Good morning. Good afternoon. Welcome to the R&D webcast of MoonLake Immunotherapeutics. My name is Matthias Bodenstedt. I'm the Chief Financial Officer of MoonLake, and I'm joined here by Jorge Santos da Silva, our CEO, and Kristian Reich, our CSO. We're very excited today to have you here to present our MIRA phase II 24 weeks data in HS. And before we get there, here, a little preview over the agenda for today. Those of you that joined our webcast in the end of June will be familiar with the setup.
So after I finish the introduction, Jorge will say a few introductory words, then Kristian will go in detail through the 24 weeks data of the MIRA study, and then Jorge will summarize the findings, put them a bit more into context, and in the end, we will have a bit of time to answer a couple of questions that you can raise through the webcast function. Before we get there, two important housekeeping items. One of them that you see on the screen right now is our disclaimer on forward-looking statements, so let me leave it here for a moment. And then a couple of logistical items here. So yes, please take note of the disclaimer. In terms of Q&A, I already mentioned it, you can raise your questions through the Q&A function that you see on the screen. So please raise your questions there.
We will try to address as many as possible in the end of this session. Also, please note that the presentation document will be available on our IR website, and also a replay of this webcast will be made available after the session. If you have any technical issues, please also use the Q&A function, and for other requests, you see the email address is listed here on the page. Now, without further ado, let me hand over to Jorge. Over to you.
Thank you, Matthias. From my side, a very warm welcome to the many of you that are connected to this webcast. We're very happy to have this session today and take you through the full data set from the MIRA trial, which we press released yesterday. As Matthias mentioned, I will take us through a brief introduction to remind ourselves of the overall data already available, how do we see it in the context of the recent EADV, and a summary of how our data stacks up versus the bar that we put ourselves in our last Capital Market Day in September. Reminder to all of you of the MIRA design. As you remember, the trial had a Part A and a Part B.
Part A, as you see there, towards the left of the chart, was presented by us in an R&D Day in June with excellent data. As you saw, this data was recapped again last week at the European Dermatology Meeting. You saw the fantastic group of KOLs that is involved with analyzing and discussing this data publicly. In our eyes, it also put a very strong peer-reviewed scientific tick to our data, which obviously we're proud of, but hopefully also perhaps silences some naysayers out there throwing shadow on this data. What we are going to discuss today is part B, which is in the middle of your chart. It's the 24-week data.
I remind you that as we move from Part A to Part B, group one and group two, so the two doses that we had selected for phase II for sonelokimab were continued all the way to week 24. Now, in the full maintenance monthly dose, group three, the placebos, were crossed over to either 120 mg or the 240 mg doses, so that we could determine if what we observed in the dose behavior in the first 12 weeks is indeed what we should expect. And group four, the small adalimumab arm that you see in the bottom, all those patients were crossed to sonelokimab, to the 240 mg dose, as you well know.
Here, the critical question is, do the non-responders of SLT, now, once they switch to the therapy with sonelokimab, do they reach sonelokimab-like levels? As you remember, we had a very successful primary analysis. We met the primary endpoint of HiSCR 75 at week 12. Go check the details of all the EADV data. We're still the first and only company that has a primary endpoint as a HiSCR 75, and you can still see that our delta to placebo continues on a pivotal-to-pivotal design comparison, continues to be around 30%. You remember the 29% we showed in June. So we continue to be the better performing drug.
Of course, we're very happy that small MoonLake inspired all the players in the field to spend their summer doing the post- hoc analysis to be able to report HiSCR 75. So we're very happy that the whole field is indeed moving to higher bars. As you remember, also, HiSCR 50, which is the primary endpoint of most of our competitors, we continue to be several-fold better, especially on the delta to placebo. Again, there was nothing to change this at EADV. You remember we talked about this, perhaps less discussed publicly, but very importantly for us and patients and physicians, we started seeing a hint of deeper responses.
So we started to see signals on HiSCR90 already at week 12, as well as remission of specific lesions, abscesses and nodules, draining tunnels, together with very strong reported outcomes. Again, go back to all the EADV data from last week. We didn't see much commentary on these, on these metrics from any of our competitors, and the same applies to something that you guys know was very dear to us in June and continues to be dear to us, which is the fact that our drug seems to have a very strong impact in the most important lesions in this disease, which are the tunnels, as measured by particular scores like IHS4, morphology, et cetera. And of course, we showed a very favorable safety profile.
Obviously, between June and now, other smaller molecules trying to hit the IL-17 pathway also struggled. So I would argue that our data aged extremely well, from June to today. Just a very, very quick visual recap. You remember, these were the deltas, on HiSCR75 on the left. That's probably the most meaningful, data in comparison to others. By the way, the analysis is as stringent as can be. Same for HiSCR50, as I mentioned. I also want to remind you that this continues to be images that you do not see from anyone else.
And we will show you more today, both on scores that relate to tunnels, as you see on the left side with the IHS4, and direct imaging for our separate study, when we look at the morphology of tunnels. And as those of you that attended the EADV last week, as I said, the data was peer-reviewed and presented at a scientific conference by a very strong group of key opinion leaders. Obviously, all the confirmations on the depth of response, on the safety profile, and on this idea that matching a great MOA, like IL-17A and IL-17F inhibition together with molecular characteristics that are unique, small Nanobody with an antibody binding domain, continues to capture the excitement of the community.
