Conference Transcript - ALMS 2026-09-08

Derek Archila, Analyst — Wells Fargo

All right, everyone. I think we'll get started here with our next session. My name is Derek Archilla. I'm one of the senior biotech analyst here at Wells. With me, we have Illumis, and from the company, we have Martin Babler, president and CEO, as well as Jordan Droppa, chief scientific officer. So, gentlemen, thank you so much for joining us.

Martin Babler, CEO

Thank you for having us.

Derek Archila, Analyst — Wells Fargo

Thank you. Excellent. So we just had some data for your lead product, envudacitinib, phase 2 in lupus. So, you know, maybe first just kind of recap what we learned, and then we can kind of dig into a little bit more of the specifics.

Jörn Drappa, Other

Yeah, so this was a phase 2b dose-ranging trial of n-vudacitinib, three different doses versus placebo in patients with moderately to severely active lupus. It was a one-year trial with a primary endpoint being BICLA at week 48. The trial did not meet the primary and its key secondary endpoints in the overall population. It became quickly apparent that in the population that has the type 1 interferon signature, there was a strong response and consistent response across multiple different endpoints that includes the BICLA, the SRI-4, the CLASI, joint counts, as well as remission. But in the type 1 interferon signature negative population, there was really no benefit at all. And in fact, some of the active group appear to be doing even worse, which is primarily due to an extremely high placebo response in that subpopulation. Since this interferon-signature-negative group constituted an unexpectedly high proportion of the overall trial participants, that sufficiently diluted the overall outcome to become negative. In the past, we've typically seen approximately 80-20 distribution between signature-positive and signature negative ones in trials in this population in our trial it was approximately 60 to 40 so this was a large enough population to render the all comers outcome negative so I guess you know what what do you think explains that lower than expected interfere in high high patient in the population it's as you said generally we see kind of that 80 20 split so like what do you think went wrong?

Derek Archila, Analyst — Wells Fargo

Was it more a geographic thing or race and ethnicity? Like what kind of mix did we end up getting here?

Jörn Drappa, Other

Yeah, we're still digging through this data. So we only got the top line data a week ago and the Biostats team is buried in a mountain of work. So we're trying to kind of dig through on a by site, by region, by country level where all these type one signature negative patients came from. My preliminary sense is that a lot of them actually came from the United States. fewer of them came from Latin America and and especially Asia in Asia typically patients have a higher proportion of the signature than in in other regions and that in our hands was also reflected in a much larger response clinical response in in Asian patients than in for example the United States in the United States we were in a situation where there's a lot of competition for patients with with moderate to severely active lupus, and especially at the time when we began to enroll in North America, because other countries joined later on, we had initial very slow enrollment and had to compete with a lot of other companies that had late-stage trials going on, and I think that probably led to the fact that we had a somewhat milder phenotype than we had expected, and that was then also reflected in the lower proportion of signature negative patients gotcha so I mean beyond just your data that you generated here you know I guess how predictive do you think the interferon gene signature is for for endo sit in its response like you know across maybe other trials maybe just kind of give us the totality of the evidence that points that way so I think it's been very very consistent observation by now in with drugs that target the type 1 interferon pathway so we've seen that first in the anifrolimab program that I was involved in many years ago where basically the type 1 interferon negative subgroup did not contribute any almost any response to the Delta was close to zero and all the Delta came basically from the type 1 interferon positive subgroup and that was primarily due to an elevated placebo response rates in the negative subgroup it's again been seen with the Ducra program where the responders mostly came from the positive subgroup and there was very little of any Delta in the negative subgroups for most of the dose arms and now we have seen it again consistently no benefit whatsoever so across three different programs now we have seen the same thing over and over again and I think we can now safely conclude that there is just no benefit for of these patients for this type of therapeutic approach.

Derek Archila, Analyst — Wells Fargo

I mean, although a failed trial, it does add to the learning of like trying to almost homogenize this patient population to a degree where you can have and run a successful trial. Is that like fair, like we're kind of narrowing the population to some degree?

