Hello. Thank you for joining us today for our presentation on the top line results from our phase III PANAMO trial of vilobelimab in severe COVID-19 patients. A replay will also be available on our website following the live event. Before we begin, I'd like to point out that we will be making forward-looking statements that are based on our current expectations and beliefs. These beliefs are subject to certain risks and uncertainties, and our actual results may differ materially. I encourage you to consult the risk factors discussed in our SEC filings for more details. Our agenda today will include an introduction and key messages, a review of the vilobelimab mode of action in COVID-19, the PANAMO trial design and phase II results review, and finally, the PANAMO phase III trial results.
We will conclude with a live Q&A session, for which I will give instructions at the end of the presentation. Today, I will be joined by our CEO, Professor Niels Riedemann, and our Chief Clinical Development Officer, Dr. Korinna Pilz. I will now hand over the call to Professor Niels Riedemann to get started. Thank you.
Thank you, Jordan. Welcome everyone to today's press call. I'm excited that we will be presenting to you the top-line results of the PANAMO study. Please allow me to make a short introductory statement before I go into the summary here. This is an important moment for InflaRx, because the company has been funded based on research that was originally conducted 20 years ago at the University of Michigan in Ann Arbor, in the U.S. Also based on the strong belief of the founders, that C5a plays a crucial role in infectious organ disease and life-threatening organ injury, in sepsis. Now, based on this belief, we founded InflaRx.
You know, the last 15 years of research, we feel, may be validated today, you know, by the data we're presenting, since we believe that the data show a robust effect, and suggests that vilobelimab, the first-in-class C5a inhibitor, has life-saving potential. With that, I would like to go right into the key messages. Please, next slide. The primary endpoint was the 28-day all-cause mortality, and you may know that this is kind of the toughest endpoint for intensive care studies recommended by the FDA and other agencies around the world. The clinically meaningful benefit was detected for vilobelimab, and now we will go into details in a minute, but we missed the statistical significance level that we put up using the pre-specified analysis method. However, we had pre-specified different analysis that shows significant improvement in the 28-day all-cause mortality.
I want to put your attention specifically on the significant treatment benefit in the predefined subset analysis of the Western European patients, which made up for more than half of the patients in the trial, and in which we showed a 43% relative reduction in 28-day all-cause mortality. We also showed a significant treatment benefit in all three predefined subgroup analysis of patients with higher disease severity at baseline. Now, this was based on our knowledge, our research, and also on the phase II data that suggested that severely sick patients may show a stronger benefit from our drug. We also will show you a continued robust improvement in all-cause mortality up to day 60, which was the end of the study.
Finally, we will show you data related to a favorable safety profile for vilobelimab, confirmed in this critically ill patient population. Next slide, please. Before we come to the data, I just want to very briefly review what we had done before in COVID-19. Next slide. This was our hypothesis really derived from in-house knowledge on other work, but also from the phase II data of the phase II/III PANAMO study. We published this work in The Lancet Rheumatology. Really what we found is that C5a seems to lower mortality by impacting neutrophil activation. Besides other factors, we know that neutrophils secrete tissue factor. They are very much involved in the organ damage, in this case, in the endothelial cell wall damage.
We hypothesized, without going into all details, that the microangiopathy with thrombosis may be influenced strongly by C5a. There were certain signals in the phase II study that I alluded to, but I do wanna point out that today there's additional evidence from other studies that suggest that some of these hypotheses, specifically on tissue factor release and coagulation, have already been proven true with other research. Next slide, please. Next, please. Just briefly to recap the design. You know, this study is the phase III study, is really about critically ill intubated patients with COVID-19-induced pneumonia, and they had to have additionally ARDS criteria. The primary endpoint was the 28-day all-cause mortality.
We had key secondary endpoints, especially the 60-day all-cause mortality, but also the 8-point ordinal scale improvement, the kidney dysfunction and renal replacement need, and of course, also the safety aspect. Now, the phase II study was a small open label, but randomized study where we only enrolled 15 patients in each arm. We did learn about the PK/PD profile. We also learned about the intubated patients showing a stronger signal. This is why we designed the phase III part of the study based on this pre-work. I just want to remind you, in the phase III part of the study, we did administer six doses of 800 mg IV vilobelimab in the first 28 days, and then we followed up the patient up to day 60. Next slide, please.