The fact, as you heard on stage, that this is a phase II designed pivotally, right? That's very important to continue underlining and making sure that people understand this. Obviously, a few scores, especially on the patient-reported outcomes, that were new, but that confirmed what we already had shown, at week 12. So if you take the totality of evidence that is accumulating already as of last week, sonelokimab continues to have a very differentiated profile in HS. Based on this, we set ourselves a pretty high bar in September when we presented our capital markets day.
We asked, "What are the criteria by which we can judge if our 24-week data is successful?" One was, can we show that we maintained the response on HiSCR 75 from week 12, or that we maybe even go a little bit higher than that? And we were pleased to see that investors share their expectations as either keep that bar or perhaps add 5 more points to it, and that would be a phenomenal, phenomenal result for patients. Another criteria is, can we see greater depth of response? We saw a hint of a 90% improvements in some scores. Can we see this going further now that we're treating patients with our monthly dose?
Number three, very important for us and for KOLs and physicians, do we see an improved score when we really talk about remission of certain lesions? And again, are the patients still happy with what they're getting, or are they even getting happier? And do they report that quality of life, that pain improvement even further as we go to the 24 weeks? Very important, mostly for investors, can we confirm that the 120 mg dose is the winning dose? Can we replicate with the placebo crossovers, the data that we saw in the first 12 weeks? And can we even corroborate that further with other analysis that we now have at 24 weeks, such as the pharmacokinetic data?
Another criteria we would want to look at is, what is the effect on the TNF patients, especially those that do not reach HiSCR 75 at week 12, which, as you all know, is the majority of patients that initiate therapy under Humira. And obviously, do we continue to see a favorable safety profile with all transient candida, no discontinuations associated with these items, et cetera. As we announced yesterday through our press release, we believe that the results are extremely exciting, and we actually hit all criteria. On the HiSCR 75, once we switched to the monthly dose, up to 50%, 57% of patients reach HiSCR 75, again, with a monthly dose in a very similar analysis than any of our competitors has done in the past.
That's, of course, an increase of over 10 percentage points, no matter how and what analysis you decide to do between Part A and Part B. We saw around 40% of patients reaching scores like HiSCR90 and IHS4- 90, which again, tells you that also on the deep responses, that improvement is being observed with our very convenient 1 ml monthly dose. Very exciting for us, in a trial with very low discontinuation rate, and we will talk about this. We see one in every four patients reaching inflammatory remission. Inflammatory remission, IHS4- 100, no detectable abscesses, no detectable nodules, no detectable draining tunnels, right?
The lesions are not there or are not visible, and in fact, the patients, 40% or more, report that they feel that their disease is absent or minimal using the PGIS score. Take a stop there and think, these are hidradenitis suppurativa patients at six months, reporting that they feel that their disease is absent or minimal. We think this is extraordinary. Very importantly, so that we continue accumulating evidence there, the 120 mg is the best performing dose. We replicated in the crossovers what you saw on the first 12 weeks. If anything, as K ristian will show you, the 120 milligram even had a little bit more response than we had in the first 12 weeks. So in our, in our minds, the road is starting to run short for the naysayers when it comes to our dose.
Finally, indeed, the TNF patients that couldn't reach the response of HiSCR75 at week 12, which as you know, is the majority, around 70%. Once they were switched to sonelokimab, in this case, the 240 mg dose, they reached a sonelokimab-like response after 12 weeks. Indicating that although the sample is very small, as we always tell you, it gives you an indication that switching is advantageous for the patients, apart from the fact that, of course, at 24 weeks, we just have better responses than you would see with PIONEER. And absolutely no new signals of note in the safety profile, it still looks extremely favorable. And very importantly, very importantly, the discontinuation rate of MIRA is under 10%.
So this is very far from JAKs and ozanimod, and all these other very large discontinuation rates. The discontinuation rate is below 10%. So every time, if you spread this through the arms, it's only a couple of patients in every arm. So no matter how you do the comparison between Part A and Part B, whatever metric you use as observed, NRIs, et cetera, the numbers are very similar. Okay? I've highlighted a few points and underlined them verbally here, but I now give it to Kristian to take us through the details of the data.
Yeah. Thank you very much, Jorge. I'm also very excited to be here.
I think we had a little technical glitch there, but I think we're back. Kristian, you were gonna start with the results.
Absolutely. Probably data too exciting for the technical platform. So what I was trying to get to is I will walk you now through the details behind the messages that you heard from Jorge. And I think the data will generate what we feel is an unequivocal view on the positioning of sonelokimab in HS. Let me start by showing you the patient disposition. And you have seen from competitors, HS patients are very sick. So normally, especially when you add significant anti-inflammatory drugs, you see dropout rates going up, and of course, this has an impact not only on the safety, but also an impact on the quality of the statistical readouts that you can do. So very importantly, among all sonelokimab-exposed patients, exposed for 24 weeks, the discontinuation rate, less than 10%.