Jörn Drappa, Other

Yeah, I think so. I mean, obviously you want to target treatments to patients who have a good chance of responding to them and not to those who have very little evidence to support that they would derive any benefit from it. So going forward, I think the rational way to proceed to next steps is to hone in on those patients that have a chance of responding, and that is the type 1 interference signature positive ones. And we have a lot of work ongoing to see whether, in addition to the interference signature, we can come up with other markers that are associated with response. We've basically obtained RNA samples at multiple time points from every single patient in the LUMIS trial, and over the next several weeks and months we will analyze all this data and to see whether in addition to the type 1 interferon signature there's other things that we can potentially use to narrow down the population and hone in on those that have the best chance of responding. I mean can you talk to the efficacy in those patients with the interferon high signature was it fairly consistent across many endpoints is there variability and what else could you show you know maybe at a future medical meeting that would kind of even reinforce kind of the the potential for you guys to move into a phase three and just the interfere on signature high patients yes so they were consistently large differences between active and placebo so with respect to the big law there was about a 30% Delta with respect to the DSRI for I can remember the exact number now top of my head but also in that order of magnitude there was a large effect on classy which is a skin specific instrument that's conceptually similar to the PASI it measures the area of skin involvement and the severity of skin rashes and lupus and there was a good proportion of patients who actually achieved the LL-DAS which is a remission like state of low disease activity so there was a more than doubling of the rate of patients that achieved the LL-DAS compared to placebo so all of these point to the fact that there was a really good treatment response in this sub population and consistent across multiple domains the one the only two endpoints that were not statistically significant although they showed a trend were steroids sparing and flare reduction there were relatively few severe flares in in this trial and that's why the year number was too small to achieve significance there but all the other key secondary endpoints were clearly positive we can you also talk about the dose you you guys were evaluating a couple doses in the trial and just you know what we should take away there in terms of you know looking forward to a phase three yeah so first of all we looked at pharmacodynamics so there was a beautiful textbook dose response so the more the the lowest dose achieved some degree of inhibition of type 1 interferon mediated genes and then the the higher you went in dose though the further it was suppressed up to almost the baseline at the highest dose the dose response was less clear when it came to clinical outcomes so we did have a dose response and for the primary endpoint which was the bickler there was no clear dose response for the sri4 and for some of the other secondary endpoints and exactly why that is we're still working through it could be just variability in the relatively complex clinical outcome measures in lupus, or it could be that you perhaps don't need the type of complete target coverage that you clearly need in psoriasis that we've consistently observed that you really need to hit the target very hard in order to achieve optimal efficacy. And it may be that in lupus you don't need to hit quite as hard, but we're still working through that.

Derek Archila, Analyst — Wells Fargo

Understood. So I guess as we think about, you know, and I think I asked this question on the call last week, but there's no established precedent for just enriching for interferon gene signature patients in a lupus trial, but there is precedence for narrowing patient populations, and as you were just kind of alluding to, going to the patients that you know are probably the highest probability of having a response. So, I don't know, maybe walk through some potential precedents that you guys are looking at and kind of the conversations that you'll have with the FDA around a future phase three in this enriched population.

Jörn Drappa, Other

Yeah, I think that the collective body of evidence that I've talked about in your previous question is now strong enough to make a case to the agency that the risk-benefit ratio is actually not appropriate for these patients, that they have very little chance of deriving benefit while still being exposed to the risks of a clinical trial. And so that's the argument we are going to make. And then there could be several different scenarios. it could be that the trial is sort of geared exclusively towards that subpopulation in the first place. It could be that we include at least some type 1 signature head negative patients to further strengthen the body of evidence supporting that these patients derive no benefit, but then analyze it in such a way as to have the primary analysis geared towards the subpopulation and then a secondary supportive set of analysis for the all-comer population. I mean do you think the base case here is that you'd have to run you know two additional like trials or do you think you can leverage some of the evidence from Loomis and just that you know population of the interferon high signature patients I think it's hard to predict I think the agency recently has shown flexibility to approve drugs based on a single phase 3 trial particularly in a situation where we have a relatively large phase phase 2 trial but you know it's hard to predict what they are what they're going to say there's going to be a topic of discussion when we meet with them towards the end of this year hopefully early next year gotcha and that's I was just gonna ask you on the timing that is that kind of the earliest you kind of probably do it that's what we're shooting for sorry we have obviously a lot of analysis still to complete it to us and so we need some time to assemble a data package but then we aim to request a conversation with them in an expeditious way depending depending on their calendar, which is not in our control, hopefully in the fourth quarter or first quarter of next year.

Derek Archila, Analyst — Wells Fargo

Gosh, and how will you communicate to the street? Will it be more just like, here's the plan, this is the phase three we're gonna run, and have the whole design? Or is it just that, yes, we can move forward? How comprehensive an update will you guys plan to provide? Martin, you wanna answer that? Let's get Martin in here.

