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

Welcome, everyone, to the 39th Annual JPMorgan Healthcare Conference. My name is Anupam Rama. I'm one of the senior analysts at JPMorgan. I'm joined by Tessa Romero and Matt Bannon from the team. Our next presenting company is InflaRx, and speaking on behalf of the company, we have CEO, Niels Riedemann. [Operator Instructions] With that, I'll pass it over to Niels. Niels?

Well, thanks so much, Anupam. Much appreciated. Thanks for inviting us to your exciting conference, and I have to give you an update on what's going on with InflaRx. So I'd like to briefly direct you to the cautionary note regarding forward-looking statements since we are a public company. So I'll move through the slide deck and will tell you where I am, so for those of you -- to be able to follow online where we are. So on Page 3, investment highlights. So we are really focusing on terminal complement inhibition with a specific focus on a very interesting target, C5a. We have highly biologically active selective blockers of C5a, monoclonal antibodies, and we have a strong patent coverage, which can be extended into late 2035 on the core patents. We have proven anti-inflammatory efficacy in various settings and proof of concept, I should say, in various settings with a favorable profile of safety and tolerability in over 300 treated patients today. And we recently also talked about encouraging early results in the Phase II study in COVID, and I'm happy to share some of them with you today. Now so we are in multiple ongoing studies, one of them is a severe COVID-19 study in Phase III. The company focus remains also on our lead indication, hidradenitis suppurativa, short form HS. And we are sharing with you today that we're going for a special protocol assessment with the FDA for a Phase III protocol assessment in order to get alignment on the primary endpoint, which is pretty much the main outstanding discussion point between the FDA and us. We have green light from the EMA on this endpoint that we're suggesting. We just very recently, last week, completed enrollment -- target enrollment in the second ANCA vasculitis study, and I'm going to talk about that as well briefly. So on Page 4, the pipeline, I mentioned the Phase III study in COVID. I want to go into a few more details here. HS, I mentioned that we are heading towards a special protocol assessment with the U.S. FDA, and I will briefly touch base on that as well. ANCA-associated vasculitis, we have 2 studies. The U.S. study completed enrollment earlier, and we had seen last patient, last visit. So we're expecting data mid-year. And the European ANCA vasculitis study, that's the study where we are exchanging corticosteroids completely for IFX-1. So it's a proof-of-concept study. It has also now reached target enrollment, and the study is ongoing, but we're expecting data in the second half of this year and more towards the end of the year. Pyoderma gangrenosum, we have an open-label study going on, a small study in this rare disease. It's a debilitating skin disease. We shared early results last year, and we hope to give you more updates on the dose escalation in the time to come here as well. We also just this week announced a new indication that we've prepared for a couple of years here, which is an oncology indication. We're very excited about that. It's cutaneous squamous cell carcinoma, so a skin cancer that is very well responsive to checkpoint inhibition. However, most patients fail to respond over time. And so we're going into second-line treatment for those that are refractory or resistant, and these are locally advanced or metastatic cSCC patients. I'm going to be speaking briefly about that, but there'll be more to come in the future. And we have the IFX-2 as a pipeline addition as well, working as a life cycle drug. And we're working on more nondisclosed assets, and we are also happy to give you updates there more towards the second half of the year as things progress here. So just very briefly on Page 5, just to remind you, we are really especially focusing on C5a as a target. It works through 2 different receptors. The main receptor, C5aR, is most prominent almost in all tissues and organs. C5L2 is a complex receptor with different ligands and different types of signaling through these ligands. When it comes to C5a signaling, this is a pro-inflammatory signaling, and there are good studies to show that, these are here quoted. And it's important because by blocking selectively C5a, we don't touch these receptors on the cell but we're able to really eliminate the C5a signaling, and that's what we've been focusing on. Maybe one important highlight here as well. For those of you familiar with C5-cleaving drugs, like the promising drugs in the market, Soliris and ULTOMIRIS, those credit the cleavage of C5 that comes through the complement pathways. We are really interested in C5a. And why is this important? Because C5a can also be generated by enzymes, for example, enzymes from coagulation pathways. And these -- this cleavage is not inhibited by those C5 blockers, so it makes a big difference to block C5a versus C5. Okay. So let's move into here Page 7 together. Let's talk about COVID a little bit. Obviously, I'm going to keep that slide short. We all learnt that this is a disease, when it comes to the later-stage critically ill patients, where these patients show a very specific to COVID, I should say, very specific feature. They have microangiopathy with -- forming thrombi like vessel, thrombi, almost in every