VolitionRx Limited (VNRX) Earnings Call Transcript & Summary

Good morning, and welcome to the Virtual Investor event for Volition, a new and exciting LifeSci Advisors client. [Operator Instructions] As a reminder, this call is being recorded, and a replay will be made available on the Volition website following the conclusion of the event. I'd now like to turn the call over to Gael Forterre, Chief Commercial Officer of Volition.

Thank you, Tara, and good morning, everyone. I'm Gael Forterre, the Chief Commercial Officer of Volition. It's a pleasure to be here this morning. I'll start with a few words on Volition before handing over to Andy for his presentations. So what is Volition? It's an epigenetic company. Epigenetic means sitting on top of the gene. We have a large IP, which we built up over the last decade, and we started to monetize it in 2021 on the vet side initially. So we achieved some success on that front in 2022, our first major contract with the Heska Corporation, a part of Antech, IDEXX and other large players. So as of today, we have a partnership distribution agreement with all the large diagnostic companies in the vet space. In terms of milestone and sales, we already received $23 million from different payments as well as sold 100,000 tests last year in 2024. So now on the human side, our activity is split between 2 main pillars, oncology and NET and NET includes sepsis. So we started the licensing discussion in the fall of 2024 and are progressing with a good number of leads on both pillars. So those discussions are based on the recent clinical evidence and upcoming papers that you'll see coming in publicly if some are not already in the public domain. In parallel, we are running an early access program with early adopters and hospital systems in Europe. So our human pillars are focused on large unmet needs and address large markets. So one example is the lung cancer screening program. So it's the work based on the -- the work we're doing with NTU, but also with other centers in Europe as well as sepsis in the ICU. So now a few quick words about technology and some of the key advantages. So our tests are very cost effective and can be adapted to a large number of existing platforms, both on the point of care as well as reference labs. That allows for a large market access. That's what we're looking for. In terms of go-to-market strategy, Volition focuses on the R&D, nurture KOL launch early access program. And there's one that we'll mention a little more later that we're running with IDS. And then we monetize the core of our IP via large commercial and licensing contracts, which include upfront, milestone, royalty and the sale of key components. So one example on the vet side is we led with clinical evidence, papers, then an early access program with the Texas A&M GI lab and then a series of licensing and distribution agreements with Antech, IDEXX, Fuji, just to name the bigger one, but we have others in Europe and in other geographies. So now similar process has been put in motion on the human side. I mentioned the recent and upcoming papers showcasing clinical utilities in partnership with KOLs and early access program with IDS, a subsidy of Revvity. And so this is on the net side. But soon, you're going to see the same on the oncology side with hopefully a large hospital system in France, which we're working with. So those early access program allow us to continue to build clinical evidence, onboard new KOLs, drive adoption and early revenue. Now it's worth mentioning that our next product is IVDD and is currently being evaluated by 3 hospitals in Europe for a range of indications. So it's not just about sepsis. We're also in discussion with another 10 hospitals and expect to launch more evaluation programs this year and hopefully move to routine shortly after. On the licensing side, our discussions are progressing well with a focus on sepsis. Now sepsis is a complex disease with more than 250 tests trying to address different parts of the market. So the focus of our first papers and discussions are around AKI, ARDS in the ICU. But I just want to highlight, it's just the beginning as a marker is able to address a large number of clinical questions. And so we believe we have a unique value proposition, both in terms of cost, workflow, but also clinical utility and can add a lot of value to the current standard of care. So [ Eli ] will share more about this in a minute. I also want to refer to Professor Djillali Annane's comments, one of the leading experts in the space.

First time I have seen so many data coming so fast and with consistent findings. So what we are likely to see now with H3.1 and more globally with NET measurements is a high likelihood of getting a treatable [indiscernible] a game changer in effectively modifying patients' trajectory. So I think this is something that is very likely to be translated by most physicians like me in the routine practice in the next couple of years or so.

So our goal is to sign a few agreements this year, both on NETs and sepsis side as well as oncology. Some might be exclusive, other nonexclusive. It will depend on the development stage of the technology, the clinical indication as well as the competitive landscape. So you stay tuned for quite a few announcements this year, and you'll see different type of agreements that we put in place. So with that said, I'll hand it over to Andy. Dr. Andy Retter is our Chief Medical Officer and one of the clinical lead at one of the largest intensive care units in the U.K. Thank you, Andy, over to you.