Number 1, this already shows you the good safety and tolerance of sonelokimab in this complicated patient population. And secondly, as Jorge said, you know that the statistical methods primarily differ in the way they impute missing data. If you have a very low rate of missing data, that means that all statistical analysis is actually very close together and will show similar results. And this is, again, I think, unlike other data where you have high dropout rates. When we talk to analysts and knowing that sonelokimab at week 8 would go from every other week to monthly dosing, there was a question: Can you even maintain the response? Best case scenario, can you do what bimekizumab was able to do? So elevate the HiSCR75, around 5%, between week 12 and week 24.
Delighted to share with you here that we can actually do even more. Whatever analysis you take, you see a 10+% in HiSCR75 between week 12 and week 24, and we feel this is clearly one of the best data that has ever been shown. Interestingly, but not unexpected, the higher you go, the higher is the elevation between week 12 and week 24. You see here, when we look at HiSCR90 response, it's a +14%. Again, whatever relevant analysis you do, you see a 14+% in delta HiSCR90 between week 12 and week 24. HiSCR100. We have been asked to show HiSCR100, so at week 24, you see 30% HiSCR100.
Just to put this in perspective with valid data, it takes bimekizumab 48 weeks to get 30% of the patients to a HiSCR100, but sonelokimab 120 mg can do it within half the time, 24 weeks, as a first indication that when it comes to these very high levels of response, and of course, this is what we want to see from an innovative drug, that there is no ceiling yet. And we do see more room for improvement, especially with these high outcomes, even beyond week 24. Important question, the dose. Can we replicate? Can we further validate the dose response pattern we shared with you in Part A?
Just to remind you, the 120 mg, clearly coming out on top, had the highest absolute number compared to placebo, not only of HiSCR75, but also of HiSCR50. You remember this group three, these are the placebo patients that are re-randomized and now are either exposed to 120 mg or to 140 mg. So this group acts like an internal control. You see here, this is not copy-paste from Part A. This is just showing to you that those patients that cross over from placebo to 120 mg, dark blue, to 140 mg, light blue, they absolutely replicate the dose response pattern that we saw in Part A, with patients starting on 120 mg or 240 mg from baseline. Second important finding here, just look at this delta.
We were always hearing, "Oh, you're 29, were you just lucky? Is your true HiSCR7 5 delta should not be somewhere between 240 mg and 120 mg." No, the 120 mg is the dose you need to look at. And if you see the results generated here in the patients that cross over to 120 mg, why is our true delta not the mixture between these two? It could easily be above 30%, just to share with you how we view the potential of the 120 mg. We also heard maybe the 120 mg works well in the overall patient population, but what in the so-called difficult to treat, high Hurley stage 3, no concomitant antibiotic use, all the smokers, knowing that smoking is a trigger factor for HS.
What about those patients that have a very high baseline count of nodules and abscesses? So we did this subgroup analysis, and the difficult to treat, you see HiSCR50 on the left, see HiSCR75 on the right, and again, a very clear picture. When you look at deltas to placebo, this is what we show here. In all these difficult to treat subgroups, the 120 comes out on top. And by the way, and I'm not showing this here, also, when we put in the 240 mg, in most of these difficult to treat subgroup analysis, the 120 mg continues to be the winning dose. And I think this is very important when we later make a suggestion to the FDA, what dose do we want to develop now in phase III?
Jorge already said, and we remind you of all these discussions that we had about being small and albumin binding. It's very clear that blocking IL-17A and IL-17F is the winning MOA in HS. The question is, what is the best way to deliver this MOA? We were always discussing that in a disease like HS, where you have deep dermal structures, the tunnels, you probably really need to deliver this MOA with a molecule that makes sure that you get enough drug deep in the tissue, around the tunnels, where you have scars. And we were always thinking that we have a significant advantage there, delivering this MOA with our nanobody. We see this actually reflected in very good outcomes whenever we look at outcomes that include tunnels.
Now, I remind you that the IHS4 is one of the established scores that not only quantifies the reduction of nodules and abscesses, as the HiSCR does, but also includes a reflection on the reduction of draining tunnels. So it's important for us to see that our already fantastic data at week 12 is further increasing in the second half, in Part B of the study. To palpate, to clinically evaluate draining tunnels requires some art. So this is one reason why we decided to include a smaller ultrasound substudy, but to generate the first unequivocal data on, is it true that our smaller molecule is really doing something with the tunnels beyond the clinical scores? Jorge shared with you one example from a patient that received 120 mg. Here's another example from a patient that received 240 mg.
You see this large tunnel at baseline. You see how this tunnel is shrinking already at week 12. You see that there's further significant morphological improvement in Part B of the study. Another thing you can measure with ultrasound is the peritunnel blood flow that relates to the inflammatory reaction around the tunnels, the increased blood flow in the blood vessels. You can measure this and quantify this with Doppler. You actually see that in addition to the shrinking of the tunnel, this peritunnel inflammation is dramatically decreased by week 12 and is actually absent at week 24. So we continue to see very strong evidence that the drug is doing something specifically with these deep dermal tunnels that, as you will understand, are the most meaningful clinical phenotype for patients.