organ, leading, of course, the lung, but in kidney, heart, liver, brain. And it's always the same picture. That seems to be like the vasculature is damaged through this -- through the virus or through the immune response to the virus, and it's really a systemic disease causing multi-organ failure. Typical laboratory findings, lymphocytopenia is a hallmark. When you go to very sick patients, almost every patient has lymphocytopenia. And then also coagulation markers given the thrombotic activity are elevated, and also those that show blood lysis -- clot lysis like D-dimers. And then, of course, something that was known early in the game, there's a dramatic activation of C5a. And I want to speak about that because that's our target. We have done a Phase II study here. We're moving into Page 8. And we developed this model, which I want to show you first before showing you some data. So SARS-CoV-2 entering through the lung, through the epithelial into the bloodstream, it causes dramatic complement activation that is known through the MBL pathway. So you do get very high levels of C5a. Now similar to a vasculitis setting, C5a engages with neutrophils, and those put out radicals, O2 radicals, granular enzymes, and then that can lead to NETosis. So these factors have been shown to be very important in the endothelial cell damage in COVID. Now on top of it, C5a is a feature that's been long forgotten sometimes, but it induces coagulation. It induces tissue factor release in neutrophils and in endothelial cells. So what we see here is an immune response that has an impact on coagulation and on neutrophil-driven endothelial cell damage. Now remember, I said microangiopathy and thrombosis, and that's the key mechanisms that lead to death, as we believe, and both are clearly fostered by C5a. I should say thrombin, for example, and enzymes from the coagulation pathway do something else. They can cleave C5, I mentioned it earlier. So it becomes a vicious circle. So C5a control is a very difficult thing. We think our drug can deliver that. So let's look at a few data together here. Starting on Page 9, this is the trial design. Phase II trial was open-label but randomized. And we published this in the Lancet Rheumatology. And the Phase III study is ongoing with double-blind placebo-controlled. It's a study that should enroll a total of 360 patients. There will be a blinded interim analysis after 180 patients. And this study is ongoing. It's rolling out in multiple countries, multiple continents, and we are very excited about this study. So why are we so excited? Because in Phase II, we saw some very interesting results, but we did not see a big difference on improvement on the primary endpoint, which was chosen as oxygenation index. But we did choose 1 random endpoint as primary, and we discussed with the authorities that this is a learning Phase II in order to fix a suitable endpoint for Phase III. And what we've really seen there, well, there's a very large variability in oxygenation. Patients may be relatively compromised with their values, oxygenation values, but they may switch to become better within 1 day. And that usually happens when the lung isn't primary damaged but when, for example, the vasculature, so the perfusion of the organ, is compromised, which if it opens up and the lung is still functioning, you can see very fast improvements. So large variability on this parameter. But we saw interesting other signals. And, for example, the mortality rate, 28-day all-cause mortality was 50% lower. Now this is small numbers. This was 30 patients, 15 in each arm, but the interesting case was that the 4 patients, the 27% that died in the control arm, they all had multi-organ failure. Now the 2 patients that died in the IFX-1 arm, Vilobelimab arm, they -- one of them had a tube complication. And when it was severe hypoxia, it was discontinued from treatment thereafter. And the other should have not been enrolled, very compromised late-stage lung disease patient, but it wasn't known at the time point of enrollment. So there is this interesting signal. There's clearly fewer patients experiencing renal impairment, which if you run stats, you can sign a p-value with Fisher's Exact Test of 0.05. We have a faster reversal of blood lymphocytopenia with the same stat value. We have reduction in tissue damage markers, like lactate dehydrogenase, and we saw a statistically significant increase of D-dimers at 2 consecutive dose -- time points, sampling points after the first dosing. Now that is a sign for blood clot lysis. It fits to all, so the fact that we saw clearly a threefold reduced severe thrombosis in the lung, which was marked as a severe adverse event. So this is interesting. Of course, it's a small prestudy. But we published this, and it's intriguing. It makes sense because it feeds to the molecular mechanism that we're going after. Here, a few shift plots. Page 11 shows you that at day 15, almost all patients are back to normal with their lymphocyte values, and a few have slight lower values, but that's not the case for the control group. Similarly, the eGFR values on Page 12, you see that there's a clear impact. Now I mentioned the potential p-value on day 15. What really is intriguing, because kind of the second organ usually is failing after the lung in COVID, that we really saw a big difference in terms of lung failure patients. And when you have a lung -- when you have a renal failure on top of your lung failure, then you are putting in -- yourself in the pocket of very high death probability. So this was an interesting