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Thank you for standing by. My name is Parilla, and I will be your conference operator today. At this time, I would like to welcome everyone to the Forte FB102 Data Call. [Operator Instructions] I would now like to turn the conference over to Paul Wagner, Chief Executive Officer. You may begin.

Well, great. Well, thank you all for joining us this morning. I'm super excited to share the results of the FB102 vitiligo trial. But before I get started, I wanted to introduce Professor David Rosmarin. Professor Rosmarin is the Chair of the Department of Dermatology at Indiana University School of Medicine. And as many of you know, he's a world-renowned leader in vitiligo. He led and published many of the important studies in the field, including his first author of the New England Journal of Medicine Phase III Opzelura publication.

And we're really fortunate that Professor Rosmarin was interested in serving as the independent central reviewer in this FB102 vitiligo study for the FVASI assessment. And having his central review, I think, provides significant confidence in the rigor of the scoring. And given his role in the study, I asked if he'd be willing to join this call to provide his perspective and he generously agreed. So thank you, Professor Rosmarin, and welcome to the call.

Thank you. It's a pleasure to be here.

Great. Well, I need to show this forward-looking statement slide here, and I'll keep it up for just a moment, and then we'll jump right in. As many of you know, vitiligo, a very large unmet need here, autoimmune disease, a disease of the skin driven by pathogenic T cells that kill the melanocytes and create a depigmentation, as you can see in that photograph over on the right. You can have sensitivity of the skin, eye abnormalities, of course, emotional challenges and predisposition to other autoimmune conditions as well, a lot of comorbidities.

It's a very large market opportunity. And while topical JAK has been approved and oral JAKs are coming along and have demonstrated activity in vitiligo, the regulatory scrutiny of the JAK class, including the black box warning has impacted -- can impact the uptake of the JAK inhibitors.

And with FB102, of course, IL-15 and IL-2 are an important part of the disease of vitiligo, and that's exactly how FB102 works by blocking that interaction. And here, you can see a cartoon showing the IL-15 stimulation of the activated pathogenic cytotoxic CD8 positive T cells. These are the tissue resident memory T cells that then attack the melanocyte and that attack of the melanocyte, killing of those melanocytes is what leads to that depigmentation.

But not just IL-15 is involved, also IL-2, and I think I've talked to a number of you about this particular study. It's a cancer study where they were actually giving high-dose IL-2 to treat the metastatic melanoma. But what was observed here is that up to 22% of those patients who were treated with high-dose IL-2 for their cancer developed treatment-related vitiligo. And I think that really highlights the activity of both IL-2 and IL-15 in vitiligo. And again, the mechanism here of FB102 blocking the receptor CD122 to prevent the pathogenic T cell activation.

There's data to show that this anti-CD22 (sic) [ anti-CD122 ] activity in a mouse model. This data from the University of Massachusetts showed that there was a statistically significant repigmentation in the tail of the mouse with a surrogate mouse antibody, surrogate CD122 antibody at 8 weeks. But I think what's really interesting is this data in that publication where they showed that after stopping therapy, there was a continuing improvement of the vitiligo became more statistically significant. And the hypothesis here has been that if you're able to deplete the tissue resident memory T cells, you may be able to affect durability. So this is a hypothesis of the mouse model, but we've got some very exciting data to share here today that I think we've been able to translate this through to humans now as well.

So now I want to walk through the vitiligo study. And this is the design of the vitiligo study. So this study, we actually were able to enroll two cohorts. We previously disclosed one of the cohorts that included that 3 milligrams every 3-week dosing cohort. We were able to enroll a second cohort. It enrolled 43 subjects, 3:1 randomized, 11 were on placebo and 32 were on FB102. The primary endpoint of this study was the mean percent FVASI improvement from baseline at week 24 as assessed by the central review, Professor Rosmarin central review.