When you want to innovate treatment of a disease, you need to be able to show that you do something that other drugs, that other drugs have not been able to do. We feel very strongly that one of these elements is, can we show that more patients achieve very high levels of response? We show you here AN100, how many patients do no longer have any abscesses or nodules. We see that with 120 mg, and again, you see this dose response pattern. It's always the 120 mg that wins. You see a 15 percentage point increase between the week 12 and the 24-week outcome. If you look at DT100, how many patients have no longer any draining tunnel? Not one new tunnel, but no longer any draining tunnel.
Again, you see an increase, and again, you see that the 120 milligram comes out on top. Very reassuring that if we now look at the placebo crossover patients, that they're also in these first 12 weeks, and I remind you, they get a new induction dose. We really give them what the patients received in Part A. You see a rapid uptake of the response when it comes to AN100 and DT100. Clearly, sonelokimab is a very fast-acting drug, but the longer you give, especially for these very high levels of response, you see a further increase. I will have to share with you that this is my favorite slide, and I believe it's the KOL's favorite slide, and let me explain to you why.
You need to be able to reduce all inflammatory lesions in patients, the inflammatory lesions being nodules, abscesses, and draining tunnels. You heard before, the only established score that really integrates the quantification of all these three lesions is the IHS4. 90 means 90% reduction in these three inflammatory lesions. 100 means no longer any of these lesions is present in the same patients. We do not call this remission, because these poor patients will still have scars from previous surgery, from the disease. They may still have non-draining tunnels, but I think this is the highest possible outcome you can get to with an anti-inflammatory drug. We call this inflammatory remission. And again, and probably not surprising, even for a strong and fast-acting drug like sonelokimab, you need some time to bring patients to this inflammatory remission.
Very, very exciting to see that actually 1 out of 4 patients receives IHS4- 100. We now want everybody to show, not HiSCR1 00. That is boring. Let's now everybody show IHS4- 100. And that four out of 10 patients achieve IHS4- 90, I think speaks to itself, and it also tells you that more than 60% of patients that achieve a 90% improvement also actually get to complete inflammatory remission. So very, very high number of patients that get to a very deep response. Probably not surprising that these amazing clinical improvements correlate with what we think are amazing improvements in relevant patient-reported outcomes. This, for me, is one of the really relevant. The patient global impression of severity means that patients reflect on the severity of their HS, all the symptoms, the pain, the discomfort that they have.
This is integrated in the PGIS. We take a very high cut of the score. We only look at patients that say, "My disease, all of the symptoms related to HS, are either completely absent or only minimally present." This is what we show you here. And you see that 30% get there at week 12, but again, correlating, I think, with this further improvement in these high levels of outcomes that I showed you, it dramatically, dramatically goes up to over 40%. More than four out of 10 patients after half a year of treatment say, "My disease is only minimally present or completely absent," looking at all relevant symptoms related to HS. Again, I think a very important outcome. When we look at clinically relevant improvement in health-related quality of life, we shared with you this dramatic and early improvement of clinically relevant DHI improvement.
Again, if anything, this goes up further. The same with pain. We shared with you that sonelokimab has this amazing early effect on pain reduction, even before you see a full reduction of symptoms. Fantastic to see that in the next 12 weeks, after week 12, so week 12 to 24, this response is not only maintained, but with a 120 mg, even increases further. Safety. You see here the safety of the sonelokimab exposed patients in Part A. You see here the safety and put side by side with the placebo and the adalimumab safety, and you see here the full 24-week safety data of patients continuously exposed to 120 mg and 240 mg. First message, no new safety signal detected. The very favorable benefit risk profile that we shared in Part A replicated in Part B.
Second message, if you look at oral candida, you do see that there is some, a little bit of a dose response. We shared this with you, four cases in Part A, eight cases with the 240 mg, and you see similar, more similar number of more cases that develop oral candida over time. I will speak to candida in a minute, but we have more and more evidence that the candida signal that we see here is really not an issue at all for patients that receive sonelokimab. Importantly, you see a lot of zeros here, important zeros. You see no case of inflammatory bowel disease. You see no major adverse cardiovascular event. We only had, in contrast to competitors, we only had typical, unproblematic mAb-like injection site reactions.
I can already share with you that not a single patient, zero patient, permanently discontinued due to candida. The candida, that the safety signals that we saw in those arms after crossover, so adalimumab to sonelokimab, placebo to sonelokimab, very similar to the safety signals that are shown here. Very reassuring safety, overall safety profile for sonelokimab. Now, there was some discussion on the candida. Actually, the KOLs can no longer hear this. When we ask KOLs, "you want to talk about candida?" They say, "don't talk about candida. It's not an issue in this disease with a drug like sonelokimab." Let's but MoonLake always tries to give you the full transparency, so let's look at candida in the whole 24-week data package. First of all, these percentages that you see, 6%, these are cumulative prevalences.