signal. And then on Page 13 here, you see the 2 D-dimer signals on day 2 and day 4 with -- given this is 15 patients per arm, I'm an intensivist, I have done an extensive studying for different mechanisms in my active times as a physician. To see that many signals in a few patients, we all felt, and our expert, we had a -- we knew a circle of experts discussing this study on a frequent basis, we all felt very positive about this, and that's why we are moving into a Phase III. So it is exciting to share that with you. The Phase III is running. We expect data -- full data set of the entire study this year. And also, we have the interim. It's a blinded interim analysis. It can result in recommendation to continue to enroll or to stop for futility, but also it's powered to also show potential stop for efficacy. Obviously, that will be a very high bar after half of the patients, 180. But we're excited looking forward to that, and we're going to share news as we have them in due course of this year. Just briefly, we have had many occasions to show the data of our SHINE study in hidradenitis suppurativa. And this is a pretty devastating skin disease where patients suffer dramatically. We had this study of 177 patients. And I'm not going to repeat the entire study results, but what I would like to share with you is through the 4 dosing groups and placebo, the idea was to show a statistically significant dose response on an established endpoint called HiSCR and then move to patients in an open-label extension, additional 28 weeks, 24 weeks of treatment, according to whether they were responders or nonresponders. And in that open label, they should receive either 800-milligram every 4 weeks if they were responders, or twice as much, 800-milligram every other week, if they were nonresponders. So unfortunately, we did not take over the higher-dose group, and we learned a lot from this trial. We've shared with the public on Page 16 that in the main period for 16 weeks, we could not show any effect on the HiSCR because we had a 47.1% placebo response rate. Now these are small groups, 35 patients. We learned that there's a dramatic variability in this score. It's very much impacted, especially by the nodules. These patients have 3 lesions: inflammatory nodules, abscesses and draining fistulas. Now draining fistulas are the most bothersome lesion, and we have now new data generated in response to our FDA meeting. And we have seen a quite strong effect on draining fistula reduction, 63.2% relative in mean media, and this is higher. And this was that sick. Of course, this was not the primary endpoint, but we've also seen that the end count had an impact and looked like a dose response. But also the IHS-4 score, which is a score that scores reduction in all 3 lesions. Now it's important for you to know, the HiSCR doesn't ask for reduction and doesn't respect reduction of draining fistulas. So the most important event for patients with draining fistulas that they stop draining and being inflamed is not captured in this score. We feel this is unjustified. We feel the HiSCR is a score with a lot of variability and it will put significant risk on studies moving forward, even though we have knowledge how to mitigate this risk through this study. So we suggested, based on our results, that we should forward this indication with our drug, specifically prompted by the Page 17 long-term results. You see here the end count on the right side. This is after 9 months of treatment. So these patients, about 2/3 of the patients completed the entire study. And at the end of treatment, we saw a marked reduction of the end count of the draining fistula count of the IHS-4 score in ANF count, and this is all after 9 months of treatment in this trial compared to the very baseline. Now we don't have a placebo-controlled group for 9 months, but we do have the placebo-controlled group after 16 weeks, after 4 months. This is a difficult comparison, but it shows you that the well-performing placebo group on the HiSCR, remember 47% response, was not so strong on all the other counts, and this shows you the problem in the score in and of itself. So we see that the majority of patients had a long-term benefit, and our KOLs, our expert advisers, all saw the same thing. So we're moving this forward. On Page 18 is our strategy, just very high level. We are very excited about discussing a new endpoint, the IHS-4, for numerous reasons. I'm not going to go into detail here today. We've chosen the special protocol assessment. That means we're going with a Phase III worked out protocol to the FDA, and we're submitting all the additional homework and evidence that we generated, including new prospective data on patient input on the importance of the lesions, including additional data that we got from the own data set. And I think they all point into one very, very clear direction: draining fistula reduction is the most meaningful event for patients that suffer from draining fistulas. And it's, in our eyes, unjustified if a score is used for approval for this disease that doesn't reflect reduction in these lesions. So we're going to share the outcome of this. Usually, the special protocol assessment allows an interactive discussion. We have a lot of additional work to submit, but I also want to share finally here a lot of the Phase III discussions were already discussed in the end of Phase II meeting relating to the chosen dose justification, preclinical package, general inclusion/exclusion criteria, set up, et cetera. So really, the main open topic here is the