InflaRx N.V. (IFRX) Earnings Call Transcript & Summary

Ladies and gentlemen, thank you for standing by. Welcome, and thank you for joining InflaRx's conference call to discuss the results announced today from the multiple ascending dose part of the Phase I study with INF904. [Operator Instructions] Please note that today's call is being recorded. The presentation will be followed by a Q&A session. [Operator Instructions] I would now like to turn the call over to Dr. Niels Riedemann, CEO and Founder of InflaRx. Niels, please go ahead.

Thank you so much, [ Laurie ]. Welcome, everyone, to our today's conference call. We're really excited to host this call today. I'll be leading you through this call here at the beginning, and I will share the presentation with Dr. Camilla Chong, our Chief Medical Officer. But before I introduce the team, just on the next couple of slides, please take note. We'll be making forward-looking statements. There's an important notice and disclaimer related to that, and we will also be talking about data, either proprietary or other data. So please take note of that disclaimer. Next slide, please. So as I mentioned already, with me today, Dr. Camilla Chong, our Chief Medical Officer. She will be leading you through the clinical data. We're very excited about this data. Also with me Co-Founder and our Chief Scientific Officer, Renfeng Guo; and Thomas Taapken, our Chief Financial Officer. Next slide, please. So the agenda for today, I'll be briefly speaking about the background and preclinical work, and then I will hand over and Camilla will lead you through the study design, the safety, PK/PD outcome and then to a summary. Next slide, please. So let's start with the background and next slide, please. Before we go into too many details. I think 1 important point I really like to make, and it's been in the meantime, published extensively in different settings is that the way that C5a and C5aR are generated -- and it's important to note that, obviously, we all know that there are complement pathways, classical, lectin, alternative. There's different ways to activate these pathways, they converge on the level of C3 and then the C5 convertases are formed. So C5 can be cleaved through these mechanisms and generating C5a and C5b. Now C5b is a drug target that we don't touch. We leave that function intact but C5a and today we'll be speaking about C5aR, which is the main signaling receptor for C5a signals. C5a is then generated. And it's really important to note that can be generated through enzymes. Some refer to that as extrinsic pathway. And we believe that this plays a very big role in certain disease settings. And it's important because upstream complement inhibition may not result in blockade of and we've published this of this enzymatic cleavage. So bottom line is if you want to have control over C5a signaling or C5aR signaling, you need a targeted drug approach. And today, we'll be speaking about INF904, which is a small chemical orally administered inhibitor for the C5aR. Next slide, please. So this is a very exciting drug target for us. It's been extensively researched in the field. C5aR is a G-protein-coupled receptor, very fast signaling, highly expressed on neutrophils, granulocytes, but also upregulated in epithelial cells, mast cells, macrophages, all sorts of different cells. So it's a very broadly present receptor and blockade of this receptor showed strong anti-inflammatory effects in numerous preclinical disease models and in the meantime, also in the clinic. So it's fair to say C5aR is a validated drug target. And when it comes to C5aR antagonism, it can be potentially a stand-alone therapy or also an adjunct treatment for a variety of inflammatory disorders. Now in all these areas listed here to the right, there's extensive research present on the role of C5a and C5aR. I think 1 of the newest fields is probably immunodermatology. It's 1 of the areas that we help pioneering when it comes to the role of C5a and C5aR but then also renal respiratory or very exciting neurology data coming out more and more on the receptor and on its role in chronic inflammatory neurological diseases as well as rheumatological diseases, autoimmune diseases. So it's a very broad applicability. And there's 1 marketed drug candidate only, that is avacopan and we believe that the PK/PD profile could be improved based on the published data of that molecule, which brings me to the next slide, please. So what could be improved? And what would you like to see for a best-in-class C5aR antagonist. So certainly, one of the areas that we wanted to improve is a different PK profile. We want to reach higher plasma levels because in plasma, neutrophils get activated and start moving into the tissue, and that drives likely many disease settings that's been shown preclinically and so with higher plasma trough levels, you should get a higher coverage. Why is this important? Because it brings me to point to that should result into an improved blocking activity. We see a high chance here to improve this blocking activity and we believe it's important because it may result in better clinical efficacy and there's also certain initial evidence for that, and that -- I will go into that on the right side of the slide in just a second. And finally, the drug strength may be improved with lesser capsules administered or less frequent dosing. So let's look at the right side here. This is the published data from the Phase I healthy human study of avacopan and this was a 7-day multiple ascending dose, and you see the dose here of 30 milligrams, which is the twice per day, which is the approved dose for avacopan. And that's the blue dotted line that is the trough level. So it is basically the last dosing at day 7 and 12 hours later, they measure the neutrophil activation with the so-called CD11b expression. It's a marker on the neutrophil surface that is very sensitive for neutrophil activation. And C5a is a strong inducer of neutrophil activation. And you can see that at levels of C5a added here. So they took the blood from the healthy volunteer after 7-day dosing with avacopan. So the signal should be covered and then they added different concentrations of C5a and saw if they could excite neutrophils. Now at 10 nanomolar roughly, which is levels you see in inflammatory diseases, you saw approximately 50% of the signal coming back. So we believe that ideally it should block more than 80% at that level, and that was 1 of our goals for the program. We've previously reported the single ascending dose and showed you that we reached over 90% blocking activity with any dosing level exceeding 30 milligrams for our drug, INF904. And so this is something that we will be looking for today -- into today to see whether that is also achieved in multiple ascending dose. And next slide, please. So just as -- just a few last words about the preclinical summary. INF904 binds to well-defined allosteric binding sites of the C5a receptor. It's a novel molecular structure. The patent in the U.S. was issued in 2021, and it's going through natural phases in other selected countries. There were no obvious toxicity findings in the so far conducted and completed preclinical studies. There's a high in vitro potency, which is important for this type of molecule. We have a higher plasma exposure compared to head-to-head avacopan in animal studies. That was 1 of the goals that was preclinically achieved. And then we also saw an increased efficacy in blocking in vivo in a hamster model, which is in the appendix of this slide deck. And then also, we also have initial therapeutic effects in preclinical disease models in renal and peritonitis models. So that brings us to a very exciting molecule, and I'm happy to hand over here to Camilla to lead you through the multiple ascending dose part of the study. Camilla, the floor is all yours.