Doesn't mean that at week 24, 12% of patients have candida, because for the vast majority of patients, as you can see here, despite staying on the drug, this is a once in their lifetime, once in their study participation event, that the oral candida comes, you get topical therapy, the oral candida goes away, you stay on the drug, it does not come back. It's not like once candida, you remain a high susceptibility for candida. That is clearly not the case. And actually, only two patients in the whole study had a recurrent candida event, and all this recurrent candida was again only oral. As I said earlier, no case led to permanent discontinuation, and I think this is also—this is very important. Do you have an adverse event? Do you have an injection site reaction?
Do you have anything that really makes patients stopping the drug, that tells you something about the limited validity, viability of your drug in the market? We had not a single case permanently discontinuing because of candida. We don't want to downplay this. As you would expect with an MOA like we have here, you see a candida signal, but I think this data clearly supports that is not an issue for the patients with HS that get the treatment with sonelokimab and this session, this improvement that we just shared with you. I know that many of you struggled with understanding what was this adalimumab arm that MoonLake decided to put in this study. So allow me to try again. As you know, many have struggled to produce valid data in phase II .
I think there was even the question about how can we interpret data that was produced in phase II? As one of the several measures that MoonLake decided to integrate into their study in order to produce valid and phase three reproducible results, as one of the many measures, we decided to put in an adalimumab anchor arm. It's not a comparator arm. Comparison means statistical significance. You need to have 200 patients in an arm. Clearly, you cannot really do this in phase II. What we want to see, can we, in our study, replicate the results with adalimumab, by the way, the only drug that had published phase three results when we designed the study, can we replicate the phase three findings of adalimumab in this arm? We could exactly replicate the PIONEER II data, as we already told you.
That means we have validated our protocol, our design, our patient population. We've ultimately validated the findings I just shared with you. We have really produced evidence against compression of this data going from phase II to phase III. Of course, the arm was very small, 33 patients. My CFO always tells me, "one patient twisting up or down changes results by 6%, 7%. Don't do comparisons." I will not do comparisons, Matthias. But of course, you want to get a feeling for a possible trend, and we decided to give you this trend in a way a payer would look at data between two drugs used for the treatment of HS. If one drug is 30%, the other is 60%, it's not 30% more patients that get the response, it's a 100% more patients that get the response.
And this is exactly what we decided to show you. Across a broad range of relevant outcomes, sonelokimab 120 mg indeed showed a trend that you get more patients to these responses with sonelokimab compared to adalimumab. That's all we wanted to share. What is probably more relevant, and now coming back to the 24-week data, number one, if you have failed to achieve a HiSCR75 response to adalimumab, will you be able to achieve the response after switching to sonelokimab? And if I would redesign the study today, I would probably switch them to the 120 mg. But we decided, we planned this, "Let's give it all we have." So they were crossed over to 240 mg. But importantly, this is the response at week 12 of patients that started on 240 mg.
This is the response of patients that had no HiSCR7 5 response after 12th week of treatment to adalimumab, after crossover to 240 mg. So my interpretation is, and again, with all limitations of this small subgroup, it was completely irrelevant if the patients had a non-response to ada limumab before. They generated the same response that we saw in adalimumab-naive patients, if you will, in the first part of the study. That is important. It means that if a later in the market, if a patient is a non-responder to adalimumab, there's probably a high, high chance that this patient will be a response to sonelokimab. Second important finding: with adalimumab, which is a good drug in HS, but where it really struggles is to maintain responses over time, which, of course, for a chronic disease, is absolutely essential.
We remind you here of the PIONEER II data. If you look, if you ask the question, how many patients at week 24 are responders of those that achieved the response in the first place, already in 12 weeks, you can see that 40% of the patients lose the response. That is the problem with adalimumab. Sonelokimab does not have this problem. We have a completely different potential to maintain response in patients primarily responding to sonelokimab. Very interesting to see that bimekizumab shared data at the EADV. And again, sonelokimab seems to be one of the best drugs out there, even vis-à-vis bimekizumab, in maintaining the response in responding patients. Now, it gets very boring. Of course, it does not get boring, but let's share some PK data with you. In contrast to what mAbs have struggled with to generate-...
understandable PK data moving from psoriasis to HS. I remind you that bimekizumab, despite, despite giving double the dose, they only saw the, the trough levels that they found in psoriasis. So there's all a big question mark, what is going on in HS with mAbs? Our Nanobody does not share this problem. You see here the PK concentrations that we would have expected using our psoriasis model. The dots show you the real trough concentrations that we measured in our MIRA trial, and it absolutely matches. So the psoriasis model proved to be a viable model also for HS. Second, what you see here, and I'll come to this again in a minute. In contrast to mAbs, if we doubled our dose, you saw really trough levels going up. When we went from every other week to monthly dosing, you see trough levels going down.
But importantly, this probably explains why 120 mg is already the winning dose. Importantly, even with the 120 mg, you stay above the trough level that we know gives you the absolute optimal anti-inflammatory response in the tissue. A concentration that you probably only need when target levels are high during the induction therapy. And again, this is now the real data from the MIRA trial. The 120 mg, the 240 mg, is a logarithmic scale. You see how the higher dose converts into higher trough levels. You see how those patients that cross over from either placebo or adalimumab get to exactly the same peripheral levels. Again, you see there's this small decline in peripheral trough levels. Target levels will be down.