The phase II study results, we originally started with an exploratory primary endpoint, which was also pre-discussed with authorities here in Europe, and looked at the oxygenation ratio, which is one part of the ARDS criteria, that is used. However, we found a very high variability, and this seemed to be not a very suitable endpoint and not even a good surrogate, because it's very dependent on patient positioning and other affecting factors. However, the key secondary endpoint showed a pretty substantial lower all-cause mortality rates. We also showed other signals, especially less renal impairment and a faster reversal of blood lymphocytopenia, which is a hallmark of COVID-19 disease, among other effects. Next slide, please. Without further ado, we would like to go now into the phase III top-line results.
The first slide here looks at the 28-day all-cause mortality given the Kaplan-Meier curves. What we've seen here is a 23.9% relative reduction of mortality. This is the full analysis set, and you see that we reduced mortality from 41.6% to 31.7%. As you see, we slightly missed the pre-specified primary endpoint with a p-value of 0.09. Besides this, what we've seen and what we really like about this is that there is an early separation starting as early on as day four and a consistent separation of improvement in the vilobelimab arm. When you calculate that into how many patients you need to treat, we have one additional life saved for every 10 vilobelimab-treated participants compared with the placebo arm. Next slide, please.
Just briefly, the Cox regression approach that we principally chose for the analysis of the primary endpoint, you know, we feel is definitely the right approach. I want to remind you that all the Cox regression analysis here is adjusted for the one factor that is known to affect mortality, which is age, in COVID-19. However, we used in the final version of the statistical analysis plan a stratification by site to be included in the Cox regression. You know, this was then the pre-specified primary endpoint. As we said, it slightly missed the statistical significance level of 0.05. However, the original suggested one was the non-stratified version, and this would have resulted in a p-value of 0.026.
Now, we did change this based on recommendations of regulatory authorities, which we felt were justified, and therefore we changed it. However, we looked at different other ways that are usually used to look at Cox regression. One of them, the so-called frailty model. Please keep in mind this is post-hoc now. This assigns random effects and random treatment effects in the sites. Also then, you know, I want to point your special attention here to the stratification by country, where we saw an even stronger p-value effect. There are certain reasons for that I will explain in a short while here. Even if not applying the Cox regression approach, but a simple kind of group comparison, if you will, with a log-rank test, even in that test, we would have hit statistical significance.
Next slide, please. We did use various pre-specified ways to look at sensitivity analysis. What that does is you look at the patients dead or alive. You see them here, the two, the table upfront. Then you look at the missing values, because some patients may withdraw consent or leave the study for other reasons. It's always a question, how do you impute this? That therefore you use sensitivity analysis. Now, it just so happened that we have nine patients missing in each arm, which is around 5%. This is a relatively low number. We are happy to see that. What you do is you impute those missing values.
The worst case in favor of placebo is when you basically say all missing patients in the vilobelimab arm would die and all missing patients in the placebo arm would survive. We did not expect to see statistical significance given the you know the trial power and the size of the trial. However, what is important is that even when this worst case scenario, we still have the signal, the risk difference here with -5.4% in the right direction. Now, if you just treat both groups similarly, like all alive, this is what you usually call last observation carried forward or all dead, then you would still yield a clear statistical significance. Probably the most valuable way of imputing missing data is the multiple imputation model. This was also pre-specified in the statistical analysis plan.
As this is really accounting for the data you know from the study, but also assigning additional random effects to basically mimic real life. Here what we see is an even stronger p-value, which further makes us believe that the data are robust. Next slide, please. Thank you. Looking at 60-day all-cause mortality, this is the same full analysis set now looking not only at 28-day but further to 60-day. The same effect principally was seen. We still have a 22.7% relative reduction in mortality and a similar hazard ratio. Again, we used the final stratified, site-stratified Cox regression analysis and you see a p-value of 0.08. Next slide, please.
We did the same analysis using the same originally per protocol analysis with no stratification or the other models that I explained just before. We have a similar effect. All the other p-values show a statistical significance if they had been chosen as the primary. That is important for us 'cause the 28-day data do not seem to be a chance finding, but are really carried forward the effect of saving lives to day 60. Next slide, please. Now I come to one of the most exciting slides here in the slide deck. This is a pre-specified analysis of the European patients. Now, the reason why we pre-specified this is we knew that we would likely have a large amount of European patients, but we also know the sites here.