Thank you, Niels. It gives me great pleasure today to present our multiple ascending dose study, which is, as you know, the second part of our Phase I study, which looked at various doses in a randomized, double-blind, placebo-controlled manner with 24 participants. And as you can see on the graph illustrated on the right-hand side, we studied 3 doses, and these were 30 milligrams given once daily, QD; 30 milligrams given twice daily, BID; And last but not least, a high dose of 90 milligrams given twice daily. Our participants were dosed daily up to 14 days. Next, please. So I would like to share with you now the results of our safety outcome, which is the primary objective of this MAD study. Next slide, please. So I'm pleased to say that 904 was very well tolerated and we didn't really see any safety signals of concern across all 3 doses that were studied as mentioned previously. In addition to that, the number of AEs in the placebo group were noted to be slightly higher at 83% compared to 77% in those who received active drug 904. The AEs were generally mild in severity with only 5 moderate cases. And more importantly, no SAE were reported at any of the dosing levels at all. There were 2 AEs, which were related in nature to 904. And these, as you can see, were mild in intensity and the cases as illustrated on the slide. No subjects were withdrawn from treatment at all. Next slide, please. I would like to take the opportunity to share with you the PK results. So next slide. Here, we are showing 2 graphs, and let me go through one by one. The one on the left is basically the concentration of INF904 versus time over the 14-day dosing period. And the table on the right-hand side are basically the 3 doses with Cmax and AUC levels shared at day 1 and day 14. And what you can see from these 2 pieces of information, these 2 graphs shared here, are that, first of all, 904 dosing either once daily as illustrated by the 30 milligrams dose on the blue line, the solid blue line, as well as those given twice daily on the orange line and on the green lines corresponded to a favorable concentration time profile. And more importantly, INF904 exposure is dose proportional. So when you go from 30 milligrams once a day to 30 milligrams BD and to 90 milligrams BD, you can see a dose proportional exposure. In the BD regimen, we've seen accumulation observed for both Cmax and AUC level of roughly around 1.3 and 1.9-fold. The other interesting observation here is, if you look at the 90-milligram dose given at day 1, the AUC and Cmax level achieved demonstrated greater exposure than that seen after 14 days dosing with the 30 milligrams BD. This has future potential for once-daily dosing as well as twice daily dosing. Next slide, please. Next, I would like to be able to share with you the PD data. Next slide. So the PD analysis was based on ex vivo whole blood assay, which upon 14 days of dosing with 904 measures the upregulation of CD11b neutrophils on the Y-axis, as you can see across these 3 nonlinear curves. After challenge with different levels of C5a, which is shown on the X-axis on all the 3 curves. So what you can see here is that measurements were taken at different time points upon last dosing from T=0 before dosing, after 24 hours dosing, T144 hours is roughly around day 6, T168 hours is basically day 7, T312 hours are at day 13 and last but not least, T336 equates to day 14. So all these are the different time points by which we took the samples to demonstrate the levels of percentage of inhibition. So upon stimulation with roughly around 12.6 nanomolar of C5a levels, which is what you would observe if you -- in disease state, if you look at that level, what we have been able to show conclusively is apart from the first day of 30 milligrams QD dosing, the percentage of blocking with INF904 is consistently at or above 90% of inhibition. And these results, as you can see, is consistent across the 3 nonlinear curves shown on this slide. In addition to that, the EC50 values also show that increasingly high values during the course of the 14 days of dosing, which is an encouraging sign. So next slide, please. And in summary, the next slide, what I'm really delighted to be able to conclude from our data from this MAD study is that INF904, our oral molecule was found to be well tolerated with no safety signals of concern in this multiple ascending dose study from the 3 doses, which we have studied. In addition to that, 904 demonstrated a favorable PK profile, which I've just shown you with the potential to achieve therapeutic doses required in chronic immuno-inflammatory diseases. And last but not least, INF904 has also been shown now to consistently block C5a at 90% or more at concentrations very often observed in human diseases. And I'm pleased to say that we believe INF904 confirms its best-in-class C5aR inhibitor potential following from our MAD study, which also confirms what we saw earlier in the SAD study, which have been previously reported last year. And with that in mind, obviously, our next steps are we are excited to be able to introduce to basically progress 904. We will be introducing a commercially viable formulation for our Phase II clinical program, complete our long-term chronic toxicology studies as planned and also start initiation of our Phase II clinical study towards the end of 2024. So with that, I'm going to hand back to our moderator. Thank you.