Now very importantly, this was only 12 weeks of treatment. We only treated for 12 weeks with either FB102 or placebo and then observed through 24 weeks. So they were off therapy for the final 12 weeks of the study. And as I mentioned, we've enrolled 2 dose cohorts in addition to the 3 mg per kg maintenance cohort we previously disclosed, Cohort A, which had 15 subjects and cohort B with 17 subjects and 11 on placebo in the intent to treat.

Now, the protocol-defined efficacy evaluable population excluded one placebo subject. So the placebo count goes from 11 in the intent to treat down to 10 in the efficacy evaluable population because that individual had facial hair, but that subject also experienced significant vitiligo progression during the study. So as a result of the protocol-defined efficacy evaluable placebo population, it provides a much more conservative assessment of the FB102 activity.

And we can see that here, this is the intent to treat. Of course, hugely positive here because we have that one placebo subject that got much worse in the study, and that really drove the placebo to have a negative response. In other words, depigmentation, so a 45, 46-point delta in the active versus placebo and of course, highly statistically significant as well.

But if we remove that placebo nonresponder and placebo subject that got much worse, again, this is protocol-defined efficacy evaluable, we still -- and again, very conservative assessment for FB102, we showed a very high statistical significance here, both each of the individual cohorts and FB102 overall, about a 30-point improvement, and we'll compare this to other therapies in development, but compares very, very favorably in terms of the percent improvement from baseline, about a 30-point improvement, 8-point improvement on the placebo when we take that one placebo that got much worse out, again, protocol-defined efficacy evaluable population for a placebo-adjusted delta of about 22 points, and again, statistically significant.

Now what's interesting here, if we look at the progression of the response, we actually were able to see a response to this therapy that was statistically significant in this very small study, statistically significant by day 64 and continued in that statistical significance through week 24. And I've highlighted in this slide where that end of treatment period is. And also note that between week 12 when they stopped treatment and week 24, that the improvement continued and of course, became more statistically significant, similar to the mouse model that was hypothesized in terms of the disease modification.

Now we also looked at patients who were extensively involved at baseline. And so those would be the subjects with an FVASI greater than or equal to 0.75. So a 0.75 FVASI corresponds to about a 20% to 25% depigmentation. That will be a complete depigmentation of about 1/4 of the face. So that will be just below your lower eyelid, the mid-section of your face and the entire cheek. That would be what approximately 0.75 baseline FVASI was. That would be very extensively involved disease.

And as you can see here, an even more robust response. So about half of the subjects had this very high baseline level of FVASI, 0.75, 17 in FB102 and 4 in placebo. And even with this smaller subset, we hit statistical significance, in fact, greater statistical significance by week 24, again, 43% on active in placebo. Again, those subjects who had some response on placebo didn't have very extensive involvement, which again, I think is an important point about a placebo-controlled trial. And so the placebo-adjusted delta in this group was only 43 points, roughly 43 points and again, p-value of 0.006.

And again, in that subgroup as well, you can see here a 14-point improvement between weeks 12 and 24. So after we stop therapy, these patients who are more significantly involved, had a very substantial improvement between weeks 12 and 24 when they were off of therapy for 3 months.

So how does this compare? If we look at the FVASI improvement at week 24 versus some of the oral JAKs, I've got the oral JAKs from their Phase II data here, you can see that it compares quite favorably. In the overall population, you can see about a 30-point improvement relative to placebo. And in the baseline with the extensive involvement, these are patients that again have about 1/4 of their face depigmented at a 43% improvement. So again, a very favorable comparison to the oral JAKs. And these oral JAKs would have been dosed for the full 24 weeks. Again, we're just dosing through 12 weeks.

In terms of the responder analysis, the FVASI50 and the FVASI75, we had a 34% FVASI50, a 12.5% FVASI75. Again, this is at week 24 after just 12 weeks of therapy. And in the baseline FVASI, these subjects that were much more extensively involved at 60% FVASI50 and the FVASI75 of 23.5%.

Now the responder endpoint was impacted by placebo FVASI75 responder. And I think that really reinforces the importance of randomized controlled studies and baseline severity when interpreting the vitiligo responder endpoints. But again, a really robust response from FB102. And even with that placebo responder, as I noted previously, we had a statistically significant improvement in the primary endpoint, so quite impressive results even with that headwind.