Hello, everyone. My name is Dr. Andrew Retter. I'm an intensive care consultant. And since April 2024, I've been Volition's Chief Medical Officer. It's tremendously exciting to work in industry and bring new diagnostic tests to the frontline in medicine to improve patient outcomes. And today, I'm going to take you through the evolving and burgeoning platform of clinical and scientific data that we've been able to put together over the last 2, 3 years in Volition. I should say that I am a shareholder in Volition. I also have another job and that I'm an intensive care consultant working in the National Health Service in the U.K. And just for clarity, the views I express here today are my own and on behalf of Volition, and they don't relate to the NHS trust I work for. Thank you. Sepsis. Why do I get up in the morning to try and improve outcomes from sepsis? Sepsis is a horrendous disease and a huge population health problem. There are almost 50 million cases a year, approaching 11 million deaths. Over 40% of the cases are in children under the age of 5. It is the #1 cause of death in hospitals and a leading cause of readmission to hospital in all advanced health care economies. It's estimated to cost a minimum of $62 billion a year in the U.S. alone, and that number is almost always increasing year-on-year. It's really important to acknowledge that over 40% of survivors of severe sepsis suffer severe long-term physical and psychological effects. Many struggle to return to work and many are unable to complete tasks they were able to do previously. This has a huge long-standing economic impact and burden on the community and on people's lives and their families. Who's at risk of sepsis? In short, everybody. It doesn't respect age, ethnicity, socioeconomic status. Sepsis is a multifaceted disease, which can affect anyone at any time. And we're desperately seeking for new ways to improve outcomes and improve recovery. And with H3.1 nucleosomes and Nu.Q NETs, we really think we have a new tool to try and unlock and move things forward. The diagnosis of sepsis is largely empirical, multifactorial and subjective. Current methods using the sepsis 3 definition published in 2016 and combining organ failure scores such as SOFA score and patch 2 scores are complicated, complex and slow. And although often useful in research, it can be difficult to translate to the real world where clinicians and practitioners need decisions real time, quickly and efficiently to direct a live situation that's going on in front of them. It's broadly and widely accepted that there's a desperate need for improved diagnostics and improved prognostic markers in sepsis to help us identify patients early and triage them and escalate care appropriately. Why did I come to work for Volition? Volition's mission has always been to develop a low-cost, easy-to-use rapid diagnostic test, which we can deploy to save lives and improve outcomes for patients worldwide. We're here today to present Nu.Q NETs, the H3.1 assay as a novel clinically relevant biomarker, which we believe has the potential to be an absolute game changer in the management of patients with sepsis. Why is H3.1 key? Let me go through some of the scientific data now. Our DNA, our genetic code is round up inside our cells. It is wrapped around nucleosomes and deeply called up inside the nucleus of cells. And you can see here, we're seeing the strandraveling. We're seeing the nucleosome and the antibody, this is looking right at the heart of the test, the antibody is picking up H3.1 histones modified on the nucleosome, and that's what we're able to detect. We can now run this test in 15 minutes. We have a lower limit of quantification of 20 nanograms per ml. The linearity in the test is maintained up to a level of 20,000 nanograms per ml. So a huge range there. And in a few moments, I'll start to explain why such a high range of 20,000 is important for us to be able to detect and some of the data we've shown about how clinically important levels that high are. We are fascinated by the process of NETosis. What does that mean? Neutrophil extracellular traps. Neutrophils are the sort of key primary infantry fighting cell of our immune system. So some of the first responders to infection, they can go blood bugs, phagocytos them, but they can also release toxins to destroy invading microorganisms. And the third newer mechanism of action that they have is to release these things NETs, neutrophil extracellular traps. And what happens there is the neutrophil changes its nucleus and it injects and spits its DNA out of it. And that DNA acts as a web. I always think about it as sort of Peter Parker spiderman firing the web from his wrist. And that -- those strands of DNA are rejected. You can see them on the slide here, and they physically act as a barrier to help trap and ensnare invading microorganisms. These strands also act to signal to and recruit other immune cells and other neutrophils say, come here and help, we're trying to fight an infection. What can happen though is that when this effect occurs to excess, it can lead to excessive inflammation and potentially damage in remote organs. This slide is modified from Ella Silk's paper published in 2017. What's it trying to say? It's trying to say that nucleosomes as detected by H3.1 can come into our circulation from a number of sources from the death of cells, from apoptosis of cells. But the really key point we're trying to get across here is that in a patient with sepsis, well over 80% of the nucleosomes are from neutrophils. So H3.1 is acting as an excellent marker of NETosis in this situation. Excessive nucleosomes, excessive NETs can be directly damaging to cell tissues. You have a really polar molecule, which is directly damaging to phospholipid bilayers, cell membrane bilayers. So you can see damage to the lining of blood vessels, this endothelial toxicity. They can also directly activate platelets, these tiny little a nuclear fragments of cells involved in blood clotting and the immune response and they can activate another part of the immune system complement. When all those bits stimulated together, you get an excessive and upregulated immune response that can cross critical thresholds, become excessive and damage organs. That's what we're detecting with H3.1. It's a really key mechanistic insight into the immune response and is a really exciting area with great potential to modify, adapt and understand further. I've tried to summarize what's a very complicated slide in a few sentences. But just to highlight to everybody, if you're interested, there's a lot more educational content related to H3.1 nucleosomes, NETs, NETosis and damage associated with [ molecular ] proteins on our website. In summary, H3.1 nucleosomes sit as a trumfort of innate immunity, inflammation and calculation, and it's a really exciting new tool available to us. The majority of the extracellular pathology is due to indiscriminate binding of [indiscernible] components of