endpoint. Good. Just a few words on ANCA vasculitis. As you know, there's proof-of-concept of the pathway established through a C5a receptor or chemical inhibitor which recently had a positive Phase III and is now on the path to approval. This is very exciting. This is derisk for us. The role of C5a in this disease has been substantially worked out before, 30 years ago, so to speak, and of course, also through the receptor antagonist success. And we feel we have a good angle here with a very tight control of C5a levels in the vasculature. Remember, this is a vascular disease. The main damage happens inside the vessel at the endothelial cell level. And we're really confident. We have 2 running trials. We think that we have rapid onset and a potential potency difference that could be envisioned when we look at the receptor antagonist that was recently tried. So we have 2 trials. Page 21 shows you the U.S. trial. This done -- this trial has completed enrollment and seen last patient, last visit. This was 2 different doses of adalimumab on top of standard of care. Not going into greater details here. We had voiced the interim blinded results that we didn't see any signs for concerns on the efficacy or on safety, of course. And then the European study here on Page 22. This is really a study with a 2-stage design. First, we test always against placebo. The one is where we reduce corticosteroids plus standard-of-care and with adalimumab. And then we are now completed also with the second part where we completely exchange corticosteroids with adalimumab. So this is a proof-of-concept-oriented study. We are eager to show data and see data towards the end of the year. And with that, I want to leave it with ANCA vasculitis. Just a few words about the remaining programs really here. Pyoderma gangrenosum are mentioned. This is a rare but a very debilitating disease. It's a skin disease, alterative skin disease. We are conducting a study that should target to enroll 18 patients. This is a very rare disease. So we've added additional sites to increase enrollment speed, but we shared the results of the first 5 patients previously. And just on Page 25, to show you the interesting early signals, 2 patients that had elevated baseline C5a levels were not just reaching the primary endpoint, which is really target ulcer shrinkage according to a score, but they completely closed the target ulcer and closed all skin ulcerations, total body, and stayed healed for many, many months after last treatment. So that was already voiced previously. So we're excited about that. Again, it's a very rare disease. And moving forward, we're hoping to update in due course on the next dose groups. Okay. So last but not least, we also want to very briefly talk about oncology here. Oncology is still a new field for us, and we are now moving into cutaneous squamous cell carcinoma. There'll be plenty of opportunity to go into more details. Just a few words why have we chosen this. Well, it's known that C5a receptor is expressed in this tumor. It's known that C5a in squamous cell carcinoma is actively involved in recruiting MDSCs, myeloid-derived suppressor cells. These are the bad guys silencing your T cells. And when you block that pathway in mouse models, beautiful data being published, showing that you will, a, keep the MDSCs outside the tumor and you get T cells back into the tumor, killing and -- the tumor and stopping progression. There's also knowledge that there could be additive effects with checkpoint inhibitors. So we designed a study that blocks C5a as a monotherapy in second-line refractory or resistant to checkpoint inhibitor locally advanced or metastatic cSCC patients. And we also want to show then that when we combine the treatment, monotherapy with adalimumab, within this case, pembrolizumab, that we can either see a similar effect like the monotherapy or have an additive effect. Again, there's some mechanistic reasons to believe that, that may work. I just want to point out, there's a few other reasons to believe C5a plays a role in the tumor and microenvironment. It may also help promoting tumor progression in and of itself, there's data showing that and suggesting that. And it's also involved in different animal models in metastatic disease, so it kind of fosters the metastasis. So blocking it may really be helpful on numerous levels, and we are excited about that. We think cSCC second-line treatment, for which no other treatment is approved and these patients are really prone to die otherwise, is a very important element to help patients here, and it's a high unmet medical need. And I just -- as a last remark, these patients respond very well to checkpoint inhibition, up to 50% primarily. But pretty much all patients over time lose response. So in the end, these patients end up at a second line no approved treatment and no available working treatment situations. And so we feel strong about this. We really spend a lot of work into that, and we're excited to give you more updates along the line. So with that, I think, clearly, the -- we come to an end here. The presentation shows that we keep a strong focus on terminal complement. We're really building out our expertise. We've learned from HS, but we still saw a very active drug, and we believe our drug is active. It's been safe and well tolerated so far. And we're very excited to share updates on these numerous programs. And with that, I would like to really thank you for your attention, and I'm happy to move into an engaged Q&A session now with the whole team. Thank you so much.