Now, you go from every other week to monthly because you need less sonelokimab to keep the disease under control, but even with 120 mg, the PK is absolutely fine. This explains to me, A, we have a very valid PK/PD. It explains to me why the 120 mg is already the optimal dose. And last but not least, just is the cherry on the whipped cream. I hope you enjoy how MoonLake always lets the pants down in these events. We show you all the data. We even show you immunogenicity. There are still many targeted therapies where I have never seen the immunogenicity in HS, so here is our immunogenicity data. We always said we have no clinically relevant immunogenicity.
This is showing you in patients with and without anti-drug antibodies, that the trough levels are absolutely the same, so the presence of ADA does not influence trough levels, and more importantly, it also does not affect the clinical response, because you see that more or less the curves are overlapping. So again, also from MIRA, a similar picture like from the psoriasis trial. With this Nanobody, there seems to be no clinically relevant immunogenicity. And with this, I hope I have convinced you that sonelokimab really has absolute fantastic data. The 24-week data, I think, quite significantly corroborates what we already saw at Part A, that this is a winning drug to treat HS. Jorge, back to you.
Thank you so much, Kristian. Hopefully, you all got those amazing details from the data package. A quick summary here. If we reflect back on what we just discussed, on what we talked at Capital Markets Days, different ones we had this year, at R&D days, at what we saw at ADV, I think we can clearly say that we're helping the field by setting a new bar here. If you think about all the research that we showed earlier in the year, a really unique molecule with a very clear MOA and very specific molecular characteristics.
As you just heard here, a really full data package, unusual for this time of development, I would argue, that MIRA shows us, and obviously a very positive optimal outcome as we start planning, and Kristian and his team start planning the further steps in development, the discussions with the FDA, et cetera. So of course, we're very, very excited about the potential that we're seeing here. There are obviously a couple of questions that are asked. For example, what does it all mean in terms of the potential, the value, of SLK? I would like to remind you of what we feel the opportunity is and how we're placed to capture this opportunity.
You remember when we started looking at this market, we looked at the perceived sales of adalimumab, which is somewhere around the 2 billion doses. We always tell you this is probably a big underestimation of the market, because as you know, this is all dynamic market. Only one-third of the patients really go for a full year of therapy, because otherwise they don't have response, and those then lose the response. So this is probably a very gross underestimation of what the market was already a year or two ago. And then, as we showed you previously, we tried to determine where will this market go. And as you know, we reached about a size of $10 billion within the next 10 years.
We really don't think that these are unreasonable numbers, and I tell you why. Number one, you remember that one of the key assumptions is that, in fact, the true prevalence of this disease is about 2%. The epidemiology data continues to accumulate to show this. We continue, and many of our competitors continue looking at real-world claims, and what you see in the real data is that the prevalence is indeed around the 2%... The other two big drivers of these numbers is that we believe that the diagnostic rate of this disease will go up in the next 10 years. We didn't assume anything unreasonable.
We just said, "Let's look at all the other immunology fields, including all the derm fields, and assume an average increase in diagnostic rate for all these diseases." We did the same for the use of biologics, as you see on the table below. We're not assuming anything unreasonable, and in fact, when we look at all the what's being published by the banks, what is being stated by Novartis, by UCB, by AbbVie itself, in terms of what is the opportunity in this disease, our numbers are actually not that different. Whether you call it $8 billion, $10 billion, $12 billion or any other many billion number, the important thing, of course, is that you have the winning molecule, and also that there are several molecules driving the market, because, of course, one is not enough.
What do we have here in the next few years driving this growth? We have the IL-17 inhibitors, the nanobody, and the antibody from us and from UCB respectively. You have Cosentyx, which you know is already approved here in Europe. You have AbbVie with the TNFs and the JAKs. You have Incyte with the JAKs. And, you know, perhaps in the future, we might also have secukinumab, we will see that. But certainly, a lot of molecules and great companies driving this market and helping it grow.
Of course, in the middle of all of this, or on top of all of this, is our Nanobody, which marries the best of both worlds in terms of the best molecular characteristics with the best MOA, and as, as we have shown, it has accumulated a data package that, again, at last week's EADV, we did not really see anybody challenge. Another question that we get asked: Will it compress? I think you've already talked about how we use the adalimumab arm in our phase II to control for that, but it's also important to clarify a few points. It is not correct that every phase III will compress versus phase II. I don't know where this has been stated, but this is not true, and we show you specific examples here.
You have several examples of molecules that did not replicate their phase III compared to their phase II results. The reason is quite simple, is that the protocol changed, and significant elements of that protocol, the types of patients, the doses being used, some of the admission criteria were different, and of course, those were not fully replicated. And that, and I'll come to that in a second, includes bimekizumab phase II, which people continue to like to quote. Bimekizumab itself, itself had a clinical trial where they replicated in phase III the results of phase II, which was in psoriasis, and because they did not change the protocol. In fact, as you see here on the right, the data is probably even better in phase III than in phase II.