the circulation and vasculature. What do patients of sepsis die of? Patients die of organ failure and multiple organ failure and sepsis. This slide is picking up how H3.1 nucleosomes or excessive nucleosomes and histones can damage organ tissues, the heart, lung, liver, kidney, spleen, pancreas. Because the lung and the kidneys have a very rich and larger vascular bed, they appear to be particularly vulnerable to high levels, and I'll pick that up in some of our clinical data in a few moments. But it's a true multisystem disease, and we're seeing multisystem damage. This is a very, very, very complicated slide. What are we trying to show here? At the very top of the slide, we've got an air sac in the lung and alveolus. We've got an invading microorganism, which has broken the lining of that air sac is entering our circulation. The invader has been detected by complement and by neutrophils. And that purple neutrophils to the left of the screen is injecting its DNA in a neutrophil extracellular trap. And you can see the yellow circle, which is H3.1 nucleosomes or the H3.1 signal where we're picking up and detecting it. It's directly related. The other message we're trying to get across in this slide is the huge amount of crosstalk in the system, how platelets talk to neutrophils, how neutrophils talk to platelets, how complement talks to neutrophils and complement talks to platelets. So we're really picking up a molecule at the very heart of our immune response. The role of H3.1 in NETosis, proving we are measuring what we say we are measuring. What does the graph show? The graph shows as neutrophils are stimulated, we have increasing levels of H3.1 detected. The pink picture at the side is NETosis in action in real life. The neutrophils are activated, they inject their nuclear material, and you can see it's being stained and picked up with this fluorescent pink stain. You can see the correlation in the graph as we are detecting H3.1 nucleosomes as they increase. We've done quite a lot of what might be considered boring work as well, but boring and really important to show that H3.1 works. In multiple studies, we have now shown that H3.1 levels in a normal population is not affected by a patient's height, age, weight or sex. It's not affected if people are premenopausal, postmenopausal, smokers or non-smokers. In more detailed kinetic studies, we've not been able to identify any circadian rhythm associated with H3.1 levels. What does all that mean? It means that we have a very tight normal range, that H3.1 is not vulnerable to sort of standard changes in the population, and it helps us interpret the signal that we're detecting in blood results, and we don't have to have any sort of compensation or fudge factors to cope for slight variation in levels. Together, I've worked with my colleagues, Terry Kelly, Kieran Zukas, Justin Cayford and others in our innovation laboratory in America. We're delighted to say we've got a strong pipeline of scientific publications. You've got 3 publications listed here, and there are many more on the way. The data in these publications focuses on NET kinetics, showing that we can stimulate neutrophils, showing that we can stimulate neutrophils reliably to produce neutrophil extracellular traps and that we can detect their release and factors that affect their release. That's led us to develop some potentially very interesting new models for sepsis and testing new compounds to see their effect on sepsis too. We've also just published a review article in the intensive care journal, Critical Care with 2 senior intensivists, Professor Mervyn Singer and Professor Djillali Annane, both world experts in the management of sepsis talking about the role and relevance of neutrophil extracellular traps as key components in this dysregulated host immune response. That's a really excessive inflammatory cascade that I was mentioning a few moments ago. So what are the key messages? NETs are a key component of the dysregulated host immune response. Neutrophils are key fighting cells fighting off pathogens. They swallow up and invading microorganisms. They can also inject the DNA from the neutrophil in the form of NETs. These webs of DNA trap pathogens. NETs act as a critical bridge between our blood coagulation system and our immune system. When these neutrophil extracellular traps are [indiscernible] in excess, blood vessels become inflamed and damaged. This process is called thromboinflammation and contributes to organ failure, disrupting the blood supply to organs. And remember, patients with sepsis die of multiple organ failure. Targeting this excessive release of NETs represents an really exciting new diagnostic and prognostic and really importantly, therapeutic strategy for patients with sepsis. We have lots of clinical data. It's incredibly exciting. I'm going to reference some of the data here. Some of the paper is actually out for review with journals at present. So I can't share it all, but more will come. We've worked with colleagues in Germany and done a retrospective analysis of data and samples collected from the German CIS-PCT trial. We've worked with colleagues at UMC Amsterdam with patients included in the MARS study. We've also worked closely with Professor Annane in France and have work ongoing in the RSU records analysis and conducted our own study in the U.S. with about just under 200 patients with sepsis submitted to emergency rooms. These studies have been presented. They now total up to over 3,000 patients. And across geographically distinct cohorts of patients presenting with sepsis, we have consistently found that an elevated H3.1 nucleosome level represents a dysregulated immune response, is associated with increased mortality, is associated with increased risk of progression to septic shock and is absolutely associated with multiple organ failure. In particular, drilling down into multiple organ failure, we see it's associated with an increased risk of renal failure and simulated intravascular calculation. And picking up on what I was mentioning from the scientific slides a few moments ago, we really think that this is a really useful diagnostic trait, but also a treatable trait and aspect of the disease that we can modify and ameliorate to try and improve outcomes. This paper is now available on bio archives from Caroline Newman, and this is really picking up the data from the CIS-PCT trial. It's the first large publication of an independent cohort of intensive care patients. We analyzed H3.1 nucleosome levels in 971 patients. The key message is that H3.1 nucleosomes are a promising biomarker for early mortality and organ dysfunction in sepsis with significantly higher levels found in those patients with septic shock as opposed to those patients with sepsis. And there was a very strong dose response relationship between the development of acute kidney injury and H3.1 nucleosome levels. The findings of this study established H3.1 nucleosomes as an independent predictor of 28-day