Martin Babler, CEO

Yeah, so we haven't decided yet how we're gonna do that I think the most important thing for us is at this point we mostly want to have an understanding on what the path forward is whether and how and when we move forward I think is is a question in the bigger context who we are as a company at that point gotcha and just going and revisiting the you know question around dosing I mean do you feel like you've done enough dose ranging to understand just to bring in one single dose into a phase 3 trial or would you still look at multiple doses I think we would ideally look to bring in one one single dose but as I said the dose response we're still we're still working on on all the analysis and to see whether we can come up with a

Jörn Drappa, Other

sufficient rationale certainly the safety seemed to be fine at the 40 BID at the highest dose so there's really no concern from that point of view to you know taking out a higher dose and having potentially more side effects that did not appear to be the case understood okay and then maybe just to talk about you know Dukas trial they're gonna have a readout you know by the end of the year in lupus as well I guess what do you hope to learn from that I don't know how much detail we'll get but you know what would you hope to kind of learn from that trial whether it be at the top line or at a future medical meeting when they actually show the granular data that support your hypothesis here so my expectation based on their Paisley phase two program is that they're going to have a positive outcome overall this is a large trial well powered I think the biggest question is what is going to be the magnitude of effect right say so they showed a really strange dose response in the in the Paisley trial where the lowest dose had a huge Delta in the middle dose had almost no Delta between active and placebo and then the highest those again had sort of an intermediate kind of Delta and so on which end of that spectrum between almost no Delta and a large Delta the phase three is going to come out I and I'm not sure how to predict that and then the second question is going to be whether they what is their proportion of type 1 signature positive versus negative going to be in house that going to influence the results and will they have the same observation that we did that really the negative patients have

Derek Archila, Analyst — Wells Fargo

no benefit whereas all the Delta really is derived from the positive sub population so if it's kind of an 80 20 split it's probably positive but if it's kind of drifting down to kind of where you guys are does that produce more risk I've been done the powering and I don't know if you guys have looked at but like I don't know I guess for you guys it would seem like if it's heavily overweighted to the interferon high and then that supports the thesis but if they hit and it's kind of like 50 50 then you know maybe maybe not so much but I don't even know if that's possible it's hard to predict it it depends on exactly where and when their phase three patients were enrolled, and of course, they now also have the ability to potentially learn from our trial and modify their analysis quite

Jörn Drappa, Other

accordingly.

Derek Archila, Analyst — Wells Fargo

I guess looking forward, we'll get some updates next year hopefully on lupus, but your other plans for NVU has been centered around potentially bringing it into CLE, so kind of a derivative of SLE, but also Sjogren. So do you think the data from the phase two LUMIS trial kind of helps validate those indications in any way? And maybe just walk us through kind of your current confidence in the development for those indications.

Jörn Drappa, Other

Yeah, we've seen a very strong response on the CLASI specifically, which is the skin instrument, which is both more quantitative and more objective than some of the composite endpoints, such as the slidai and the bilag. so based on that I think it would increase my confidence in in CLE of course in CLE there's the same or a similar distribution between type 1 positive and type 1 negative patients so we will need to take that into consideration as we expand it to CLE as well and then Sjogren's is it is it slightly different or Sjogren's is slightly different because there's really no prior evidence up to this point of TIC-2 drugs in Sjogren's. We know that there is a type 1 interferon signature in Sjogren's, but there is no prior sort of clinical validation. I think the first point of validation is going to come from Bristol's trial of Ducra in Sjogren's. And then just revisiting, so one of the components of the LUMIS trial was enrolling patients that had some skin manifestations, but ultimately that didn't translate to, whatever their interferon signature was like I guess like what actually happened I mean ultimately that's what we thought we were enriching but ultimately it seems like we didn't yes what it seems like in my mind is that the association only works in in one direction right so those patients with the interference those patients with skin manifestations tend to have a good response to type 1 interferon directed drugs but the presence of skin disease in and of itself is not necessarily sufficient to ensure that they actually have to have the signature so there may be skin manifestations in the type in the negative subpopulation as well and so that is an important learning so in the future they will just need to directly test the the signature in a prospective way and then you know select accordingly gotcha okay anything else that we should be paying attention to you know near term around you know the SLE program for envu you know either internally or externally No, I think we covered it. An important inflection point is obviously going to be the outcome of the Ducra trial in lupus. And then our next inflection point internally is the conversation with the agency. And then we'll need to decide whether or not to move forward in SLE or whether to focus on psoriasis or potentially to change directions and go into CLE.