Thanks, Camilla. I'll be taking on for just a few last words before handing back to [ Laurie ]. So just to reiterate what you just said, I think the team is both very proud of this development and very excited because the MAD data really confirmed the potential we've previously reported with the SAD data. And we really believe that this drug holds a large potential given the research background that I explained. So with that, you see the team very excited about this data. Many years of development and knowledge in component development went into this. Big kudos also to Professor Renfeng Guo, our Chief Scientific Officer, who led this discovery. And with that, I would love to hand back to [ Laurie ] for Q&A. Thank you.

Thank you, Niels. This concludes the formal presentation. We will now open the call to questions. [Operator Instructions] Our first question comes from Yatin Suneja.

Can you hear me?

Yes.

Perfect. I have a few questions on the development part first. So it seems like you're implying that there could be some short term studies that could be started by the end of this year. So the question is, could you just talk about like how you're really thinking about that? Would you start some sort of a basket study where there is a biomarker that could enable an earlier read on the efficacy before you go into the longer-term study. So that's one. What exactly is -- would be the gating factor for you to start the short term and the long term? Is it just the toxicology study or anything else you need to do? And then finally, if you look at the 90-milligram BID, I'm just curious if you can sort of I know the cross-trial comparison is not always ideal, but love to hear from you how differentiated that is relative to avacopan. So basically 3 questions, sorry.