This is the Netherlands, this is Belgium, this is France and Germany, and we can assume relatively similar treatment algorithms and also equipment in these areas. What we've seen here is an all-cause mortality reduction at day 28 of 43% relative reduction. When you look at the Kaplan-Meier point estimates, we have reduced the mortality in the placebo arm of 37.2% down to 21.2%. These were also statistically significant from p-value 0.0142. You see on the right side that this effect was just, you know, as present when carried forward to day 60. Now, this brought up the question, why was this effect so strong? We looked at the different regions, and we also pre-specified for other regions.
Before I show you, just wanna remind you, this would project here in Western Europe that one additional life was saved for every six patients at day 28 and for every seven patients at day 60 who were treated with vilobelimab versus placebo. Next slide, please. When looking at the pre-specified other regions, one thing becomes relatively clear. Now, these are not the same numbers. As you see, it's 209 patients in Western Europe. This is more than half of the trial. You expect more variability in lower numbers, obviously. But there is a clear trend towards improvement in Western Europe as well as in the, what we call rest of world, South Africa, Russian Federation. However, in South America, this effect was much lower. South America here means Brazil, Mexico and Peru, where we recruited patients.
Without being able to tell you all the data yet, because there are still analysis ongoing, one thing we can already share is that we have identified quite substantial baseline differences in that patient population compared to the Western Europe one. The effects seems to be clearly impacted by the region of the world. There may be various reasons for that. Next slide, please. This is also exciting really because these were pre-specified analysis in patients that have a higher baseline severity in looking at 28-day all-cause mortality. Now why is this important? Our earlier research, also the phase II data showed a more substantiated effect in the most severe patients.
We looked at three ways here to say baseline severe patients. One is the ordinal scale. An ordinal scale of seven means that next to being intubated you have to have one additional organ support. That could be vasopressors or other organ support like renal replacement. These make up for roughly 100 - 130 patients here per group. The second one was the ARDS severity criteria. We looked at patients that have oxygenation index as below 100. This would be severe ARDS. Last but not least, we looked at patients with impaired kidney function using the estimated glomerular filtration rate. All three pre-specified analysis showed a clear benefit and reached statistical significance here. You see that on the right side.
With these forest plots, you know, and the variability really not reaching one. These were very convincing data that showed that the drug seems to be working even more, even stronger in patients that are more severely diseased. Next slide, please. We're coming now to the other secondary endpoints. One of them was the change in the ordinal scale. What we found is that the change in the ordinal scale at day 15 and day 28 followed the 28-day baseline mortality rates. We did not see an effect where patients would be earlier out of the ICU. In a way this is also not to be expected because patients who survive a near-death situation are usually known to have some longer stay on the ICU.
We do see a shift, but this really follows mortality clearly. Next slide, please. Now, another, secondary or two secondary endpoints dealing with kidney function. Now this was the proportion of patients developing acute kidney failure. Now, surprisingly, and this was kidney failure derived from, data that were entered at pre-specified time points, in the data set, in the data analysis. Patient reaching criteria for acute kidney failure were only eight patients in the velo arm and 12 in the placebo arm. Now, these are clearly less patients in the velo arm, but of course, as you can see, these are very low numbers, so not to be expected that the statistical significance can be reached with that few patients going into acute kidney failure. However, next slide, please.
In the next slide, we looked at the proportion of patients free of any renal replacement therapy within the 28 days of randomization. We used the Fine and Gray model here to look at hazard ratios. This shows you a rather nice separation. Even though acute kidney injury was detected only in a few patients, the need for renal replacement therapy using this model was really showing a nice separation. The P value almost reached the 0.05 limit here with 0.0696. Next slide, please. Just coming to safety, there are two slides looking at safety. This is really the overview, just looking at all treatment-emergent adverse events.
You see on the left side here that any treatment emergent adverse events, they are equally distributed. There is any related treatment emergent adverse events, and then serious, any serious TEAEs, any serious related, TEAEs and any fatal. You said that overall there is of course, a really good distribution, so no peaking out signal. Of course, for the fatal TEAEs, it's actually lower in the vilobelimab arm. Next slide, please. Now, another pre-specified look was focusing on infections, and these are the MedDRA high-level group terms that you see here. These are, you know, a prefix, so to speak. They are not invented by us. Also here we see a very even distribution between vilobelimab arm and the placebo arm. Nothing really peaking out.