And this is how that compares. So again, we look at the oral JAKs here from the Phase II data, the FB102 at 34.4%, again, right in that range of the oral JAKs that were dosed for the full 24 weeks as opposed to our study, again, just dosed for 12 weeks. And the FB102 baseline FVASI greater than 0.75, so again, very extensively involved, actually at 58.8%, well above what was seen with the JAK inhibitors.

And likewise, in that range of the JAK inhibitors, even with that placebo responder in there in the 102 group and in the baseline group, which had the FVASI greater than 0.75, you can see that, that placebo responder actually was not extensively involved. So that, I think, is a very important point. If you have less involvement, so a small area that improves by 50%, you could have an area that's, for example, the size of a quarter and half of that improves, that's in the range of the placebo fluctuation, and that would get represented as an FVASI50.

So here, I think this is a more accurate assessment if you look at very extensive involvement in terms of an important responder index like FVASI75 by looking at those subjects who are more extensively involved as we did here with the FVASI greater than 0.75. And here it's a 23.5% benefit even ahead of the oral JAK inhibitors at 24 weeks, again, with them treating through 24 weeks with us just again through 12 weeks.

And this is an image. I think images are really important, and this is the UV, you can really see the clear demarcation of the depigmentation. And I think this is an important image as well because it represents what a subject looks like if they've got an FVASI 0.75, so pretty clear involvement around the eyes into the forehead, around the nose and around the lips and the lips tend to be a harder area to treat as well. You can see by week 12 already a 73% improvement. And as we get to week 24, an 87% improvement. So nearly a complete clearance of the vitiligo.

And note too, the difference between week 12 and 24. The average, as I noted before, in this population that had this extensive facial involvement was about 14 points. So this subject here is exactly representative of that, showing that 14-point benefit between stopping therapy at week 12 out to week 24.

And so this is the safety profile. Again, a very strong safety profile, all mild to moderate with FB102 actually looking favorable relative to placebo. So this is very consistent with what we saw also in the Phase Ib in the celiac study. And so again, continue to see a really nice safety profile.

And so just to give the quick summary here, this was a double-blind, placebo-controlled study. FB102 demonstrated robust activity. This is pretty remarkable for a study this small, I think, to show the statistical significant improvement in this primary endpoint from baseline up to 24 weeks. The responses occurring very early, statistically significant already by day 64, a very robust responder analysis, particularly looking at those subjects who are more involved and seeing that continuing improvement through week 24 after just 12 weeks of therapy is, I think, very meaningful in terms of the biology of how FB102 is working, really supporting some of the hypotheses that were generated by that mouse model data that we reviewed earlier.

So again, overall, another interesting point here, too, that I want to make is 84%, 84% of the FB102-treated subjects improved over that 24-week period following the 12-week treatment, none worsened, while in placebo, we had 27% or 3 out of 11 of those placebo subjects worsened. And I think that's another interesting point in addition to the summary I'm showing here of the data that we just described.

And so with that, I'd like to actually turn it over to Professor Rosmarin, again, very generous in his time in participating in the study as our independent central reviewer. But also just his expertise and perspective, I think, would be very helpful. So Professor Rosmarin would be -- I'm just going to turn it over to you if you wanted just to comment on some of the things that you saw in your general impressions of the data.

Thank you for the presentation and the time. So first, this study is a resounding success, and I'm going to explain why. As a dermatologist who treats vitiligo patients, I have 3 goals: One, I want to prevent progression; two, I want to repigment patients; and three, I want to be able to maintain them and maintain that repigmentation.

And amazingly, this Phase I presents evidence of all 3 for FB102. So first, for preventing progression, you just heard Paul say that there was no worsening of patients who were treated with FB102 at week 24 compared to their baseline. However, there were 3 who worsened on the placebo arm. This is notable and a key point that I think can even be further explored in later studies.