Niels, if you want to just introduce the broader team on the line, we can get started with the Q&A.

Absolutely. So on the line with me is the entire team. So I'd love to introduce, first of all, my business partner and Co-Founder, our Chief Scientific Officer, Renfeng.

Hi.

Renfeng and I met at the University of Michigan and studied complement together as post docs in the laboratory of Peter Ward. So this is really where we are today, and we did this all the way along together. Then I would like to introduce also Thomas Taapken, our new CFO. He just joined in October. Thomas is a very seasoned CFO. He's been in CEO and CFO roles in different public and private companies, and I think he's also been 8 years venture capitalist, so it makes him likely dangerous for the rest of the team. And then we have Jordan Zwick. Jordan's our new Chief Strategy Officer. Jordan is with us for a while now. Very excited to have Jordan on the line with us, and he's really heading strategy and business development activities and has been a great addition to this leadership team. So that's the team here for you today, and happy to move into Q&A.

And maybe we'll start with the COVID-19 program. You've got the potential scenarios around an interim. What's the bar for futility? And then what's the bar for stopping for efficacy? Like what are those ranges here that we should be thinking about?

Yes. So I mean we haven't concretely voiced the exact bars. I mean futility is clear. We set a certain statistical bar that if we see very little activity, or no, that then the study would be stopped. So this is a 2-stage design. We don't adapt the second part, so the decision is either to move into a full additional 180 or not. That's because if you do it dynamically, you lose power in the study. And so what we've done is we modeled all types of scenarios and said, okay, at what point it becomes rather unlikely that with a very successful second part, we could still make up for it, and that becomes a bar for futility. On the efficacy side, with 180 patients, this is pretty much determined. So you need to be relatively close to a high bar, showing what you were supposed to be showing. So without giving you concrete numbers, clearing that bar is really high -- is really a high bar. Clearly that high bar is something that we'll be looking forward to, but it's not a given. So the study is powered with a 90%-plus power for enrolling 360 patients. The most likely scenarios is that we complete the 360 and see how it works out.

Got it. Okay. And then in the HS indication, there's obviously some regulatory differences, right, in the U.S. and the EU. And I guess with the SPA that you guys are submitting this quarter, what if the FDA doesn't agree, right? Like what happens, right? Would you run 2 parallel trials? I mean, obviously, I think your goal has always been 1 global trial, but -- so what are the scenarios around the SPA that we should be thinking about? After you submit the SPA, what are the time lines for feedback?

Yes. Let me maybe pass that question to Jordan. He's been very involved with the team, with me together, in designing this. And Jordan, do you want -- do you mind?

Yes, absolutely. No, thanks, Niels, and great to be on the phone. With the SPA, essentially, once you submit the SPA, the FDA has 45 days to respond. Typically, that response will be quicker, but that is their time frame. And that will be a back and forth conversation. The reason we decided on this process is given what a SPA is and it's an opportunity to reach an agreement with the FDA on a Phase III design, it's the way to move this forward as opposed to going to an advice meeting. And given the interaction we've had with the FDA, all is open at the endpoint at this moment. So it's a good way for us to get agreement on an endpoint and move forward that way. Now in the interaction with a SPA, written back and forth, if we don't reach an agreement, we can submit a 30-day request for a Type A meeting, which is a meeting for a stalled development plan, which typically comes in reference to a SPA. So the nice thing about the FDA is there's a lot of guidance for timings of these meetings and allows additional FDA personnel to attend the meeting beyond just the Type C advice meeting. So we're excited to go through that process with the FDA.

And competitively, how are you thinking about the HS space? You've had one complement competitor go into Hurley stage 3 patients, only based on what they saw in Phase II. Are there subpopulations that are maybe more attractive, given maybe, I think, in HS, the hardest thing to do is kind of control placebo? So if you go into a more severe population, maybe you can control placebo a little bit more? How are you guys thinking about that?