mortality and the need for renal replacement therapy. The paper demonstrates that H3.1 nucleosomes provide additional information to the clinician. And that's really a key point to get across. And It was providing independent information over and above the other biomarkers that are available to clinicians. And that's really useful as it provides new and novel information to help decision-making of the bedside. It's potentially extremely useful for risk classification and early identifications of the patients most likely to deteriorate with sepsis or most likely to develop organ failure. This is some very raw data taken from that study. What did it show? All the patients with an H3.1 level greater than 20,000 died and they died early in their hospital admission. It's clearly linked with severity of disease. Interpreting that raw graphical data a little bit more, any patient presenting with an H3.1 nucleosome level greater than 20,000 died. Levels between 10,000 and 20,000 was a 25% mortality and there was a clear increase in mortality for any patient who presented with sepsis with H3.1 nucleosome levels greater than 1,000. It's a really important number because it helps facilitate and support decision-making. You're clearly identifying patients at greater risk. In the paper, you will see the hazard ratios expressed in this fashion. What does this mean? It's a forest plot demonstrating the hazard ratios with a 95% confidence intervals for mortality at day 7, 14, 28 and 90. And it's picking up the prognostic importance of H3.1 nucleosomes. For every tenfold increase in H3.1 levels, there is a hazard ratio of 2.2, more than a doubling of mortality. The confidence interval clearly is distinct from and away from one, emphasizing its significance. And you can see how its significance and value continues through day 14, day 28 and day 90. And that's just raw data shown from the paper showing its importance and its effect and risk of high levels of mortality. A similar forest plot looks at the risk of a patient requiring renal replacement therapy. We chose renal replacement therapy as that's a hard outcome. It's clear evidence of organ failure, we're having to step in and provide dialysis for the patient. This forest plot, again, showing adjusted hazard ratios with 95% confidence intervals at different points [indiscernible] on admissions. The analysis demonstrates that the hazard ratios are consistent with an approximately 3.5 to 4x risk of renal replacement therapy at all times when patients have H3.1 nucleosome levels greater than 2,500 nanograms per ml. It's really associated with a strong increased risk of requiring renal replacement therapy. How might we use this? Well, you could use it in the bed space to try and identify patients who are at risk of going into renal replacement therapy, could help you triage your patients, stratify your patients and potentially consider interventions to try and stop or perhaps even affect timing or influence your decision on timing of starting renal replacement therapy. There's lots more to do in that area, but it's a really interesting and consistent signal. This is very exciting as it's our largest study, and it's just been submitted for review and publication. We worked with the team in UMC Amsterdam and have analyzed 1,700 patients with over 4,000 samples from the MARS study group. The key take-home messages from the study are that organ failure and inflammation and sepsis are closely associated with NETosis as measured through our H3.1 nucleosome assay. Patients with acute kidney injury disseminated intravascular caglation and acute respiratory stress syndrome all exhibited significantly higher H3.1 levels compared to patients without those conditions. Additionally, H3.1 levels showed promise differentiating between hyper and hypo-inflammatory subtypes of sepsis. What's so exciting is just like the paper published by Newman and colleagues I just mentioned just a moment ago, this data consistently showed that H3.1 nucleosomes provide additional information to the clinician and suggest its potential clinical utility for risk stratification and early intervention in critically ill patients presenting with sepsis. The differentiation between hyper and hypo-inflammatory types is particularly interesting in that H3.1 could help us personalize and tailor personalized medicine and treatments for patients going forward. This is a key figure from the table. And actually, it's picking up something very similar from what we've seen before. It's showing this increased odds ratio, increased risk of death with high H3.1 levels. And you can see a 1.65 increased odds ratio. The confidence interval is 1.4 to 1.95. It's clearly significant. That significance is coming in the group in the hyperinflammatory group in that 538 patients who were particularly claimed and had very high H3.1 levels. And that's why we're confident it's helping us pick up this hyperinflammatory, this really inflamed perhaps the dysregulated host immune response group of sepsis. It's a really exciting bedside test. And if we go back to the beginning, it's lining up with Volition's core principle, which is to produce a low-cost, high-volume test, which is widely available to help us identify and potentially treat patients with sepsis. It's a key link back to that mission statement and mission objective for us. This isn't sequencing. This isn't thousands of pounds of analysis or complex analysis away from the bedside. This is scalable and deliverable in real time to affect patient care. We have shared a taste of our clinical data and scientific evidence. We feel we're building an increasingly strong case to support the use of our proprietary Nu.Q NET H3.1 assay. We believe the data supports the fact that H3.1 has great potential to become an integral biomarker in the management of sepsis. It's both a marker of badness and a cause of badness too, which in turn means it's a really exciting therapeutic target. Doctors will be able to use it to diagnose patients. Doctors might be able to reduce it or remove it to improve patient outcomes. I'd like to finish by also adding that we're not the only ones thinking this. We're really excited our review article has been published. You will have seen an announcement in the last few days that we've just started collaboration with pharmaceutical industry using our high-throughput NETosis assay. It's a really exciting time for us. Our basic science, the skills of our scientists to stimulate neutrophils has enabled us to develop a platform where we can test drugs and see the effect of drugs on NETosis. And so we think there's a huge potential to develop that further. Most importantly, we are increasingly encouraged we've got something that we can bring to the bedside to help patients, and we're pursuing multiple parallel streams to try and make that a reality. Thank you for listening. I'd now like to hand you back to Gael. He's going to continue to take us through our commercial strategy.