Second, I think Paul presented really well, and I think showing that there was definitive repigmentation with this mechanism of action, which was the primary goal of the study. And then the third concept for maintenance, there's also evidence. In fact, the patients aren't just maintaining off of treatment, they're actually improving even after drug is out of the patient's system, which is, again, consistent with the mechanism from what we saw from John Harris' mouse studies. So this is all amazing to see.

Now I also want to comment that the Phase II for me has been derisked, given the design and the execution of the Phase I. This Phase I was almost like a Phase II. And I'm confident we'll see positive results in a Phase II. First, this was placebo-controlled, which is important to give us confidence. As Paul mentioned, in the upadacitinib and povorcitinib Phase II, the crossover arms that were no longer placebo-controlled had about double the efficacy when -- as compared when the study was placebo-controlled. So it's very helpful and important to have that placebo arm.

Second, the repigmentation is statistically significant even at week 9 here. Usually, we think of JAK inhibitors as extremely powerful and rapid. And what we're seeing is even a week 9 improvement in a Phase Ib, that to me is very impressive. Further, I have confidence in the Phase II because where -- if patients are treated throughout the 24-week period or later and not stopped at just week 12, that also has potential to improve efficacy. Paul also showed the more severe patients do better with that FVASI 0.75, or more at baseline, which also can be potentially leveraged in future studies.

Now I always like to comment on safety. So with the caveat that N is small, and we won't fully know until a Phase III, the safety is also looking good so far, and I'm optimistic given the targeted nature. So my final comment is that with all the available data we have for treating vitiligo systemically, this would be my first option. And I think my colleagues will also view this as their preferred agents as well.

That was excellent Professor Rosmarin. Thank you much for your perspective. Really appreciate that and for being our central reviewer. Parilla, I would like to turn it over to you if there's any questions in the queue.

[Operator Instructions] With that, your first question comes from the line of Yatin Suneja with Guggenheim.

Excellent results. Maybe 3 quick questions for me, if I may. So the first one is around the cutoff of 0.75. What is the relevance of that? Is there a meaningful difference between a cutoff of 0.5 versus 0.75? So that's one.

Second question is -- and that question is also for the KOL, if they can opine on this disease-modifying or the deepening of effect that we are seeing post treatment. Do we see that with JAK inhibitors or things that are available right now, whether it's the oral JAKs or the topical JAKs?

And then maybe a question for the company. I mean, we have recently seen a data from IL-15. Your mechanism is more -- it's a dual mechanism. So could you maybe talk about the benefit that we might be seeing here from the IL-2 arm?

Great. Well, thank you very much. I'll take that. I'll take the first question, and then we'll get Professor Rosmarin's perspective as well. I think it gets to the point that I was making during the call, first of all, thank you for dialing in, and thank you for acknowledging that it's really, really stunning results. I was a little bit blown away myself when I saw them.

But the cutoff, I think, is important because that really involves a substantial portion of the face that's depigmented. So again, 1/4 of the face would just be below the lower islet all the way through the mid-section and the entire chief. So that's a very extensive level of involvement. And if you have smaller levels of involvement, less involvement, you can have fluctuations, placebo fluctuations that would give you an impression of a responder in FVASI50 and FVASI75 when in fact, there was really less absolute surface area repigmentation going on.

So it's -- these patients that would have much mental health, emotional issues with extensive depigmentation on the face, and they were able to show that we get a very substantial repigmentation in those subjects.

On the IL-15, I'll let Professor Rosmarin comment on that and also on the disease modification. Maybe Professor Rosmarin, you could provide your perspective on that 0.75 cutoff and around the disease modification results we're seeing here relative to JAK inhibitors, oral and topical. And then also maybe your thoughts on the IL-15 data and how that compares to what we presented here.

Yes. So first, I agree with Paul's comments on the meaning of the FVASI 0.75 cutoff. That -- first, the reason why it's helpful to present is that it gets further evidence. This is not due to placebo fluctuations or fluctuations due to having a smaller baseline involvement to start. You're seeing that improvement is happening for the patients who are more severe. So I think that that's part of the meaning and the relevance to Paul presenting that data.