So if you don't change the protocol, you're likely to replicate your data. It's not a rule that every phase III necessarily gets compressed. Specifically on bimekizumab phase II, we just saw an analyst report, again, harping on this point this morning. Let's put the facts on the table. What you see here on the left is all the key characteristics, and you can go and check them on the bimekizumab phase II. What you see in the middle column is what bimekizumab used in their phase III. In green, we labeled green the protocol elements that are designed as a pivotal trial, and in red, what is typically used for a proof of concept trial. What you see is that almost nothing, nothing was conserved between the phase II protocol and the phase III protocol.
No wonder the results are not going to be the same. Doses changed, analysis changed, cohort characteristics changed. You should not be surprised that, of course, the data changes. Now, what you see all the way here to the far right is the MIRA design, which is all pivotal, which is all replicated in the protocol we're currently preparing for the FDA, and where even in some cases, we use more stringent protocol designs, elements that are more stringent than bimekizumab. So for those that continue telling us that we should compare to bimekizumab phase II, hopefully, this is yet another example of why these comparisons make no sense. We even have been compared to, "Could you not be an example like Allakos?" Many investors will remember this situation. Again, the same story.
Different diseases, phase II is designed in one way, and then completely different in phase III. We're happy to share with you the details. So very low likelihood that our clinical data will compress in phase III. Very quickly, just to finish off, to leave some space for our questions. I think if we move on to what does it all mean to SLK, I think we can continue saying that the evidence is accumulating across multiple large inflammatory diseases, that the MOA that we work on and the type of molecule we have allow us to aim for the top position in solving these excruciating problems for many of these patients. We've had it in HS, we've showed you PSO, and soon enough, we'll be here to discuss psoriatic arthritis, and obviously a lot more in the future.
Again, a reminder to everybody, why is IL-17A and IL-17F this good at creating responses in clinical trials? And we believe that the reason is that there's a lot of targets upstream. Many of those are very familiar to you. There are many targets on the effectors downstream, but ultimately, a lot of our immunity and the different type of cells that drive it actually all signal through IL-17A and IL-17F. So this is a bottleneck that we're targeting with these drugs. And obviously, that's true for us and bimekizumab. We share this winning MOA. We are showing the highest responses, the arguably safer inhibition in many of these indications, and obviously there's only the two of us.
But we believe there are several evidence, and I think EADV is another example of that we are clearly differentiating. We have an elevated performance. We've reached the scores in times or in levels that we have not seen for bimekizumab, and Kristian pointed out several of them today. We've reached higher goals in our primary analysis. This is what we will go out to the market with, and we don't see that being challenged by bimekizumab. And of course, we have a very important point on convenience. I think it's important to underline again, all the data that you saw, all these improvement that you see towards 24 weeks is 1 ml being injected once per month.
Not every day, 2 pills, not injections every week, not 2 injections every other week, 1 ml once a month, and that matters for patients and for physicians. I think ultimately, in terms of positioning, what this means in our mind is that obviously there are different spaces to compete in, in immunology and inflammation. As you've seen before, we split the world, and many others do the same in type 1, type 2, and type 3 diseases. We believe, and I think the evidence continues to show us this, sonelokimab is likely the potential leader for this whole pillar of type 3 inflammation, which obviously includes many diseases. Where do we go from here? We've showed you the HS primary data. In June, as you know, Capital Markets Day and EADV have happened.
Today, we showed you the 24-week data, exactly when we told you that we would show it, with the results that, as you can see, we're extremely excited about and KOLs are very excited about. We will come soon enough to discuss about yet another indication. We plan to go for our FDA derm and the phase II meeting in December, so that we can start discussing with you all soon enough about what the catalysts are gonna be for next year. Obviously, we're expecting the 24 weeks PsA. We're expecting to start HS and PsA phase III. Obviously, another FDA and the phase II meeting on the rheumatology side, and we will be announcing new programs in due time.
We will be ready at the end of this year with a very large safety database and a very stable supply capacity, already ready for three indications for phase III. And as you can see here, and I'll just briefly go through this, but I will again want to be transparent with you. We have a very strong cash position, about $500 million, and all of this giving us plenty of runway to deliver on the elements that that we said that we would deliver. Maybe, Matthias, I will finish here, so let me allow some questions. I'll just leave this on the screen. I think you've seen this before. If anything, all these 5 bullet points continue to be underlined by our data.
Yeah. Thank you, Jorge, and in the interest of time, maybe we only get to a couple of questions, unfortunately. But I saw a few questions coming in still on the dose, so let me pick this one here. "Do you have shown new evidence to confirm 120 mg as the best dose in HS? Is that the dose that you will take forward in phase III?" Kind of question.
Yeah. So Matthias, I'll try to be very brief. Let's quickly look at the evidence. Part A, the 120 mg comes out on top. I showed you here that even if you go to complicated to these subgroups, the 120 mg comes out on top. If you continue giving the two doses, the 120 mg, even in the second part, comes out on top. Finally, if you cross over your placebo patients, you replicate this dose-response pattern that we already saw in Part A. So clearly, for me, the 120 mg is the best dose. You bring in safety, you clearly have to see this is the dose with the optimal benefit-risk profile. There's no magic going on with the PK. The more you give, the higher is your trough level, the higher is the concentration in the tissue.