Thank you very much, Andy. We've started our monetization process a few years ago. We started on the vet side with the indication that we already licensed and more coming. We also just started now on the human side that monetization process for a large number of indications, and you'll see some of those on the screen. Now just a quick parenthesis on oncology. We didn't discuss it at length today, but we're doing a lot of work there with a lot of good things coming, and we hope to have over the next few weeks or month a webinar to share more information about it. We expect a few agreements this year and look forward to update you as we bring those partners on board. Now with that said, I'll hand it over to Louise and Tara for Q&A. Thank you.

[Operator Instructions] So our first question comes from Boris Tolkachev from Freedom Broker.

I think the first one goes to Andrew. Andrew, during the presentation of clinical data last year, you gave a snapshot of German study data. And there, you were mentioning serial H3.1 measurements. However, in the available manuscript, only levels measured on admission are analyzed. So I was just wondering what are the reasons to separate that pieces of information? And should we expect analysis of serum measurements in later publications?

Thank you, Boris, for that question. So the pragmatic decision in publishing the paper was to just stick with the initial presentation to help with the clarity of the message and just be consistent with publishing the journal, figure numbers, table numbers, et cetera. So that was the predominant decision behind that, and that paper is published. There is some extra work going on looking at serial measurements as well, and that may well be published. I don't want to completely commit to that because there's lots going on at the moment, but there's certainly a wish to publish the serial measurements later.

Okay. Can I ask a second question? We've noticed that German study data was finished more than 10 years ago. Just wondering why did it take so long to analyze that information? And I'm curious whether the analytical performance of the tests used in this study 10 years ago could be different from the current generational tests. So is there a possibility of an issue here?

So there's a couple of things to unpack there. Thank you very much for that question. So the trial data set that we used is a very, very rich trial data set. So that was very useful to us. The samples were frozen for 10 years at minus 80, and we're happy that they're stable when stored at that time. So the samples were actually processed and run last year, about this time last year, actually, I think if I remember correctly, it was January and February that we processed the samples. So it's not that the samples were processed 10 years ago. It's the samples were process -- the patients entered the study, the samples were taken and they were frozen, and we use samples that were still available. And so I hope that makes sense. So all the analysis was done on a very modern test, which has been developed in the last 10 years and was run on the latest version of the test, around this time last year, and it's taken about 8 to 9 months to write up the data. I hope that makes -- I hope that's clear.

Yes. And you don't think that there will be any issues with the nucleosome stability over that time?

We haven't seen any alert signs with the nucleosome stability. It's a very reasonable question. We're particularly, so we haven't seen any warning signs about deterioration in quality, and that's very reassuring. The data is also remarkably consistent with the other study as well, and we're seeing a consistent signal there. So we find those 2 bits together very reassuring. It's a quite boring technical part of the methods of the paper, but the samples were all stored at minus 80 and in both the study from Germany and in the study from the Netherlands, the samples are processed in identical ways. So we're not concerned about our methodology of sample processing.

Maybe if I can add, we were not in touch for any -- in case there is any doubt, we're not in touch with those centers 10 years ago. So we just started the collaboration a couple of years ago with them.

Our next question comes from Bruce Jackson at Benchmark.

I'd like to start with the workflow. So setting the scientific basis for doing the test is great. A question for Dr. Retter from a practical perspective, when you're actually using the test in practice, is it a fairly -- tell me about the -- is the workflow easy to adopt? And how does that work if you're in the ICU, for example?