In regards to the deepening of the effect, that's, again, very impressive to see here. In terms of JAK inhibitors for both -- so for the topical primarily, we really don't have oral data that from an RCT yet, but we do have anecdotal evidence. For JAK inhibitors orally, we know that after some time, the patients start to depigment again once they're stopped. There isn't anything published about a deepening of response with those JAK inhibitors, either oral or topically. The best data we have is from the topical that some patients can help -- can maintain off of treatment, but not have this deepening effect.

And lastly, I do like the CD122 mechanism because you do have the IL-2 blockade along with the IL-15 and IL-2 is involved with the pathogenesis. So again, what matters is what we see in the clinical trial results. So we'll need more data to truly understand how important that is. But I do view it as helpful mechanistically from what we know.

Great. Thanks Professor Rosmarin. I just want to add to that last point as well. I mean the tissue resident memory T cells, the CD8-positive cytotoxic T cells in part driven by IL-15, but the CD4 positive T cells as well are involved in the IL-2 release that helps to signal for the activation of those pathogenic T cells that are in the skin, the tissue resident memory T cells. And so by blocking that, I think that in itself, I think, could have a significant impact on this improvement and durability that we're seeing here differentiated from IL-15.

So I do think it's very important to have both the IL-2 and the IL-15. I highlighted the data that was shown with high-dose IL-2 that subjects that didn't even have vitiligo previously, the IL-2 actually caused vitiligo in those subjects who are on cancer therapy, high-dose IL-2 for their cancer therapy. So very clear implication of IL-2 in vitiligo, but also in that tissue resident memory T cell and the impact and potential for FB102 and CD122 in durability and improvement beyond stopping therapy.

And the next question comes from the line of Gavin Clark-Gartner with Evercore ISI.

Great to see this data. I have a couple of questions. I'll go one by one now. Just first on the population severity. So I appreciate that about half of the patients in the study had over 0.75 FVASI involvement. Do you know what the mean FVASI was either across the whole study or in the subgroup or anything about BSA involvement?

Yes. I don't have that number right in front of me right now. But again, it would have been between that 0.5 and 0.75 is where the overall would have been brought up by that 0.75. It was -- I'll get back to you on that. I don't have that right in front of me right now.

Okay. Great. And I guess this question might be for you, Paul or for Dr. Rosmarin. I was surprised to see that in the subset of patients with higher FVASI involvement, there was deeper responses. But looking at a lot of other vitiligo studies, you kind of see the opposite of that trend. So I'm curious if you guys have any hypothesis for why this was the case.

Again, I think that it just shows the level of activity of FB102. It was interesting looking at the pattern of the repigmentation as well. I think you saw it in that image. The pattern of the depigmentation wasn't really coming in from the outside the borders out, in which case, you might think that a lower surface -- excuse me, a lower FVASI, a lower FVASI would show a better response because you're coming in from the periphery and this -- the edges relative to that surface area would be greater, so you'd actually get better involvement.

But actually, what we were seeing and again, sort of hinted by that image pretty consistent as well and Professor Rosmarin can comment on this, is that the repigmentation was occurring throughout the depigmented zone. It wasn't necessarily coming from the outside in. And so I think that is a big contributor to why this more extensive involvement in terms of the baseline FVASI we're showing these better results. But Professor Rosmarin, what's your perspective?

Yes. So we haven't -- so the data that we really have is mostly from the TRuE-V1, TRuE-V2 rux cream studies and that have published on dividing it, the baseline FVASI from 1 or less or is it 1.5 or less or 1.5 or more. So there is that breakdown. And we do not see a lower response with the higher severity, but we do see a lower placebo response in that population.

So again, I think the key point here is that when you're looking at the -- it gives you more confidence this is a true effect. This is not going to be a negative Phase II. It's -- if you can improve the more severe patients, those are less likely to improve on their own. This is less likely to be due to placebo. To me, that's what I think the takeaway is from that result.

Yes, that's really helpful. And Paul, what's the difference between Cohort A and B?

