All right, good to go. All right, everyone, thank you so much for coming to the Jefferies Healthcare Conference, and I'd like to warmly welcome the CEO of Zura Bio, Robert Lisicki.
Thank you very much for that introduction, and I'd like to, on behalf of Zura Bio, just extend my regards and thanks to Jefferies for the invitation today and the chance to share what I think is a very exciting update on Zura Bio and the company. Just as a reminder, over the course of the discussion, I will be making some forward-looking statements, our standard disclaimer. You can also refer to our website, zurabio.com, for further review. The company, Zura Bio, was formed as a private company in 2022 and went public in 2023. Over the course of that two-year journey, they in-licensed three novel biospecific antibodies. I joined the company in January of 2024, and what I outlined for the company was three clear objectives.
The first was that we would successfully secure two new INDs, that we would initiate two phase two trials, and that we would raise sufficient funds to execute on those trials and provide a cash run post data readout. Really impressed and proud of the accomplishments of the organization, we were successfully able to secure an IND for systemic sclerosis. That study initiated in December of 2024. That study is TibuSURE, and an IND was cleared for hidradenitis suppurativa in March of 2025, and that study was also activated, and that study is TibuSHIELD. Really excited about what the next 15-18 months will look like for the organization. While we have three assets, I'm going to focus my time and discussion today on our lead asset, which is tibulizumab.
Tibulizumab was in-licensed from Eli Lilly, and it is a quadrivalent bispecific antibody that inhibits both IL-17 as well as BAFF. The quadrivalent aspect is unique and provides some really unique attributes for this product in disease. If you look at the structure of this molecule on the BAFF side, this is tibulizumab. Tibulizumab is ligand-bound, and it forms a trimer with the BAFF receptor, BCMA, and TACI. That gives it a broad application against a long lineage of B cells. On the IL-17 side, it forms a heterodimer with IL-17A and IL-17AF. This particular molecule spares IL-17F, the isoform 17F, and we think that is advantageous given some of the offset effects that have been reported with IL-17F inhibition. What also makes this particularly, I think, appealing combination is that this is a quadrivalent bispecific antibody, meaning that it can bind to just IL-17, just BAFF, or both.
It does not require co-location or dual engagement to be activated. Given the heterogeneity of a broad range of INI diseases, you can, I'm sure, think of the potential for this molecule across a broad subset of those indications. I want to spend the remainder of our discussion talking about the two phase 2 programs that we have in place, the validation for those programs, the design of the trials, and our expectations on when we will see top-line data. The initial indication is systemic sclerosis. Systemic sclerosis globally affects around 300,000 individuals. This is a disease with a lifetime mortality, or a 10-year mortality, I should say, of 50%. There's also a high degree of morbidity, and despite the challenge of this disease, there still is no advanced line agent that's approved for the whole of the disease.
There are two therapies that are approved to treat SSc ILD, but they provide a relatively modest effect, and some of the trade-off of those agents is challenging for both patients and physicians. The aspiration we have with this program is to demonstrate effect in both skin and in lung. In a phase 2 endpoint, the typical primary endpoint is the change in the modified Rodnan Skin Score, and you will also explore lung. In a phase 3 trial, the modified CRISS, the CRISS score is used, which is a composite index of five different endpoints. Based on the responses and the results in the phase 2, that will inform our phase 3 plan. It's always helpful if there's a strong scientific hypothesis and rationale, and if there's preclinical data that supports that. In our case, we choose to pursue indications that have validated clinical results.
So in the case of tibulizumab, on the IL-17 arm of the asset, we have a phase three study that we can look at that was conducted by Kyowa Kirin with brodalumab. Brodalumab is an IL-17 receptor. This was a phase three study that was specific just to Japanese patients with 50 patients per arm. This was a unique trial in that the primary endpoint in this trial was a modified Rodnan Skin Score at 24 weeks. This was not a traditional 52-week trial, but you can see that in this 24-week trial, you saw a very robust response in the modified skin score where the delta was close to 20. It's been an unprecedented response.
This was very early disease, and in part, the goal or the aim of this study was to determine if you could change the natural course and trajectory of disease, and in that regard, the sponsor appears to have been successful. We also see benefit in FVC. FVC is an objective endpoint and gives more support and validation to the hypothesis we have on the role that IL-17 plays in systemic sclerosis. There is also a broad subset of validating data with B cell disrupting or inhibiting therapies, where rituximab, as an example, is approved in Japan for SSc. In the U.S., GSK sponsored an investigator-initiated trial of belimumab that was conducted at the Hospital for Special Surgery. This was an exploratory study that was 52 weeks in a double-blind, and again, we see evidence of effect in both skin and lung.
This generates the question on what is the potential of combining these two interventions in a single molecule with the goal of trying to provide something new and novel that treats the whole of the disease and scleroderma. That is precisely what the aim of our phase two trial is. Phase two trial will have 80 participants with one active arm and one placebo arm. This study is active today. The study is expected to provide, or I should say to complete enrollment by Q1 of 2026 and provide top-line data by Q4 of 2026. One of the challenges that you can often have in a phase 2 study is your sample size is insufficient to fully understand the benefit of FVC. We will measure FVC in this study, but one of the mitigation strategies that you can use is high-res CT imaging of the lung.
This has been used in IPF, and it's been used in ILD studies as well. The benefit is you can detect early whether or not there is benefit from the intervention that's being used, and this is a highly concordant approach to FVC. It's not an acceptable endpoint by the agency, but it does help support whether or not there is strong rationale or validation of the role of this drug in helping or supporting lung fibrosis, and it will ultimately inform how we think about the sizing of our phase 3 program. Again, we're very excited about the next 15-18 months for this trial. The second trial that was IND cleared was for hidradenitis suppurativa.