Yes. So these were 3 questions. Thanks so much, Yatin, for tuning in for asking the questions. I will hand question 2 and 1 over to Camilla in just a second and maybe start with question 3 and Renfeng feel free to chime in. So that was the question on how similar or how different is the 90-milligram dosing. So I think it's quite different. I mean you'd have to consider 2 things. First of all, the data that we've shown here is a 14-day multiple ascending dose. The data reported for avacopan's Phase I study was a 7-day data. The other thing is that the curves that we see at 90 milligrams twice daily are much flat -- more flattened and more moved to the right side of the curve. So in other words, you see close to 100% blockade. I think it's around 96%, 97%. So this is as good as it gets in this assay. And you see it consistently and you see it consistently basically for all time points. In other words, with the first dose -- with the first day of dosing, we see a coverage, and we see a C5a inhibition on the receptor level on neutrophils, that is more or less close to complete. So I would say it's impressive with my background. And I would definitely say it's very different from the data that I showed earlier for the Phase I MAD data reported for avacopan in as much as they've achieved at 10 nanomolar a 50% inhibition. We showed you at 12.6 nanomolar, so that's 25% more, 26% more we showed you above 90% inhibition. Again, this was not a head-to-head study, obviously, but it's just the data that we reported. So it's just a much higher inhibition. It's very consistent over longer-term dosing and the curve is much more flattened and moved to the right side, meaning you have a broader range of C5a that you can cover, even clearly exceeding 12.6 nanomolar. Renfeng, anything to add from your end that you wanted to contribute here?

Yes, sure, Niels. I think -- 1 thing I think we should also look at is AUC. I think if you look at 30 mg BID and the 90 mg BID, we're able to see that [indiscernible] able to reach a really high level of AUC in the very rapid fashion. And I think that's a differentiating factor from avacopan because avacopan you'll see that from their clinical trial [indiscernible] able to see like 13 weeks, they see a reach to a high level of AUC. So I think that's the differentiating factor that you're able to see, [indiscernible] can reach the very high level, you'll see it very rapidly.

Thanks, thanks, Renfeng. So for the first 2 questions related to the potential for a basket study and the potential for starting a short-term study and whether the gating factor is -- the chronic talks, I would hand over to Camilla.

Thank you. And thank you, Yatin, for your question. So basket studies are definitely a possibility because as Niels had alluded to earlier, the potential areas of which we can go to is vast, and we have to be smart and shortlist that. Nevertheless, you don't want to not take the opportunity whilst we can. So therefore, basket studies is still a possibility. In terms of gating factors, I think we do have to complete our chronic toxicology study and I think that's the main path to doing a longer-term Phase II study. So that is in the plan. I wish it could be sooner. But however, we have the opportunity to be able to do an interesting 4 weeks study, whether it's basket or not we have that opportunity given the potential where 904 can go.

Yes. And maybe if I may add, Camilla, there is a certain gating factor in the long-term 9 months, which is the long term we do that allows us for real chronic dosing in any other disease. And that we could follow on after initiating the short-term dosing just maybe within the half year or so later or with maybe less than that. So it is a certain gating factor, but it also gives us the interesting opportunity to move into it with a bit more meaningful information. Good. I would hand back to [ Laurie ] then.

Our next question comes from Joseph Schwartz.

Thanks so much, and congrats on all the progress. I was wondering, I think avacopan is a CYP3A4 inhibitor and also has some liver caution associated with it. So I was wondering if you could talk a little bit about the pharmacophore for INF904 and discuss the ADME profile and how that might be differentiated?

Absolutely. Thanks so much for tuning in, Joe. Really happy to see you here. This is certainly something I hand over to Renfeng. But the answer upfront is there is a big difference in what we've seen in CYP3A4 inhibition. So Renfeng, floor is yours.