This is why the 240 mg has a somewhat higher candida signal. So my interpretation is, we also showed that already with the 120 mg, the dose that we know is optimal in psoriasis, we have the concentrations that we need. I think that is the clear finding. My view here, if you significantly go beyond the dose, that gives you the optimal anti-inflammatory. Obviously, you start to put your foot, if I'm allowed to say this metaphorically, on the gas pedal and at the brake at the same time. Importantly, we have a winning dose. That is the goal of a phase II study, that you generate a winning dose that has the optimal benefit-risk, and very clearly, we think that this is the dose, the 120 mg, that we will take into phase III and that we will discuss with the FDA.
Perfect. Thank you. Maybe one other one that, I saw some questions here on HiSCR1 00, IHS4-1 00. Here's one: "Please explain more about the IHS4- 100 score. This is not routinely reported by others. How does it compare to, for example, a PASI 100 in psoriasis?
And again, in terms of time, I'll try to be very brief. We were always hesitating to use HiSCR 100 because it gives people the wrong impression that this is remission, as PASI 100 remission is in psoriasis. We don't have this in HS. I think the closest parameter, as close as we can get to, we call it inflammatory remission, is IHS4-1 00. People may say, "Yeah, but what about the weighting factors? It includes nodules, abscesses, and draining tunnels." Yes, but it also has a weighting factor that is irrelevant when you look at IHS4-1 00 because it just means zero across all three inflammatory lesions in IHS. So we think it is as good as you can get with an anti-inflammatory response.
... We will do further work correlated with patient-reported outcomes. We'll do further work, look at ultrasound, what do we do with tunnels? But this is a terrible disease. The only way to stop patients from getting irreversible tissue damage is to treat them even earlier. This would be our vision for the future, but in the meantime, I think IHS4- 100, inflammatory remission, is as best, as good as it can, can get.
Perfect. Then I think a few questions, one more time on the Humira arm, even though way less than last time. Here is one: Does the week 24 Humira data, quote, unquote, "Put the discussion on adalimumab to bed?" Question mark.
Shall I take that one?
Yep.
I think the answer is clearly yes, it should put this argument to bed. It is very clear that patients that are on SLK simply do better than those that are treated in, with adalimumab, as Kristian showed with that particular chart, that again, I invite you all to consult after this session. Not only in Part A, our best dose was already clearly better, but also when you look at the cohort of adalimumab non-responders, which I remind everybody, more importantly, than looking at numbers that you can compare to make a point, what matters out there is that patients that get adalimumab, their majority doesn't reach HiSCR 75 at week 12. And the non-responders you saw in our cohort have very strong results, that they wouldn't have any other option to reach.
120 milligrams is clearly the better dose, in that it has achieved a far higher response compared to adalimumab in, in HS, in our main and our crossover arms. I think the other thing that everybody has to ask themselves, where is the data for, for adalimumab on the effect size, on the long-term data, on the tunnel evidence, on the inflammatory remission, on the patient-reported outcomes? I challenge all the naysayers to find this data. It is not there, it's missing, and you see that SLK provides that for, for patients. There may be, Matthias, more discussions about specific data points.
Skeptics will for sure raise some analysis, but I think if you take a step back and if you look at the totality of evidence, it is clear, at least to me, that sonelokimab has a much better benefit-risk profile than adalimumab in HS.
Perfect. Then maybe one very last question, and probably that one is for you, Kristian. Last week at EADV, data was shared on other molecules in the HS space. What were relevant findings for you at MoonLake?
Yeah. So we have 2 more hours, right? And we are already above the full hour. Yeah, maybe just two things. Number one, and there is good and bad in this. Number one, many MOAs continue to fail or not showing convincing data, and that includes the Janus kinase inhibitors. Although they are broad, they obviously don't directly inhibit IL-17, and they do not really work. That includes PDE4, 36% inhibition, other mechanism. It's really the IL-17A and IL-17F inhibition that shines. And I have to say, and of course, with all the limitations, we are phase II, bimekizumab is phase III, but if I look at all these parameters, we always seem to be 5%-15% better than bimekizumab. So if I'm allowed to use this a little bit rhetorical words, I think there's little else out there.
And even if you go to the IL-17A and IL-17F inhibitors, it seems to be more and more the case that we have a gold medalist here, which I think is extremely good news, not only for those that treat these complicated patients, but really for the patients themselves. And again, I think this IHS4- 100, one out of four, that is a message that is really taking off.
Wonderful. I think we're at the end of the hour, so maybe thank you, Jorge, thank you, Kristian-
Thank you.
For joining me here for the webcast. Thank you, everyone, for dialing in. As I mentioned in the beginning, a replay of the webcast will be made available on our IR website. You should find the presentation there already now. And last message, we will see each other soon again, at least for those that want to dial in. As Jorge laid out, our PsA data is coming very soon. We always said it is coming in the beginning or first half of November, and that still remains true. So we're looking forward to seeing you again when we get to present our PsA data. Until then, thank you very much for joining. Have a good day.
Thank you.