Derek Archila, Analyst — Wells Fargo

Yeah, so maybe, yeah, let's move to psoriasis. So, you know, the NWU data there look great. So I guess, you know, how should we be thinking about, you know, kind of the next steps there with the NDA filing, but, you know, ultimately the strategy, whether to commercialize, partner. So what's kind of the update there?

Martin Babler, CEO

Yeah, well, let's start by saying that, you know, we're having some additional data, especially long-term data that will further define the benefit of NWU and psoriasis. And we really, you know, especially when you have a setback like this, you have to remember what you actually have and we actually have a very strong highly competitive drug and psoriasis in a market that seems to be growing quite substantially and when you look at the July date at least it looks like you know the oral launch actually is going really well for J&J and so that tells us that that market is indeed actually going to grow the way we anticipated so we have a molecule for a growing market and a very substantial market we always said we're going to plan to partner this asset and I think the reason why I also want to remind everybody we always said the reason is that we want to first see how to value the asset and whether this is actually a broad asset we kind of have one and a half pieces to the answer here we we have a strong psoriasis drug and and it's getting stronger by the day in our minds and in the interferon side the hypothesis actually is validated that there should be several indications on the interferon side that it works and I think the other piece that we've shown is and we had a slide in our deck that even with patients that have very very high interferon compared to psoriasis we actually really reduce interferon levels down to normal levels and very very low, and do so actually at least as good if not better than the competition. So from that standpoint, the validation we have there, we just don't have a clear, large positive trial, but we have a lot of learning. So now we know how to evaluate it, and now it's really about can we find somebody, can we find the structure of a partnership that that maximizes and optimizes this asset in the meantime we are continuing to prepare for the launch we're submitting the NDA by the end of the year in the fourth quarter and and really prepare the market in every way that is necessarily time wise and then we will see how that partnership shapes up if we have a partnership or whether we actually will go it alone but our intent remains that we partner this asset for at least the psoriasis launch.

Derek Archila, Analyst — Wells Fargo

Got it so I guess as we think about you know post AAD you and ZASO like so NVU and ZASO data you kind of shine you know in the TIC2 class can you maybe talk about the enthusiasm amongst kind of you know physicians and as well as maybe strategics around kind of the TIC2 class and is it more centered around the IL-12-23 diseases or a kind of growing enthusiasm around interferon related diseases?

Martin Babler, CEO

I would say in the dermatology community the L23 axis is the most important one because I think what they've seen there is that there is a clearly definable patient population that TIC2 seems to benefit and actually seems to help patients even more on certain aspects than other drugs so that's very clear on the dermatology space there remains very significant interest for example from CLE from dermatologists and also for other smaller diseases. I would say on the rheumatology side it is clearly the the interferon side that drives it and then there's always the the key question which we will get some answers to is gastroenterology an area where where this would could really become an interesting target. In our minds that they're the most interesting aspect for TIC2 is not just as monotherapy but possibly combinations and so we're waiting to see what whether the experiment that the Takeda is currently running in that field is successful because they are actually pushing the dose and we believe that's an important part to understand the effect of TIC2 and IBD we know the AL-23 pass works so it should work but how well it works is to be seen gotcha so still broad opportunities and so I guess when I think about you know maybe the future here and when you look at a potential partnership what's kind of like the most optimal for you guys like is it more about you know completely splitting cost or you know kind of having someone completely build out you know Envu's you know indication set while you maybe focus on A005 like what would be optimal for you and most value creating for the company yeah you know this is the most fascinating and puzzling piece of Tick2 because TIC-2 already has shown today that it works in about four different diseases and a year from now we know about ten different diseases any other mechanism that actually aims at ten different diseases people would be super excited about and we see this in other areas because of the history of TIC-2 and especially Ducron and Ventix people are a little bit more shy about this but the reality is when you look in CLE at least when you look in psoriasis actually TIC2 so far outperforms every other modality and I think for us the ideal partnership of course would be somebody that shares our vision that this should be a drug that is developed in about five to ten indications and we're going to do this together and we're going to do it on a global basis that requires a lot of resources on both sides and so I think we will have to see how how strongly we can materialize that vision over time at least and and so the ideal partnership for us certainly would be one where we believe that the pie that we're creating together is significantly larger and our piece is

Derek Archila, Analyst — Wells Fargo

significantly larger than the pie we would have if we actually did it ourselves got it so I think you know there's two I think important updates maybe that you know help de-risk that partnership at least in our view would be, you know, number one, the FDA meeting on SLE, what the path is there, because that certainly would create value in terms of, like, you know, a partner coming and being able to go right into phase three. And the other maybe would be around, you know, QD formulation. So, you know, you kind of gave us the update on, you know, the FDA stuff and the timing there.