Yes. Okay. Thanks for the question. For the CYP, we did some study data in the preclinical study -- preclinical studies showed that there is a big difference between 904 and avacopan in that the inhibitory effect from the 904 is quite low, very minimal and compared to avacopan and we did have a comparison with the study. I think we reported some data before and meanwhile, we're doing metabolites and all that, the preclinical study with [indiscernible] tried to understand a little bit better about metabolites and also the CYP inhibition, that we are still working on. But from preclinal study that we already see pretty big differences.

Okay. Great. And then I think TAVNEOS is generally dosed around twice a day at 3 pills times 10 milligrams. So I was just wondering if you can talk about the pill size currently and the formulation and what additional formulation work you anticipate undertaking?

Thanks for the question. I think I can handle this question. For avacopan, you're right, it's 30 mg BID [indiscernible] 10 mg per capsule, so that's why you need 3 capsules per time, 6 capsules per day. And for us, we actually -- that's where we are trying to improve our strength. So currently, our strength is 30 mg per capsule. So that's why we're able to dose 1 pill, for 30 mg BID we dose 2 pills. For the 90 mg, we can dose 3 pills, right? So if you see the data that's I think we can reach a pretty high exposure with 3 pills like daily dosing. So for that, I think that we have a good advantage with that. For the second question, for the formulation, we are trying to develop very similar formulation that are from the SAD study, close to the SAD study because this is all lipid-based formulation, and we are trying to establish a commercial viable formulation and then improve stability and the shell and the manufacturing. So that's currently we are working on.

Our next question comes from Steve Seedhouse with Raymond James.

Thanks so much for hosting the call and congrats on the progress with this molecule, looking forward to seeing the Phase II plan. So I wanted to ask just about dose selection going forward, how you're thinking about that given the data in hand? And specifically, do you think once daily dosing is feasible and important here and along the lines of dose selection, is -- do you have flexibility to use different doses for different diseases if that's warranted? If it requires more inhibition of neutrophil activation than other diseases or if exposure is maybe different in different diseases? I would love just your general comments on all those thoughts on dose selection.

Yes. Thanks so much, Steve, also for joining and for this very great question. So I think this is exactly why we developed this molecule, right? We -- and I guess in the past, especially you and I had discussions about the right dose. We talked about the data generated in hidradenitis suppurativa back then with the molecule avacopan and the necessity to really control neutrophil function. So we do strongly believe that there are diseases we know, talking about like certain neutrophilic derm diseases, that may require a very high level of blockade higher than what you could probably achieve with avacopan at 30 mg. That's something we believe, and we designed this entire molecule and the entire program to give us that flexibility. Remember, in single ascending dose, we dosed up to 240-milligram without any safety signals detected. Now here we dosed twice daily 90, which is a lot of dosing. So I think it's exactly this flexibility and our, I would say, knowledge also generally in the complement space that there may be diseases where you may have to go to 90. Now the data we've seen here probably suggest that we don't have to go to 90 in other diseases without having tested it, it's hard to say because you have to, in the end, test it in disease. But just from the coverage and the inhibitory potential on the neutrophil function in blood, that we see here, we believe that doses between 30 and 90 are very feasible. And with that, the question can we go to 1 term dosing? I think this is why Camilla made the comment that the 90 mg at the first day give you already an exposure, which is basically exceeding the 30 mg twice daily at 14 days. So that means you could have a rapid onset of a more or less close to complete inhibition of [indiscernible] neutrophils, C5a excitation with 1 dose at that level. And so this gives us great flexibility and to also sum this up here. We do believe that there are diseases that require a higher inhibitory dose than others. And with that, we have the flexibility to go there. And it remains to be seen, but we do hope that maybe a onetime dosing per day may be still in the game here with these data.

Okay. I appreciate that. I wanted to just lastly ask a clarification question on the PK data for the MAD study. So this is from Slide 15, just the longitudinal PK curve. So just so I understand this correct, so you basically have captured the data points to determine Cmax for only the first and last doses, and then there's some sort of like between day 1 and 14, we're just not capturing the peaks at each individual dose. Is that effectively what these curves are showing?