HS is a particularly challenging disease with relatively few options for patients, and there has been a real flurry of activity by the biotech and pharma industry in identifying potential targets for HS because the need is high, and there are choices today, but the benefits have been relatively modest. The epidata in the U.S., which suggests that there's somewhere in the neighborhood of 300,000 patients with HS, there is emerging data from a number of different sponsors that would suggest that this epidata is understating the actual opportunity. We continue to do work to understand that opportunity, but we expect the actual number of patients to increase as a better understanding of the disease becomes clear. As I've shared, there are approved agents for HS, but when you look at the relative benefit or response of those agents, I think it's fair to classify it as helpful but modest.
There's been no breakthrough therapy to date in HS. I think you always want to be careful when you do these indirect comparisons of trials because trials are conducted at different times by different sponsors with different baseline characteristics, sometimes different endpoints and concomitant medications. You want to be cautious in how you interpret this. When you look at the last 10 to 15 years of drug development in HS, you've not seen anything break through the ceiling of a HiSCR75 delta of approximately 20%. It's good to have alternative therapies. It's good for patients. It's good for physicians. It's good for sponsors. It's good for investors, but ultimately getting to a higher rate of efficacy remains a need within this space. In part, it may be driven by the heterogeneity of HS. These patients are complex.
They have a number of different drivers of disease. Having and identifying an approach that actually addresses the heterogeneity could provide a better outcome. When you look at the emerging data with B cell reduction or B cell inhibition, you see very encouraging results. The most recent was part of a basket study conducted by Novartis. One arm of that basket study was their BTK inhibitor, Remibrutinib. Remibrutinib was studied in this basket study and demonstrated a robust HiSCR75 delta at the end of this trial. This was a 16-week trial. The delta was 25. That is in line with other phase two trials that have been reported.
Again, it generates the question that if you use a combinatory approach where you're using the validation of an IL-17 agent with validated B cell diminishing therapy, is there a reason to believe that you could have a better overall response or you could get a broader response? You can get either more patients that have a good outcome or a deeper level of response in those patients that have any outcome. One proof of concept study that adds some support to this hypothesis is J&J's Vega study. This was a study in a very challenging disease, ulcerative colitis. It was a proof of concept study. Historically, there has been a reticence on the part of large pharma to do these combination studies because there's a concern about offset effects that you may see in these trials and potentially jeopardizing their approved assets.
This study looked at the change in modified male score at 12 weeks with just an anti-TNF, anti-IL-23, the combination, and really a remarkable result was reported and observed. It actually showed a doubling of remission in UC at the end of the 12-week period of time, the end of the exposure period. Just as encouraging, though, was that you did not see redundant offset effects or increased risk of SAEs in the trial. We think this is very encouraging, and it provides at least some evidence of the potential effect of combinatory therapy in disease. Now, keep in mind in this study, these were two separate agents used in two separate injections. Our molecule is a single molecule that is intended to be injected q-weekly in our studies.
When you take the validation of IL-17 plus B cell, could that give you the potential to break through the current ceiling that you're seeing across these phase 2, phase 3 HS studies? To provide some additional support, what gives us confidence is the binding affinity for IL-17 agents. Ixekizumab, which is the active IL-17 arm of this drug, has class-leading affinity. Better affinity leads to higher target engagement. Higher target engagement potentially leads to better clinical outcomes. When you look at the relative binding affinity, you can see bimekizumab, for example, has much better affinity than secukinumab. Perhaps that offers some explanation as to why the differences in psoriasis in HS have been reported. When you compare bimekizumab to ixekizumab, you can see ixekizumab is far more potent than bimekizumab. Our view is that sparing the IL-17F isoform is beneficial.
It's unclear that it's additive based on the clinical trial results we see, but we do know that it conveys additional risk on suicidal ideation and behavior as well as candidiasis. We have a combination approach with class-leading affinity in an area of high unmet need in a market that is growing in terms of its prevalence and in terms of the patient need as well. When you look at the combination of the benefits that are offered, we have class-leading affinity against two validated pathways, 17 as well as B cells. We spare the IL-17F isoform, which we think will be relevant, and we're actively enrolling patients for this study. This study is expected to provide top-line data in Q3 of 2026.
It's a 16-week study, primarily U.S., at much larger population, so it starts later than the scleroderma study, but our guidance is that this study will read out prior to that. If you look at the design, the other approach that we want to just share is that we added a loading dose to both arms. There's a low dose and a high dose arm. As a sponsor, you have a choice when you want to study your minimally effective dose, either in a phase two or a phase three. We wanted to get clarity on dose effect in a phase two study.
We also included a loading dose at week two with the goal of getting patients to therapeutic levels of drug as quickly as possible and try to mitigate some of the risk you see with attrition in these studies, which can cause challenges at the 16-week period of time. There will be an open label portion of the study as well. We will collect additional safety data. Again, really excited about the progress that we are making against this trial. The team has worked very actively in activating sites and screening patients and getting patients enrolled into the trial. When you look at the next 18 months, it is really exciting from a company standpoint.
Since the day I arrived at the company, the most common question that I received is, "When are you going to have internal catalysts?" Really excited to say that we're in a position now where we can give guidance to those catalysts. Initiated two phase 2 studies with two top-line data readouts in 2026. As a company, our cash position is strong. We have cash through all of 2027, which is four to five quarters post data catalyst. It puts us in a relatively unique position given some of the challenges that most biotech companies are facing today. In summary, excited about all of the progress that has been made by the company, by the team.
Really excited to get these drugs actively involved in the clinic and in patients and to see that we can validate the hypothesis we have in both of these diseases and look forward to additional updates in the coming months for all of our current investors as well as all of our interested investors as well. Thank you, everyone, for your time and attention. I appreciate it. Thank you.