Nice to see you again, Bruce, and thank you very much for your question. So the -- there's a couple of questions to unpack there. The test is very easy to use and easy adopt to use because it's processed on a K2EBTA sample. And what does that mean in the real world, that's a purple top bottle, and that's the most common blood sampling bottle used and it's the sample that a full blood count is run on or a complete blood count in the U.S. In my hospital, the machine sits at the end of our full blood count counters and so the technician just has to walk it across. We absolutely have aspirations where you can transfer the technology, the basic nuts and bolts of the test into other analyzers. So you can see in the future that it might just be run in sequence as part of the chain of doing a full blood count and so be really useful and really empowering that way. The current version of it that we are using takes about 15 to 16 minutes to run to give a result. So that's awesome. That's really real-world data that's available and turn around. There are standard operating procedures in countries and sort of quality control metrics about how quickly you're supposed to turn a blood test round. And they vary slightly from one country to the next. In the United Kingdom, we have a minimum standard of turning a test like the full blood count round or important -- really important blood test round in 4 hours. And that's just a pragmatic realization of you've got to see the patient, you've got to get consent, you've got to take the blood, you've got to send it off. It's got to be processed, it's got to be checked and got to be sent out. So I think in my presentation, I talked about the boring stuff. This is part of the boring stuff. The test is easy to adopt. It's easy to run. It can be run in the time frame, which is very compatible with hospital production lines or laboratory production lines producing results out. Any questions back on that, Bruce?

Yes. And I love the boring stuff, too. So it's really super important. And where I'm going with this is I believe one of the studies used the IDS immunoassay analyzer. This...

So both studies use the IDSi-10 analyzer, yes.

Right, right. They've got an installed base of about 1,500 units out there. So if I've got -- if I'm in a hospital and I want to use this test, how easy is it for me to take the scientific literature that you've published and order a few kits and start using it.

So can I tease that apart if that's possible. So we have the -- it depends how much you want to do. So the advantage of the IDSi-10 that we operationalize is that it can process about 450 samples a day. So if you need to do that many, it can do that. There is the possibility to do technology transfer onto other analyzers with a much larger install base, and that will be required ultimately, I suppose, to get it to a much bigger market. If you wanted to use it now for a research study, and we're in contact with a lot of people doing research studies because the kit works well, still basic ingredient is the H3.1 antibody. And we can go through that more if you would like to, but that's available in our ELISA kits. And you can buy our ELISA kits available commercially, both in the U.S., Europe and in Asia, and we're in contact with lots of partners there that way. So if you wanted to start using it in a research study or in a small scale, you would have the ELISA kit available to you. That's processed in a slightly different way, and that takes longer and you need a plate reader to do it. But a lot of the earlier scientific work came from the ELISA plates. You can see how we've upscaled to move to the open platform that's the IDSi-10.

Sorry, I can add just a little word on the commercial side. So obviously, to get wide distribution, we'll need additional licensing and distribution agreements. This partnership with IDS initially was a technology partnerships to allow us to transfer to chemiluminescence platform. And it was not a distribution. Then we expanded for early access to clinicians for research purpose mostly. As far as routine, we have our NETs test is CIVDD. That currently is being evaluated by centers in Europe, and we have a pipeline of centers that are either starting evaluation or going to start evaluation this year. But obviously, as Andy said, to reach really scale, we will need additional distribution agreement, and that's what we're in discussions with large players already.

Okay. And then one more question, if I may. So with the technology transfer, which was going to be my last question, there are slightly different flavors of electrochemiluminescence out there and slightly different protocols on the instruments. You've already gone through this process on the vet side of adapting the test to various analyzers. Just hypothetically speaking, how easy or difficult do you think it would be to adapt the test to one of these larger analyzers that are out there in the market?

You want to -- maybe I can say.

I'm not quite sure what I'm allowed to say, get going, you go to first Gael, and then I'll add.

So without naming them, we already transfer technology to quite a few platforms already. So we're very confident that it's feasible. And actually, now we're kind of get it done reasonably quickly. We're a matter of weeks and months.

I'm really glad Gael said that because I'm very confident and we can do it repeatedly.

So our next question comes from Steven Ralston at Zacks.

You've had a lot of papers and posters, et cetera, of showing that it appears that these high level of NETs are significant. But could you address the next step, the subsequent therapeutic treatments. For example, Dr. Retter, in a previous webinar, you mentioned that the progress of sepsis was quite irregular. And in each, let's say, step in the progression of the disease, there would be a different therapeutic treatment. And the NETs would swing from very high levels to, let's say, midrange levels. But in the organ failure with concerning kidney, it seems like you only mentioned one treatment. It seems that -- and that the progress seems to be more linear. Could you compare and contrast what you expect the therapeutic treatments to be in sepsis and in kidney failure? And a tag-on question to this, and I think this is probably more in Gael's area, that given that there's this variability of treatments and it hasn't been actually designated or laid out clearly or the lack of information about them, does that impede the progress of commercialization?

Let's start with that last one or -- so the short answer is no, it doesn't. It's -- if you think of how we structured the deal with Heska, we started to monetize really what we have, the indications we had and then you build a framework for additional milestone or additional payments or additional consideration as additional clinical data and evidence come along. So no, we already have enough to discuss with partners.