Obviously we have to keep in mind that we had significant more patients, number of patients surviving, so being longer in the hospital because they survived. And when you're in the hospital, specifically when you're on the ICU, principally, you have a higher chance to catch a fungal or viral infection or a bacterial infection. Even though the numbers here show really very small differences, if at all, there'll be additional analysis following to also look at that. For example, looking at that per treatment days applied. Okay, next slide, please. I come to the key learning and the summary again. The primary endpoint of 28-day all-cause mortality showed a clinically meaningful benefit in the vilobelimab arm but missed the statistical significance level here with the pre-specified analysis method.
Now, prespecified and post hoc analysis both suggest a robust reduction in mortality for both day 28 and day 60 in the entire treatment set, the trial analysis set for the vilobelimab treatment compared to placebo. In the Western European patients, we saw a significant treatment benefit. This was a predefined analysis, just want to recap that. We saw 43% relative reduction in 28-day all-cause mortality. Similarly, in the three predefined subgroup analysis of more severely diseased patients, we saw also significant treatment benefit comparing vilobelimab to placebo. The safety profile really does not pose any concern for us and really confirms that vilobelimab seems to be safe and well-tolerated in this critically ill patient population.
We are excited about presenting this data, and the company clearly plans to discuss these results with regulatory authorities, and then to learn how next steps could be, and we will definitely update the public once we are there. With that, you see a happy founder and a happy team. I would hand back now to Jordan to go into the Q&A session.
Thank you for joining us for today's event. This concludes the formal presentation, and we are now opening the call up to questions. You can ask questions in one of two ways. By raising your hand icon under the presentation window, or if you would prefer, you can submit a question in writing via the Q&A button below the presentation window. I will then read the questions aloud. It seems we have questions from the line. Our first question comes from Yatin Suneja at Guggenheim. Yatin, the line is yours.
Can you guys hear me?
Perfectly.
All right. Very good. A couple questions. Thank you for all the details. With regard to the change in the statistical method, which regulatory agency asked you to change it? Was it the U.S. or the Europeans? In terms of the Western European, can you just comment a little bit more on, you know, what might be driving that difference? Is it more aggressive use of SOC or standard of care, or there is somehow changes or change in the patient population? You know, maybe they have different virus strain or core morbidities. Just get to these two questions, and then I have another follow-up.
Niels, take it away.
Yes. Thank you, Yatin, for the two questions. I wanna start with your first question. Just wanna clarify, we have not been asked to change. It's not that this was you should change it. This was a recommendation, and we looked deeply into this recommendation. It was the U.S. FDA making this recommendation. I think we can share that here freely. We chose to take that recommendation. It was not really an ask to change. It's important for us that we make that clear. It was a company decision based on that recommendation. The second question was, how can we further allude to why we see this relatively strong effect in Western Europe? As I said, we have not fully concluded yet the analysis. There's numerous analysis going on.
We do see quite substantial baseline differences. They are pointing to especially the patients being admitted in Brazil and in Peru, which make up for this effect mostly, that these patients may be significantly younger and may be also less severely diseased. We have to further look into this. We can't make definitive statements today. This analysis is still ongoing, but I would say it really points out that especially in the two countries that drove this effect, we seem to have looked at different patient populations. We can't fully comment on the viral strains 'cause we didn't test for each viral strain in each patient.
Obviously, if we can match, and that's work that's ongoing, we can match the time and the reported strains and strain dominance per region. That of course carries a certain uncertainty whether that is true for each individual patient. We do, however, have concluded the study with the last patient being enrolled in October last year, so this was before the Omicron variant was reported. We do anticipate that most of these patients carry Delta and other variants, but not necessarily the Omicron variant.
Got it. And then in terms of, again, focusing on the Western European, were there any significant differences in the ICU stay or acute kidney failure in that subgroup relative to the overall? Just trying to get a sense of, you know, how supportive some of these secondary endpoints were in Western European. Just talk a little bit about your next step for COVID, for this particular indication. Are you gonna engage focus mostly on the Western European? Like, which regulatory agency are you gonna sort of try to hone in on? Just give a little bit more color there. Thank you.