Yes. We just -- so Cohort B -- so we haven't defined -- we previously disclosed that we had the dosing cohort with the maintenance every 3 weeks at 3 mg per kg. There was a lot of interest and demand in the study. We opened a second cohort just to look at some other dosing options. And for proprietary reasons, we're not disclosing what that was. But the 2 cohorts, as you saw by the FVASI improvement at week 24 performed pretty similarly.

And the next question comes from the line of Yaron Werber with TD Cowen.

Congrats on the data. So maybe, yes, just a follow-up on Gavin's question. Any sense is arm is Cohort A or Cohort B will be taking forward? And are you testing either of those in the current celiac study?

Yes. Look, we -- first of all, I would say your point about the celiac study is an interesting one. I think that these results are really encouraging. I'd say, personally, I thought that vitiligo is going to be a pretty tough area and to see these impressive results just shows the level of activity of FB102. We've shown the Phase Ib celiac data really impressive, particularly around the IELs, which to me kind of informed this study, right? The IELs are the intraepithelial lymphocytes that were measured from the histology in the celiac study. I think those are exactly the same dysfunctional cells that become autoreactive in vitiligo and alopecia.

So I would also say that I think now we have the celiac data, we have this data. I think it reads through very positively to alopecia. In terms of the dosing, we've looked at different doses. And again, just for proprietary reasons, we're not going to say exactly what that was, but very consistent. They're very consistent across the studies.

Okay. The -- for the FVASI data -- for the -- I'm sorry, the FVASI50 and 75, did those hit stat sig or were those just underpowered?

Yes, they were underpowered. This is a really small study. And when you -- I think you used like a Fisher's exact test. And so you're looking at 23% in the active arm versus 0, on a study that's this small where you've got 17 and 4 or even 32 and 10 that with those -- with that Fisher's exact test on those small numbers, it's hard. But very strong trends there, not -- in fact, one of them was right around 0.5 (sic) [ 0.05 ].

Okay. And when you're looking at the FVASI50 and 75, you're looking at the full ITT...

Yes, yes, yes. No, actually -- let me clarify that, right? So the intent to treat and the efficacy evaluable had the exact same active in it. The only difference between intent to treat and efficacy valuable is that there was one placebo subject who got much worse, right, got much worse. And so first of all, by protocol defined efficacy evaluable, that individual had facial hair. The reason they had facial hair, I think, is because they were getting so much worse that they decided to grow facial hair to try to cover it up.

But that's the difference. So that's the only one subject that came out, and that made it a harder comparison. So if we would have included it in intent to treat, well, then the placebo response rate would have been lower because there would have been an N of 11, not an N of 10, but there is no difference in the active arm.

And so can you put that in context? Because I think in the Teva study, they looked at 4 out of 19 to get their 21% FVASI75. But I think that study had actually 38 patients, [ were they ] doing 4 out of 38? Can you maybe explain that, what that means?

Yes, absolutely. Well, I think that, for example, in -- if you look at our study, again, the 12% on the 32 came out to 4 subjects that were positive on the active arm. And most of those, if you look then again at the more extensively involved, those -- all of them were more extensively involved, and I showed you a picture of that.

So again, I think that our results are very robust. I think you're right. If you take the implied 4 responders, now I'd be interested in Professor Rosmarin's comments on this. I don't want to speak negatively about other companies, but I did look at their slide deck, and it was a bit hard. I mean, I think conservatively, if you said 4 out of 38, I know that there was sort of an or in between their FVASI 0.5 and their TVASI greater than 5. So there might have been fewer subjects in there. But without having disclosed that, it would seem that their number is closer to probably 4 out of 38.

So again, I'm pretty pleased with the results we have and 4 out of 17 on those who are more extensive. So every one of those responders, every one of those FVASI75 that got better than 75% improvement had very extensive involvement. So there wasn't the subjects in there that just had maybe a quarter size depigmentation and had a fluctuation in that quarter size depigmentation. And on paper, they hit one of these responder endpoints. These were extensively involved that showed great improvement.