Thank you for your question for me. So I'm going to try -- in the presentation, I talked about -- I think I showed that the basic table of raw data taken from the patients in [indiscernible] where -- and the table I have in mind is where everyone with an H3.1 nucleosome level greater than 20,000 died, and there was a 25% mortality for patients over 10,000. And then you can see that the mortality has increased over 1,000 as well. So that's really quite important because we've seen in 3 studies now that there is a clear inflection point in people's mortality when you have a level over 1,000. So that's an important level. Before I pick that up, we've also done work in -- to develop the normal range, and we're really quite confident now that the normal range is less than 30. We've got a lot of data there, too. So that's very useful for clinicians. So we have a study going forward trying to use those numbers. So one of those numbers and it's a big study that we're trying to take forward, combining H3.1 with the National Early Morning score. So this is really trying to help people or help clinicians, nurses, health care practitioners in emergency rooms. If a patient has H3.1 of 30 or less and a new score of 2, which is they get sent home. If it's on the other extreme, if their new score, if their physiology is 5 and H3.1 is greater than 1,000, they're absolutely admitted. And we're trying to do that because for every health care system in the world, triage and management of patients presenting their emergency room or accident emergency department is a real problem and a real challenge. The group in the middle, we will reassess after 2 to 3 hours to see how they go. So we're really interested to see how that will go. So that's using H3.1 in the real world to help with clinical decision-making. In terms of therapeutic interventions, there are a number of studies that have been published where H3.1 has been a key component of those studies. There are studies looking at transplant rejection, a rejection of lungs, rejection of kidneys, rejection of livers. H3.1 is high. If you reduce it when the organ is being rejected, if you reduce it, you get less organ impairment, less organ failure. So that's a really strong biological model that you're removing something and you're having an effect. There's 2 whole organism models. There's a sheep study and a pig study where sepsis was induced in those animals and removing H3.1, removing NETs made the animals better. So there's really strong signal towards therapeutic potential. What do I think currently? Currently, from the clinical data that we have available to us, the cutoff of 1,000 is really important. So it's going to suggest you want to do something different. Now that might be a cutoff for steroids. It might be a cutoff for other mechanistic aids such as anti-NETs treatments. There are lots of potential medicines on the shelf that could be anti-NETs treatments. And we're really excited because we've done a huge amount of basic science work to understand neutrophil biology and neutrophil stimulation, and we can test those in our innovation laboratory in California. Over 10,000, so we are trying to -- it's not there yet. Look at a study where we use a level of H3.1 as an enrichment criteria for entry into the study and where you would remove the nucleosomes. Why have we chosen 10,000 and 10,000? You've seen it in that table. That's a data where patients are really sick and their mortality is really high. And the risk of these patients get disseminated in vascular calculation, these micro clots sort of chaos in the [indiscernible] and they can frequently lose their hands and feet. So we're trying to take that forward as a way of using it for life and limb potential as an indication for those treatments for the immunoadsorption comes to remove H3.1. So that's our thoughts and strategies moving forward for its adoption or how be used in clinical practice.

Just one more question for Gael. It took several months, actually maybe a few quarters for Heska to put it onto their platform. You just indicated that, that process appears to have been shortened going forward, is that because of lessons learned at Heska or maybe the platform is a little more difficult or...

So no, it's a very interesting question. It was a different underlying technology. It was not chemiluminescence in the center point of care. So -- but I'm not the technical expert here. So I'll be careful when I say to avoid a mistake. But it was a different underlying technology. On the pure chemiluminescence, we're getting really good. And we've done some -- quite a few now successfully. And so we have a high level of confidence.

And you haven't announced anything about who you're with or...

No, we're not announcing when we do the tech transfer with partners. It's the initial phase for them to validate the assay. We're not announcing that.

So when you're talking to these potential partners, they will be in a more advanced stage to continue on if an agreement is signed as opposed to -- like Greenfield starting from square one.

You're correct. I think Heska was -- and I don't want to talk for Kevin Wilson, who was really at the forefront of the deal, but they were willing to take a chance on signing a deal without knowing if the technology was going to be transferable. I mean they had a high probability, but there was no guarantee. Seven partners are interested in the other way around, making sure it's transferable. So it was also a different mindset.

So I'll now turn the call over to Lou to read any questions that came over the webcast.

Sure. Thanks a lot Tara, and good morning, everybody. And there's been a lot of interest on this chat. So I think, Gael, I'll start with a question for you. So this is a very interesting webinar, thanks very much. And could you elaborate a little more about the success you've had on the veterinary side and how that success and strategy might translate to sepsis?

Yes. Thank you. So we did a few things work well on the vet side. We published a paper and a series of papers with a very highly regarded KOL. And so papers attached to people that have an importance in the field and the space and the following. So those were 2 things that we did, and we are reproducing that on the human side. As you're seeing, we're part of the ISF. We are part of international societies. We're publishing papers with renowned KOLs. We did an early access program where the test then became available at Texas CNM. Same thing on the NETs side. And actually, we're not talking about cancer today, but we also have a program like that on the cancer side. This is a program that you heard with IDS and this like smaller, but still a significant installed base. And in Europe, we're able to now work with quite a few hospitals now to evaluate and then potentially later this year on board the test. We have centers of excellence that are working with us to add to the clinical -- the body of clinical evidence. And then the next stage is we worked with large companies like in the case of vets, the 2 largest in -- well, at the time, it was one of the largest and a slightly smaller one, Heska, but some of the largest in the diagnostic vet space. And again, we're doing that on the human side. Now in discussions with more than 10 of them with NDAs in place and different level of progress.