Sure. Yeah. For your first question, Yatin, you know, this work has not been yet concluded on the detailed differences. This is something that will be ongoing, and we hope to report further in upcoming conferences. Also, we have not yet the full analysis, right? These are just top-line results that we went through. We will probably learn more about that, and I cannot share more than we have, as of today, obviously. You know, please stay tuned. We're gonna look into this in real great detail. The second question is, whom are we trying to engage, like, in terms of regulatory authorities? I mean, the obviously for us important regulatory agencies would be the European EMA and the FDA.
Now, we can't make any representations if these agencies will be open for submission or how they're gonna view the data. I do think we have it here and also in the press release, we plan to have these discussions with the regulatory agencies and see you know how they view the data and whether we will be encouraged to submit or encouraged to have further discussions. As this plays out, we would definitely update the public.
Thank you.
Thank you, Yatin. You know, our next question, 'cause it's, you know, relevant, it comes from the written questions. Anupam Rama from JP Morgan, who just wanted to just be clear, we'll be meeting with regulators globally versus EU only. That is correct. Anupam, as Niels indicated, we will be meeting and engaging with EMA on the EU side as well as FDA in the U.S., given we had engaged both these agencies in the beginning and want to follow up the next steps with both. Hopefully that answers your question there. The next question comes from the phone line. Ed White from H.C. Wainwright. Ed, the line is yours.
Good morning. Can you hear me okay?
Yes.
Great. Just a couple of questions. In general, can you make any comments on the standard of care in Brazil and Peru versus the rest of the world when it comes to COVID patients?
Yeah, I think I can. I mean, Jordan, I'm just gonna take the question.
Go ahead.
Korinna, please chime in. I mean, this is a difficult question because obviously it's very difficult, and we are not really in the position to say on a detailed level what the standard of care looks like. Obviously, what we have done is an in-depth feasibility study before we started, and we have selected trials that are both from the equivalent standard as well as from their standard of care, principally in the same, I would say, league or in the same arena as centers here.
That is not true for all the centers in Peru, but there are centers, specialized centers that treat these patients, and we have really tried to be very careful in selecting centers that principally have the same equipment and have similar guidelines. However, as you know, I have an intensive care physician background and I run a large ICU here. I must say that this is known in intensive care trials. It's always a big problem because even though you may have the equipment, even though you may have similar guidelines, standard of care can differ substantially depending on local, I would say, use of the guidelines, and that's not necessarily something that you can fully capture.
To really make a substantiated statement on standard of care as per the sites, that's going to be extremely difficult. I mean, I think we've done what we could to confirm that these sites operate on a similar level, but I know that standard of care differs a lot, and that's why we pre-specified the regions for the subgroup analysis. I don't know, Korinna, if you had something to add here, please feel free.
The only thing I could maybe add here is that we do have information about the COVID-specific standard of care that was introduced over the time, and here we do not see any differences between the regions. As Niels alluded, we don't have a full picture of the, let's say, ICU-linked standards, and we have also not a real grasp on it in the pandemic situation if all units were operating under their optimal conditions during the waves they experienced as well.
Okay. Thank you. Do you have any guidance or any thoughts at all on the timing to the meetings with the FDA and EMA?
Niels, I don't know if you have any comments on that.
Yeah, I think we cannot concretely guide. I think at this point in time, there is still a rather rapid response, so we don't anticipate like, that we would meet on a usual three months kind of pre-notice schedule, but rather faster. But I can't make representations. I know in Europe that can work within several weeks, and the same thing is true for the U.S. It's gonna be difficult for us to understand whether that changes currently or whether they are fully operating under the same time schedules. At this point, we anticipate it will be faster than usual, so not in several months, but rather in several weeks. But I can't make clear like representations if that's going to be the case. But we definitely gonna be trying that.
Okay. My last question is just from a strategy standpoint. You're developing vilobelimab for several indications. If the agencies request that you do another large study, is it worth to you to do that large study, or would you focus your resources elsewhere?
Yeah. Thanks, Ed. You know, I guess I'll take that one and pitch it to Niels and Korinna. You know, I think it's difficult to know what they're gonna say, but I would say that, you know, given this data, it really opens up evidence to suggest this works in a critical care setting. This is the largest, you know, data set for us in one study, and it is really encouraging. We would certainly, you know, consider how to, you know, pursue vilobelimab in this general area. I think, will we do a specific COVID-19 study? You know, I think that's something that we would have to seriously consider given, you know, where COVID is moving, and it's a moving target as we see every day in different regions.