Yes. Maybe I can -- we can take that. Anupam, I think you're absolutely right on there's no biological plausibility why a drug should be working much better in the Hurley stage 3 or 2 because there's no clear definition difference, it's just more anatomically regions involved in stage 3. And typically, stage 3 patients show exactly what you pointed to is they have very unlikely -- only low abscesses and nodule accounts. So the group of patients with very low baseline abscesses nodule counts is the one that shows you, in placebo group traditionally through published studies, especially through the AbbVie studies, high placebo response rate. By the way, we found data showing that this can be over 50%. So we're not alone, that has been shown before. The point is, when you're choosing Hurley stage 3 you are -- yes, you are reducing the risk that you see a very high placebo response rate on that very difficult HiSCR endpoint, but you then may also discuss what's the other side of the spectrum going to look like. So there are risks associated to the HiSCR that can mitigate it when you really deeply understand the signs and, I would say, this disease and the lesions and the statistical importance behind it. But we really felt that there's no biological plausibility to talk about Hurley stage 3 versus 2. However, you ask me, are there subgroups? Yes, there are subgroups. If you think about the one subgroup that would come to my mind that is specific subgroup because that growth -- that actually shows active draining fistulas, right? Because even in Hurley stage 3, you can have fistula that are nondraining and quiet and kind of existing as a lesion but not as something that bothers you. So this subgroup, you could call it fistulizing HS, is, of course, of interest if you show effects on fistulas. However, the nature of the disease is that you have ups and downs in all the lesions. So we still feel with all the biological plausibility that we should use a score that shows reduction in all 3 lesions, and we believe our drug shows this regardless, has efficacy in this regardless of whether we're talking to Hurley 3 or Hurley 2. And so we really want to work this out. And I think we have now very strong arguments to use scores that show -- or reflect reduction in all 3 lesions.

I'm going to turn it over to Tess to ask a couple of questions on ANCA.

Yes. Thanks, Anupam. Yes, so guys, I think we're headed towards 2 datasets in AAV this year. And I think, in particular, I think, the European study is focused on efficacy with -- so maybe perhaps could you set up for us kind of a win scenario in particular on that European study?

Yes. So first of all, the study is set to provide a certain proof-of-concept to say, look, we can safely and effectively treat patients, just as you would treat them with high-dose corticosteroids. So meaning we can bring you in remission, which is the main focus for this life-threatening ill patients, without using long-term high-dose corticosteroids. So if we achieve this goal, if there's no trends towards less effective remission compared to our placebo control group, they -- the placebo control group does receive high-dose corticosteroids, then that would be the primary win, right? If we saw a safety issue or clearly less patients getting into remission, that would be difficult for us. So that's the first stage. However, I mean, one thing that -- besides exchanging the drug, corticosteroid long term, which has a lot of side effects and which is -- I just want to point that out, in and of itself, it is a strong signal. This is -- name me any other pathway, any other drug you can block to exchange corticosteroid high-dose treatment. So it is a strong thing. However, of course, the community hopes for any signal to also improve standard of care aside from the side effect profile, which means, a, can you bring patients faster in remission? That would be -- any signal to faster remission would be fantastic. Or can you bring more patients in full remission? That's a high bar because standard of care gets most patients in full remission, clearly, over 60%, 70% go in full remission, however, any signal towards that would be very positively received. And I do want to make one analogy to the avacopan story, the C5a receptor inhibitor. They saw a very interesting late signal, which is very well received with rheumatologists as well, and that was an improved kidney function. The trial was not primarily powered for that, but as a secondary endpoint, I think that was a strong signal. So anything that -- on top of exchanging corticosteroids which show a certain improvement to the current standard of care is really a double win scenario for us.

Maybe a final question to wrap up here, maybe to get Thomas involved, the newest member of the team. Just remind us of the cash position and how you are thinking about the runway with sort of multiple inflections coming in 2021?

Right. Yes, thank you very much, and pleased to be here, indeed. Yes, so the latest reported figure was EUR 95.7 million. That was in the third quarter of 2020. And with that money, we are funded over 2 years to fund the existing programs that are in place. However, it's quite obvious that if we are to embark on a Phase III program for HS, we would certainly have to consider a significant amount of additional cost that would require us to go out and raise the money for that. The same is also true for the COVID-19 situation. If we assume that we're successful in this study, which we, of course, hope, then by the year-end, we would be in a situation where we could potentially file for some sort of accelerated approval, which would then require us to build the infrastructure that is necessary to be able to commercialize the product. So all of these, positive outcomes, the positive outcome of the SBA that we're doing with the FDA, the positive outcome of the COVID trial, they would be catalysts for us to go out and consider financing. But at the same time, we would also look opportunistically at the market and see how the situation evolves because, obviously, it's clear that for us to be able to further the programs, we will need additional funds.

Okay. Well, Niels and team, I want to thank you all so much for a really productive session. Thank you, guys, for kicking off the first session of the conference today.

Yes. Pleasure, Anupam and Tess. Thanks so much for inviting us. We really enjoyed it, and we'll stay connected. Thanks so much. Thank you.

Thank you, Anupam. Thank you, Tess.