And so we do hope to share more as the year goes on in the appropriate settings.
Got it. And then, what, how should we think about C-peptide preservation in these four patients? And then what about the timeline? Like, is it, like, time point that you need a minimum, whether it's three-month cut off the data or six-month cut off the data?
Yeah. So to show efficacy in this patient population, you need to look at the C-peptide compared to C-peptide in a placebo group at one year. So, as expected, there's a natural history of this disease, and at one year is where a drug would hope to have stat sig. Now, it is interesting, so you need a certain sample size because there's variability. You need a certain patient type because you need to have C-peptide to preserve, and you need the disease to be new. And so in order to show efficacy, which is why we did the SAFEGUARD study, you need a certain sample size, and you need a year. And that's what the SAFEGUARD study is for.
With that said, you know, we did study the drug in four patients, so, we'll share what we have, and just keep in mind that it's just a glimpse, an early glimpse at a small group of patients. At 120 days was the Phase 1, not 360.
Got it. Got it. So we get that. Okay. Then in terms of the pivotal SAFEGUARD study, the study started in third quarter. It's a two-stage study or two-part study, Part A and Part B. Could you just talk about both the like, how what is the study design, what type of dosing you are using? And I also noted that you are going as early as age five. How comfortable with you are you with age five, these younger kids, what data you might have already in those patients?
So I'll start with the study design. SAFEGUARD is a study in newly diagnosed patients with Type 1 Diabetes, so they are within 100 days of their diagnosis. It's from ages five to 40, 159 patients, 50 per arm in the efficacy study, I think, something like that. And the primary endpoint is C-peptide at one year. There are three arms: a 2.5 mg per kg, a 1.5 mg per kg, and placebo. And it's a global study being conducted in the U.S., U.K., Europe, and Australia. And the primary efficacy endpoint is C-peptide at one year. There are secondary endpoints. The one that people are most interested in is HbA1c, which is the first secondary we'll look at, which should show that the patients have better glycemic control.
In terms of going to five, there you know, we met with the regulatory agencies, and we have a plan. That's a step-down plan where you study in a group of adults before going to adolescents, before going to peds. So by the time we get to that age, we'll have established a nice, acceptable AE profile in older patients.
So in.
I think there was a question about part A. You want-.
Part A and B, which yeah, talk about that. Yeah.
Let's talk about Part A. So, the study has two parts, a Part A and a Part B. Part B is the efficacy study. That's the patient population that we're doing the statistical analysis on, C-peptide and HbA1c, and other endpoints, to prove efficacy. The reason why we have a Part A has to do with the kids, which is that the modeling for stats, in order to, you know, be confident we'll hit our endpoints, involves stratification by age and having a balance of adults, adolescents, and pediatrics. We have to enroll a certain number of adults before we can step down to adolescents. And if we were to do that all in one study, that would throw off our stratification.
We have sequestered the first 12 adults outside of the scope of the Part B so that the Part B has the right stratification of age group.
The part A has those 12 adults in there?
Part A is 12 adults, six on 2.5 and six on 1.5.
I see.
That they are not included in the efficacy component of the study because then we'd have too many adults in the area.
Correct. Yeah. But then you don't need to generate any additional data in younger patients for you to enable Part B because Part A, those 12 adults, should enable you to go into younger patients.
Yeah. Part A and the first group in Part B.
First group in part B. Oh, I see. So, okay. That's one thing. Do we know how many of these cohort adolescents and patients that you need to enroll in Part B?
In Part B, it's approximately a third, a third, a third.
A third. Is that the prevalence of those 65,000 patients? Like, how would you characterize the age-wise distribution?
Yeah. I don't think that matches up perfectly with the prevalence. That we want to study all the patient populations, and we want to be looking at, you know, each age group appropriately, to establish, you know, the efficacy.
Got it. So what is the timeline for study enrollment and the data for SAFEGUARD?
We are planning to complete enrollment by the end of this year. That's last patient in by the end of 2026. It is a one-year endpoint. So we hope to have data in the second half of 2027.
Got it. Could you talk about the powering and then in terms of how would you describe success on the primary endpoint of AUC C-peptide?