I would say that that's still dependent on, you know, what we hear from regulators. Any other comments, Niels?
No, nothing to add, really, Jordan. You captured that perfectly. You know, obviously what we have done, maybe just one aspect, but we have vetted with both the U.S. and EMA whether principally, you know, one trial in this area that is adequately powered would be, you know, seen as appropriate for potential approval, and we did not get a no from either one of them. Always it depends on the data robustness. But you know, if they came around and said, "You need another trial," we need to see what they concretely say, what they're suggesting, how the trial would look like. This took a lot from our team. This is the largest trial we conducted. It's a true global study for us.
It really, like, I think no one else has, in a randomized fashion, in these intubated patients, like, used more in a study with a new agent. It is not easy to conduct this large study in an ICU setting. We would definitely wait and see what we hear back to make a decision on that one.
Okay. Thanks for taking my questions.
Sure.
Thank you, Ed. I appreciate your support. The next question comes from the written portion from Will Soghikian from Leerink . You know, a number of questions. The first was, how do these data change your strategy moving forward? You know, I think we briefly commented on that. We had come out with a press release statement based on the COVID data we would review kind of our corporate strategy and moving forward. I would say, you know, Joseph, you know, that's still under development, but what we are promising is that we're gonna take this data to find out next steps for these programs.
You know, as Niels indicated, you know, we hope that won't take very long. Certainly we are gonna, you know, utilize this in conjunction with what we're going to do in our other indications. I would say that strategy is gonna come together pretty quickly, and we will certainly inform the public as soon as that is developed. I don't know, Niels, if you have any comments on that.
No, not really. I mean, you know, our principal focus is here in immunodermatology. We have voiced that and obviously this opens a second chance here to look into whether that drug can help real patients ad hoc or relatively acutely here in COVID. We're going to have these discussions and see whether there's a step, a moving forward. Based on that, we will determine the COVID situation. I would say as of today, we haven't changed our focus. We're doing this review, and we will come back as soon as we can here.
Great. Thanks, Niels. Also, you know, Will, you mentioned reviewing the government funding and, you know, how this would impact that and the structure of this. As you can recall, we had announced government funding approximately up to about, you know, EUR 43.7 million. The way this works is in tranches that we will be reimbursed up to 80% of kind of pre-specified expenses. If we continue to progress the program, you know, we will continue to be reimbursed. If we decide to continue this and start additional activities, including manufacturing, et cetera, you know, this will continue. It's not contingent on some data point. Hopefully that's helpful for that. Anything additional to add to that, Niels?
Oh, perfect. Nothing further.
You know, in terms of financing for this indication moving forward, you know, I think and you know, this is something that you know, we don't fully have what next steps are until we meet with the regulatory authorities and you know, we would come back to the markets to understand what additional capital would be needed. You know, we do have significant capital as we covered in our quarterly, in our annual press release, and definitely we have enough money to continue to pursue some of these near-term objectives. Thank you, Will. Our next call comes from the line, Ryan Deschner from Raymond James. Ryan, the line is yours.
Hi there. Just curious, if you could comment on the feasibility of a potential U.S. EUA given you know the lack of study sites there and what else may be required from the FDA in that case. Also, how much of the grant from the German government has been used and what IP considerations are associated with it?
Niels, do you wanna answer the first question?
Yeah. You know, it's always difficult to comment on what the regulatory authorities would say. I would say this was operated under an IND, and this was also pre-discussed in the U.S. We made significant efforts to recruit patients in the U.S. as well, and had sites ready to recruit. You know, at least that door and that is open, and we have from the beginning focused also to recruit and to be in dialogue with the FDA. Whether or not the FDA will comment or look at the fact that there are no U.S. patients in it is something that is really difficult for me to comment on. We don't know that.
From an ethnic kind of background standpoint, we have covered quite a substantial area of the world from South America, you know, to South Africa, Russia, Europe. From a patient perspective, that should not be a problem. We cannot comment on how the FDA will view that. That was the first question.
I think the second question, Ryan, you had was around, you know, the amount of funding we've received from the grant from Germany. You know, we put in our annual report, as of December 31st of last year, we have received EUR 8.3 million of the grant funding. You know, I don't know what your question was around intellectual property. What was that referring to?