Professor Rosmarin, what are your thoughts -- Yes, I just wanted to reach out and see if Professor Rosmarin has some thoughts on that Teva data.

Yes. So for the Teva, I think, first, they were not designed like a -- this study from Forte was more designed like a Phase II. So you can -- there's more data here that's presented and more that can be read into the information. For Teva, I think we have to be more cautious. And for Phase I, we're trying to show -- I think the right takeaway from the Teva data is that the mechanism does work. And I think that's the main takeaway there. I think it's hard to read into the efficacy data for how well it works for several reasons.

One is the design. It did not have a placebo control. Further, it was a completer analysis rather than intention to treat. And I think you have to be very careful making judgments on comparisons and efficacy. Now in general, from the TVASI50 and the FVASI75 tend to correlate pretty closely, with the TVASI50 typically trailing slightly the FVASI75. So the fact that the TVASI50 was 7% tells me that, well, it's possible that the FVASI75 in future studies may be just a little around there or a little bit more than that. So I think there could be a big spread in efficacy from what was presented.

And again, that wasn't the goal of their Phase I. Their goal was, again, to show some safety, and they showed some proof of principle in that population that there can be repigmentation. But again, I don't think we can take away how well it worked from their data.

Right. And -- but Paul, your valuable population is either FVASI more than 0.5 or TVASI equal to greater than 5, right? So it's the same.

Whose -- no, no. I mean we enrolled subjects that had the BSA, I think it was greater than 0.5 -- that had greater than 0.5. BSA, the actual BSA enrollment was pretty extensive. We haven't highlighted exactly what the criteria was. But again, over half of these subjects had extensive involvement.

So I think you can see here that, again, we're taking all 32, and it's 4 out of 32 for 12.5% FVASI75, and it turns out that every one of those 4 responders were extensively involved. And so if you take those 0.75, the ones are extensively involved, it's 4 out of the 17 that had 0.75 baseline or more on the active and that's the 23.5%. So I think we've been -- I think it's abundantly clear the activity we're showing here.

And that concludes our question-and-answer session. I would like to hand it back to Paul Wagner for closing remarks.

Excellent. Well, thank you so much, Professor Rosmarin, for joining us on the call. We really appreciate your perspective and your insights. And I also want to congratulate the entire team that I work alongside here at Forte. They've been putting in tremendous effort. And I know it's really satisfying for them to see these results in the context of all that hard work. So thank you all for that.

So just -- I'm just going to summarize here very quickly. This is a double-blind, placebo-controlled study. We demonstrated, I think, impressive activity, statistically significant improvement in the vitiligo, the primary endpoint from baseline to week 24, statistically significant responses that are happening early, robust responder analysis, particularly in those more involved, not just durability after stopping therapy, but continuing to see improvement through week 24 after 12 weeks of treatment and consistently strong safety profile.

So we put a lot of effort into designing FB102 in order to make sure that we optimize the blockade of CD122 to modulate both IL-2 and IL-15 dependent pathogenic T cell biology and preserve the regulatory T cells. I think by optimizing the blockade of the intermediate affinity receptor for IL-2 and IL-15, FB102 may have a broader immune pathway modulation than IL-15 blockade alone. And by not blocking the high-affinity IL-2 receptor. Again, it was an extensive design effort. FB102 clinically appears to avoid regulatory T cell modulation that can occur with overly potent CD122 inhibition.

So I want to make one final point here, and that is the data from this Ib vitiligo study and the previously reported Ib trial in celiac disease, reinforced the activity and the broad potential for FB102 and we're looking forward to reading out the Phase II celiac disease study imminently. So that study is going to read out very soon. And I think based on the data we presented here and the Ib celiac data we previously disclosed, I remain very optimistic, and I'm looking forward to that readout.

So thank you again for joining. And hopefully, in the not-too-distant future, we'll be on another call like this talking about the celiac study. Thank you again.

Thank you. And this concludes today's conference call. Thank you all for joining. You may now disconnect.