Martin Babler, CEO

Where are you kind of on QD formulation and how important is that, you think, for a future partnership or just, again, you know, being able to play you know competitively in the psoriasis market yeah so we're actually working on multiple approaches and they're entering the clinic in the coming in the near future we have not given an update because our plan originally was to basically be able to tell you this is what we picked and this is the time frame associated with it I think at this point I want to make sure that everybody understands we actually have things in our hands that we're working with and and we're pretty excited about we will give a more detailed update once we have more data from from the healthy volunteer studies

Derek Archila, Analyst — Wells Fargo

but we are basically moving into the clinic with several options to make sure that we have a once a day and we do believe that the likelihood of once a day remains extremely high we just basically want one that that we believe is commercially as attractive as it can be gotcha okay and then maybe just to shift gears to a zero zero five so I mean this is your brain penetrant tick to so maybe talk about how this it could be really interesting for neuroinflammatory diseases and I know you had initially thought around MS you know kind of moving forward there you kind of it seems like maybe move forward Parkinson's so what's really the rationale maybe for for that change or reprioritization and I guess the confidence level in in understanding good proof of concept in PD based on and kind of the biomarkers that are out there.

Martin Babler, CEO

Yeah, so maybe I'll start on the decision, then Joran can talk a little bit more about the Parkinson's program itself. So I think it's actually a really great example of how disciplined we are as an organization, because we had chosen MS, we were ready to move as MS, but then did a, based on some new information and additional market assessment, and realized that the possibility to create significant value in the short to medium term on MS was a lot harder and we knew that long term we would have to partner the asset anyway and and in parallel we basically developed internal capabilities and actually found a biomarker associated with Parkinson's that is unique to TIC2 and that really we wanted to explore and that's ultimately why we made the switch and decided that the opportunity in Parkinson's is actually significantly larger for us we can really do additional work there and and that's why we decided to engage in the program and I'll let Jorn talk a little bit more about the program what we hope to learn.

Jörn Drappa, Other

Yes I mean to add to this so the the issue in MS is that this is a very good way to run a proof of concept trial because you have an imaging biomarker that you can evaluate but then the problem is as a small company afterwards you're stuck right so you there's no way you can in you can finance or enroll these huge trials and long trials that are required in MS and so that's ultimately what contributed to the decision I think there's growing interest in Parkinson's disease and growing realization that a lot of the neurodegenerative processes are actually associated with inflammation and at least we are now in the early stages of being able to look at biomarkers that reflect inflammation in the CNS but also neuronal destruction over the longer term so I think our first step is really going to be answering two questions number one does a5 inhibits the target in the CNS as it does in in the periphery so that's question number one and then as it as it does inhibit this pathway how does that actually influence biomarkers that reflect both inflammation and neuronal destruction in the in the CNS and so that's going to be the question we'll attempt to answer we will try to run the trial over a sufficiently long period of time and with the sufficient power that it actually at least maybe give us a hint on some some clinical outcomes it's not going to be fully powered for clinical outcomes it's got to be you know size based on observing a biomarker effect but you know from our conversations with experts in the field it does appear like if we run it for a sufficient amount of time at least we might have a chance of having a hint of a clinical effect what's sufficient amount like 12 weeks 24 weeks or a year like what do you need to see so different there's different outcome measures at different time points like the PD you can measure as soon as four weeks or even at 12 weeks and then for a biomarker readout you probably want to run it for at least six months and for a clinical outcome perhaps even longer than that.

Derek Archila, Analyst — Wells Fargo

So as you think about the trial design was it kind of like a multi-stage trial or is it mostly like an open-label extension and you know what level of chronic tox have you done you know with with A005 already so that you can kind of put to play you know these these different types of biomarkers in the trial?