Yes, that's correct, Steve. So we did more time points at the day 1 and day 14 to understand the PK profile.

Our next question is from Sam Slutsky with LifeSci Capital.

Can you guys hear me?

Yes.

Just kind of building off of 1 of Steve's questions before. Just as we think about what's known with other complement-targeting drugs, what's the typical dose response curve look like? Essentially, is more inhibition always better or is there expected to be a threshold effect at a certain point?

Yes. I think this is a very good question. First of all, thanks also for joining. I'm glad to see you on the call. I think it's hard to give a general statement on this because it may be very disease specific. So it may not be that is the same for every disease. However, we -- with our knowledge and with our knowledge from inhibiting the ligand C5a with our monoclonal antibody in different disease settings, we learned that you need to have the ability to come to as much as you can to close to 100% inhibition, if you can. Now that may never be 100% possible, but to have a molecule that gets you up 90% of such a signal is really very valuable because neutrophils, when they're not excited by C5a, for example, they can still work. They can still do their job. They're not depleted, they're not inactive, but they're not overactivated. So if you have a disease setting where neutrophils, for example, play an important role, I think the ability to reach close to 100% is very important. Now we had a head-to-head comparison data point in a preclinical hamster model where we've shown that at the exact same dose, the same formulation head-to-head administered to hamsters, avacopan next to INF904, we saw a doubling of the inhibitory effect. So if, for example, in that model, your goal was to prevent neutrophils from moving into the tissue, you could reach close to 100% or pretty much 100% with our molecule and only 50. So whether that translates into a medical benefit is something we still have to prove, but we certainly believe that it does.

Okay. And then just 1 more for me. Just in terms of characterization and preclinical work, just what's the timing on completing the long-term chronic tox studies? And then as you're characterizing the molecule, is it known if it's CNS penetrant or not?

So maybe the first question, I'll cover first. So the long-term tox studies are 1 of the studies that are ongoing, and they will more or less last next year. So as from our press release, we will be able to initiate a longer-term Phase II study then going into 2025. When they're completed and the report is there, we can hand that in. So your second question was related to if it's known how much tissue penetration you get?

CNS penetrants.

CNS penetrants. I don't think we have concrete data yet to suggest how far this goes in terms of human data. So we certainly believe that the size of the molecule should allow to a certain extent, a coverage, which is something that we're very interested in.

We now have some written questions. The first 1 is from Edward Tenthoff with Piper Sandler, who also asked what do you envision as next development steps?

Yes. So maybe I can also cover this real quick. So I think right now, we are really making good progress on many fronts. There are certain studies that we are still in the completion models. Again, the longest lasting is the 9-month chronic tox in monkeys. And we have made a lot of progress also on the indication selection. We decided to press release this in a separate press release in due course. We are generally very excited about the applicability, but we want to choose the right field to start with and the right indications to move forward in. So I think the next steps are really completing all the necessary steps for the long-term dosing and to initiate the Phase II study. For that, we are also putting up a plan. And Camilla already mentioned, it may be a basket study, but that's not fully decided yet, but that's not off the grid. So one thing that we are generally excited about is whenever the C5a is known to be involved or neutrophils are known to be involved, and that is true for many diseases. So without being more concrete at this point in time, these are the next steps on INF904.

We have a written question from Chang Liu. How does InflaRx plan to finance further studies? Is a partnership plan for the financing and conduct of the further phases of the study?

Happy to hand this over to our Chief Financial Officer. Tom, do you want to take that?

Sure. Happy to do that, and thank you for the question. Indeed, it's an area where we have been initiating conversations with pharma companies throughout the last year. Clearly, there is an interest in what we're doing in the complement field, especially with 904. Small molecules always excite big companies. And so there is ongoing conversations. At this stage, there's nothing decided in terms of what we want to do because it's obvious that for a small biotech company, we want to maximize the value as much as we can. And we think that what we're doing right now will add value, including this data that we published today, but also additional steps going into 2024, should increase the attractiveness of this program, but we are in an ongoing dialogue with a number of companies, and we will consider collaborations in the future.