So the study has 80% power to show 40% preservation of C-peptide. Based on sort of MELD and TN19, it's about the same power for HbA1c to show a 0.5 reduction in absolute HbA1c. Hitting the endpoint is success. I mean clinically meaningful preservation of C-peptide is a drug that works. That's success. We hope to hit it on HbA1c. In both the two other Thymoglobulin trials, the drug worked to reduce HbA1c, so we hope to show that. But success to establish efficacy is preserving C-peptide.
Yeah.
40% preservation is considered clinically meaningful. We're powered to show 40% preservation, and Thymoglobulin has shown 50% preservation, so we, of course, you know, hope that we get that, but 40 would be enough.
Got it. Then moving on to the commercial side, I know it's early, but how are you thinking about like, what are your thoughts on the commercial strategy? How are you preparing for that? If you can just, you know, of these 64,000 patients, if you can break it down for us who are the addressable ones, and then, again, on the pricing front also, if you can comment?
Yeah. So, it's early days for commercial, but we are starting to think about commercial. We're doing early commercial activities. We, we recently brought on David Zaccardelli as chairman, so I'm not the chairman anymore. You introduced me as a chairman. In January, we announced that Dave Zaccardelli is our chairman. He was the CEO of Verona. And a marker of success there, and the reason why we invited him to be our chairman, is that at Verona, he launched his drug Ohtuvayre, and that was one of the most successful commercial launches in the last decade in biotech. So we're bringing in that capability. We're starting to build out, do early commercial work, which is to understand the patient, payer, provider journey, what they're going through and how we address them. And we'll do early commercial work in 2026, building out an organization.
So we are starting to focus on that. This is a very addressable market as it's an institutionally treated disease, so these patients get referred to academic centers. It's something that a small company like us could certainly address. We're preparing to launch the drug as we're highly confident in it, doing early commercial now and having a plan to launch on our own, is something we're working on. As far as pricing, we hope to show that and we expect to show that our drug is superior to Tzield. It's early days. You know, we haven't established pricing, but we can look at standard of care being superior to that and having a premium on standard of care.
Got it. Got it. What about other indications, or other stages of Type 1 Diabetes? Is that a plan for you with 142?
Yeah. So, Type 1 Diabetes is diagnosed in stages, which are the progression of beta cell loss. So when a patient has started to lose beta cells, but they are still insulin-independent, they still make enough insulin to not need other insulin, that's called Stage 2. We will go after Stage 2 next, sort of in a staggered fashion, not sequential. And that's kind of the holy grail. If we can capture Stage 2 and have efficacy, which we believe we will, it's the same disease, preserve their beta cells in Stage 2, there is the promise that a patient will not need to go on insulin, and there's a functional cure. So the ability to preserve a Stage 2 patient's beta cells and to redose and give it chronically offers the hope that we can keep a patient insulin-free.
So Stage 2 is an indication that's important to us. And then we have later Stage 3 patients. So in the SAFEGUARD study, and our initial label is patients within 100 days of diagnosis. And that limits the opportunity for patients to get dosed because once a patient falls out, that if they haven't gotten the drug yet, it's they're not on label for the indication. So we're also interested in those patients that are 100 days past diagnosis but have meaningful C-peptide to preserve so we can capture and treat those patients. And that really, really opens up a giant market. The addressable market on our first label, our first indication, is 64,000 new patients diagnosed every year. Those newly diagnosed patients, 100 days from when they get that diagnosis, are all addressable as an addressable market. In addition to that, this is a chronic therapy.
So if a patient has gotten dosed in year one, one of those 64,000 patients, we keep those patients so they accumulate because it's chronic dosing.
Got it. Helpful. Then on the competition front, what is the landscape there? I think Tzield has this, BLA under review under the commissioner's voucher. Any read-through to you?
Oh, it certainly reads through for us. The Tzield PROTECT study was in Stage 3. The commissioner's priority voucher is for approval in Stage 3. And what that will be is the first approval in this indication showing regulatory clarity, showing a regulatory path. And on top of that, PROTECT study, they only, only showed benefit on C-peptide, did not hit any secondary endpoints. So it shows a regulatory path with C-peptide being sufficient for an approval.
So that's okay. Then maybe finally, how is the financial health? What is the cash runway and the burn rate?
So, I mean, last year we burned about $40 million. We expected to increase, but we had $140 million more in cash at the end of 2025. We have cash sufficient through this trial if we're funded for the trial and a year-end, runway past data, so we have cash through 2028.