So well, actually, just in saying that, Gael, one of the follow-up questions was, I appreciate you're not able to name names, so to speak. But could you advise on the sort of commercial partnerships that you're exploring? What types of organizations seem most interested in partnering with you for success?

So because of the underlying technology, we're partnering with -- or we're seeking to partner with actors that are large and have a large install base of chemiluminescence platform or knowledge. There are some exceptions where maybe the market share in the hospital space, it can be quite broken in terms of -- there's not a main actor that owns 80% of the market or even 50% of the market like IDEXX or Antech on the vet side. But we're discussing with those that can either on their own as a nonexclusive, be able to reach a large number of hospitals or have the track record of doing sublicensing, so potentially an exclusive and then they would take on the sublicensing. So -- and as of now, we're in active discussions.

Excellent. And then one for you, Andy. Thanks, Dr. Retter for another engaging presentation. I've been following your webinar series for a while now. And I wondered how well understood by kind of a regular clinician do you think NETs are in the context of both their benefits and potential risks? And how much education do you think hospitals or clinicians will require?

I think the tide is slowly turning, if I'm honest. I left medical school in 2000. We won't dwell on that. That was a while ago now. And NETs weren't discovered until 2004. And actually, I go to quite a lot of medical conferences. And this year at the Brussels Intensive Care meeting, there's, I think, 4 or maybe 5 presentation on NETs. So that's a huge change. Last year, there wasn't even really one. So that's a step change moving forward. There will be discussions in other intensive care conferences, the programs aren't completely finalized yet. And there was a lot more interest at the American Society of Hematology meeting last year and at the International Society of Thrombosis and Hemostasis, -- there are more and more presentations [indiscernible] in NETs sessions. So I think interest is significantly increasing. We're able to drive and facilitate that interest because we've been able to support a lot of research, particularly with the ELISA kits and people are seeing increasing uses for studying NETs. It's a mark of activation of the innate immune system. We see the very strongest signal in sepsis because that's where it's most arranged, but there are a host of potential other applications as well. So we're very, very excited there. I don't want to shy away from the challenge all though. There is a challenge to bring education material and teach people. I talked at a National Intensive Care study Day just before Christmas. And part of the teaching material is all hosted on Volition's website actually. And it's -- we have a duty to educate. And so that's part of our sort of mission statement and work that we do. So a lot has been done, and there is a lot more to do.

Okay. And I'm conscious of time, chat. So I'm just going to wrap up with this one last one. And apologies that we've not managed to get to all of the questions on the chat today. There's a question that maybe both of you could just provide a 2-line answer to, but I appreciate you focused on sepsis and Nu.Q NETs today. But could you just provide a quick update as to where you are with regards to Nu.Q cancer. So Andy, if you want to go first and then Gael, I'll hand across to you for a wrap-up.

So I apologize for always talking about sepsis and betraying my background. It's really exciting, and I'm delighted to share that we're making strong progress with Nu.Q Cancer. We've completed some studies spanning the disease continuum. We've got work that we've done with our colleagues at the National Taiwan University, which is now up on med archives, and there's more work to follow in that series too. And Louise, our lucky host here, is working on another webinar in the near future focused on our upcoming oncology and cancer data. So I look forward to seeing you again soon, but very exciting that we're making progress on the -- very much making progress on the oncology front. Thank you, Lou.

You want me to add, I can say that we are also engaging in conversation on the oncology side. Broad interest, we have a portfolio that goes beyond the nucleosome quantification on the oncology. We have additional technologies or variation of that technology that are also in that portfolio. So there is interest and different actors depending on what the underlying technology or the applications are. But definitely for the chemiluminescence players, the lung package is very interesting. And I just want to mention, so Taiwan, you've seen the lung screening, but there's -- we're working with other centers in different countries to try to see if we could be present in other national screening programs. So this is not for tomorrow. But definitely, we're making progress on that side as well.

Sure. So I would just add actually that the European Lung Cancer Congress at the end of March, there's certainly some new data will be presented at that, which is one of the big key conferences of the year and also at the AACR in April. So you've got quite a lot of new evidence coming for lung cancer this year and indeed across other cancers. So I'm just going to wrap up there because we're on the hour, but thank you so much to everybody that's joined us today. I do hope that you enjoyed the webinar and that you felt that you've gained some insights. The replay will be available if you do want to share with any colleagues or other potential investors, then that would be fantastic. And it will be put up on our website as well as Tara said at the top of the call. But with that, we look forward to seeing you next time. Thanks very much.

Thank you.