Question about any sort of contingencies or restrictions on IP in Germany or elsewhere associated with that grant?
Yeah. There you know, to my knowledge, and Niels can confirm that there's no intellectual property restrictions based on this.
Yeah. That's also my knowledge. I mean, all the IP rights we have were generated completely independently, even our filed patents in the COVID arena. You know, from that point of view, our generated IP that we're operating under was even basically constructed completely outside any funding. There's not a link to the funding as well. I'm not aware of any additional restrictions. Yeah.
Okay. Thank you very much.
Thank you, Ryan. Our next question comes from the written section, Sam Slutsky at LifeSci Capital. You know, what do you anticipate the FDA will say on these data? Do you think they'll suggest running another study, or is there precedent for a data set like this to result in approval without additional studies? You know, I would say, Sam, as Niels had indicated, you know, we don't know yet. The best we can do is kind of present the data. You know, what we did was, you know, initially engage them and they gave us feedback, which we you know clearly on the statistical method decided to follow.
We will go to them and certainly there's been other COVID drugs that have gotten, you know, approved and under emergency use authorization and then full approval for things. We will have to see. We don't know quite yet, but Niels or Korinna, you may wanna comment additionally.
Yeah. Maybe Corinna has additional thoughts. You know, for the U.S., again, it's difficult to say. Also for Europe, I think when you look at precedents, you know, the anakinra anti-IL-1 receptor antagonist was, you know, recently approved to be also or authorized to also be used in COVID-19 on a dataset that was not as substantial, not as large, and did not have mortality as the pre-specified primary endpoint of the studies to my knowledge. I think there are areas where an approval took place. As I said, we are not here to make any representations or warranties what the agencies will do.
I do think there's general interest, also on the European side for our data, and we would just have to go and discuss and, you know, we would update the public as soon as we know more. Korinna, I don't know if there was something you wanted to add.
Actually, no. You said everything. Yeah.
Thank you both.
We have to see.
Yeah. I think our last question was in reference to when we would see a presentation on the full dataset. I don't know, Niels or Korinna, you have any comments on that?
If I may take this on, Niels. Actually, yes, we will try to get as soon as possible out to a conference which will be represented with a good target audience. We have not entirely decided which one. As soon as possible.
Great. You know what, we'll take one more from the written questions to be our last question. You know, given this encouraging results in COVID-19 sepsis, are you considering to look also to address sepsis patients from other pathogens? Niels, why don't you considering this is your research area, why don't you take this one?
Yeah, that's a great question. Let me just start by saying like, I mean, sepsis has been an extremely difficult field to be developing drugs in. Despite that, we always said this drug should work. Now, we had difficulties funding this even though we had a small encouraging early study. When COVID-19 came back, the evidence was just so overwhelming, and it looked like even though this is viral sepsis, that these patients, you know, kind of have a different pattern that first of all, you have one agent, the one virus, maybe some variants that drive it. On the other hand, it looked like these patients develop a pretty severe disease, but relatively slowly compared to some of the other sepsis diseases.
It opened the window for us to prove that the drug works, and also to prove that it works best in very severe patients. Now, you know, I think these data robustly suggests that the drug may have activity and, you know, that's really encouraging. Now, running a larger study in sepsis is an endeavor that, I would say from where we are right now today, that's not a plan that the company has. You know, maybe in conjunction with a strong partner that feels strong about the data, that's a different story, and that's something that's as always is up in the air for a smaller company to discuss and to see whether that comes to play.
You know, I'm very cautious and I'm very optimistic on the other hand, because even tougher than in sepsis, the history of ARDS, viral ARDS has been one of the toughest spots to develop in. The data we have here are, from a scientific point of view, probably the most substantial phase III data to date on 28-day mortality with a new agent in this disease area. You know, we feel pretty encouraged. That doesn't mean that we are like jumping to the conclusion that we are starting a huge sepsis trial next. We wouldn't do it. You know, if the company grows and we have the funds or a partner available to look into this, I think we have now substantial proof that there could be a way towards that endeavor.
Thank you, Niels. This brings us to the end of our event. Thank you for your interest in InflaRx and for everyone's questions. Today's slide deck and a recording of the event will be available on the website in the investor relations section of Events and Presentations of our website very shortly. Thank you and have a great day.
Thank you.