Jörn Drappa, Other

Yeah so the tox is tox is done so we have sufficient tox to run long-term long-term trials and in any disease basically and so the the exact design we have not really disclosed at this point and it is actually still to some degree a work in progress that we're trying to to optimize and then finalize so you can't really comment on so exact powering and design at this at this stage gotcha and then I guess I don't know if Martin we were kind of alluding to some maybe tick to specific biomarkers that you can look I don't know if I caught that right but you know I guess there are specific biomarkers that you know I think we've done a little bit of work in Parkinson's that you know people are

Martin Babler, CEO

starting to look and whether they translate to outcomes but which ones do you think are kind of like the most important and particularly if there are mechanistic specific ones that we should be focused on you know in this trial yeah so the the biomarker that we discovered is actually something that is proprietary okay we haven't disclosed at this point and it goes exactly the question you just asked is this what's the chicken and what's the egg and but it's an interesting one because we found it we found it associated with Parkinson's then we could go back to phase one data and see actually whether that biomarker is indeed influenced by our drug and it turned out it was and so now it's really a question of is that a predictive biomarker or is it just a consequence of something that we see and so but This is what we started out as a company to do, which was basically we wanted to be a precision immunology company and figure out can we actually identify a specific population that might benefit from certain drugs. And so, for us, that's a really interesting aspect. And ultimately, this is very similar to what just happened in lupus, where we basically now have an ability to really look at what actually changes with a TIC2 therapy, and is there a predictive value on that, or is it just a consequence of TIC2 administration? And certainly, we've already dug through some of that, but there's a lot more work to do on both of those to see whether ultimately you can identify a subpopulation in a simple way, and maybe even without running a diagnostic test, but just a certain subtype of people that you recognize because of certain features. In psoriasis, we've been able to do that at least with certain subtypes where we can basically describe you the patient that probably is the better patient for a tick to compare to other modalities with with special areas with itch etc etc can we do something similar or even with a diagnostic identify a patient that should really benefit from the drug gotcha and I'm sure you guys are monitoring kind of the field there's you know a couple other brain penetrant tick toos out there like pseudo and Sundance I mean have you guys kind of looked at to see how you guys are differentiated it was more about brain penetrance or selectivity like what do you think will ultimately rule the day you know across some of these other molecules? So I think there's two aspects here and one is the piece that we learned in the periphery which is you really have to hit this target hard to get the right effect and then with that for brain penetrant ones it really comes how well does it get into the brain and then what is the safety and and you know that there's a certain window of safety because we had three out of the four tick tooth that had to dose reduce because of safety and so what we've seen so far is that our drug actually from the data we've seen to date when all the all the CNS penetrant ones gets into the brain the best and we have a one-to-one ratio and if we apply these principles we do believe we might have an advantage to because we can push the dose to maximal inhibition in the brain without

Derek Archila, Analyst — Wells Fargo

hopefully having in introducing some of the side effects and having to dose reduce we'll have to see that that will come out in the clinic but you know that's why we're running the trials that we're running but at least from the phase one so far the data looked really good and we hope we can repeat that in the phase two as well I mean will there be anything that we could take from the Parkinson's experience and and start to apply I mean it sounds like you we were pretty confident in terms of the biological rationale for MS but maybe just not good commercially but you know how do you think about other neuroinflammatory disorders and where you know other or where again a brain penetrant tick to can go I think there's potential the potential for

Jörn Drappa, Other

applicability across other neurodegenerative processes as well there's only so many questions we can address clinically at a time but you know certainly if we do get positive proof of concept that would certainly open up a window into additional indications that also are characterized us by neurodegeneration, whether that's Alzheimer's or other diseases.

Derek Archila, Analyst — Wells Fargo

And then maybe the last one for Martin, just in terms of the overall, like, you know, next 12 to 18 months, we probably will find out a variety of different things, including, you know, thoughts on psoriasis and what you're doing there, also potentially approval within that 18-month period.

Martin Babler, CEO

But maybe just kind of tee up the next 12 to 18 months and other things that we might be missing in terms of the pipeline and updates. yeah the one thing that we will have to think about very carefully is we do have additional things in the pipeline we basically said we're going to put another molecule into a clinic next year we didn't feel like we wanted to share that necessarily earlier on but we'll we certainly will get there I think as you said the most important things coming up here is that data from our own filing then we have another molecule and then we will get some additional data from from the psoriasis program coming out in the not too distant future. And then it's really about preparing for launch. And then we have external catalysts as well. And with the Parkinson's program and with what comes behind it, we really also wanna make sure that people realize that there's more to this company than just any lucidinib. And we just have to advance those to make sure that people are recognized as a value in those assets as well.

Derek Archila, Analyst — Wells Fargo

Okay, well, Martin, Jorn, thanks so much for joining us and we really appreciate it thanks for having you