Thank you. We have a couple of questions from [ Marcell Walden ], also 1 related to partnerships, both for INF904, but also for vilobelimab to advance the pipeline or marketing of the products with additional financial resources or to develop new study designs for the compounds.

Yes. Maybe if I may add also, I mean, at this point, the last reported cash figure of the company was EUR 113 million, which is a good situation to be in, in this market. So we know that we can finance the activities well into 2026. So we are, at this stage, not in a situation where we are under any sort of pressure to do something. And that puts us in the situation that we can really develop our ideas in terms of the future developments, the areas we want to go in. And we will also listen very carefully what the interest areas are of the large companies we're talking to in order to really target our programs in the different areas. So we are in a dialogue. We're moving forward, but we're not under pressure. And we feel that at least in 2024, we will make additional very important steps towards moving 904 into a clear path towards the development -- clinical development program.

And maybe if I can add to 1 aspect here, Tom, also because the question also related to vilobelimab a little bit. Obviously, this is a pathway that we're extremely excited about and have invested in really with our whole team and the company. The C5a, C5aR signaling pathway now having 2 drugs in that, I would say, in that pathway that allow us to address different diseases. We are also -- we remain very excited about vilobelimab and the potential of [indiscernible]. We have made it public that we had a very constructive dialogue with the FDA, and this dialogue is ongoing with 1 potential additional trial needed to potentially get a broader label for an ARDS. That is a huge unmet medical need worldwide and it's quite unique to have that type of commitment and that level of, I would say, flexibility from a regulatory authority to work together, obviously, would need to be a meaningful study well conducted, adequately planned and powered. But this is -- I mean, there is development prospects that are very exciting for us. And as Tom mentioned, we are not excluding partnerships, obviously, in these markets. but we're also able to advance all the programs currently with our cash. And that's really a good position to be in. And with that, we -- as we all, we're waiting for the markets to turn better, but we are prepared to work in between, and that's what the company should do. So thanks for that question.

We have another question from [ Marcel Walden ]. Has the team already developed an idea of what a potential indication for INF904 in Phase II could be?

Yes, we clearly have done this for, I would say, a couple of years now. We have actually a few areas that we have identified as potential to start development in. Now we are not prepared to announce 1 today, but we have a very clear idea of our key indications. And that, as Tom said, it links into our BD efforts to see how can we maximize the value, right? Obviously, right now, we would not necessarily start several indications unless within a basket trial situation. But if a partnership should allow us to do so, that would really maximize value to go into maybe more than 1 indication. And we have a clear idea where that is, it's in some of the areas that we depicted as general areas today.

Thank you. We have a final question from [ Dan Elsworth ], and this is related to vilobelimab. Is there any update on revenue estimates or expectations regarding vilobelimab in the treatment of severe COVID? And in addition, are there any updates on discussions with European regulatory authorities related to vilobelimab?

Yes, I can -- I mean, we are not prepared to make any updates on commercial figures today. We would -- kindly refer here to the next quarter update coming in regards to that. With regards to the second part of the question, yes, we have made public that we're in an ongoing dialogue. We have submitted for MAA this -- in Europe. This is progressing, and this is a process that usually takes all in all about one year. So we're in the middle of it, and we will also give further updates in our next quarter reporting, but this is moving along as we previously stated.

This concludes the question-and-answer session. I will now turn the call back over to Dr. Riedemann for closing remarks. Niels?

Yes. Thanks so much. First of all, thanks to everyone joining this call. We've seen great interest with clearly over 60 people participating, also thanks to our analysts for asking these important questions, thanks to the team. We're very excited. We're really happy to move this molecule forward. And with that, thank you for joining, and stay tuned for more positive news. Thank you. Bye.