A very warm welcome to all of you to this press event, to everyone in this room, and to those of you watching. My name is Eva Lundborg. I am a pharmacist, I'm the medical editor, and I will be moderating today's event. With me here, I have two professors. I have here Professor Glenn Davison, and you are a professor of sports and exercise sciences at the School of Natural Sciences at the University of Kent in the U.K. I also have Professor Doris Wilflingseder, and you are the university professor of infectiology at the Ignaz Semmelweis Institute and also the Vet Med Uni in Vienna. The two of you share a special interest in the immune system and the way it handles infectious diseases.
That is actually the very reason we are here today, that you recently published an article with two research studies about ColdZyme. The studies were published online in the Journal of Physiology on Friday, and they are independent of the company Enzymatica, but involve the company's product. In just a little while, we will have the pleasure to listen to you, if you can see the agenda. For today, we will have the presentations from Glen Davison and Doris Wilflingseder, and after that, we will have a Q&A session. To those of you listening in, you can send your questions in the upper right corner, you will find "Ask a Question," and you just press there and you can send it in. After that, we will have a short break, and that will be followed by a corporate update from Enzymatica.
With that, I hand over to you.
Thank you very much, Eva, for the introduction. Yeah, my name is Glen Davison, my colleague here is Doris, and we're going to talk to you today about some of the key headlines from our recently published study. On this slide here, you can see the title of the study, and on this slide here, we have the graphical abstract, which just gives us a graphical representation of an overview of the main parts of the study and the main findings from the study. What we've done here in this publication is we've combined two different types of approach. We've got what we call the in vivo approach with a real-world setting, studying naturally acquired upper respiratory tract infections in an athlete model, and we've got the in vitro model using airway epithelial cells that are infected with rhinovirus.
Basically, to summarize, we found that there was a significantly lower incident, sorry, a lower duration of upper respiratory infection in the in vivo study. We found that the symptom ratings were lower, and we found that viral load was lower. In the in vitro studies, we, or Doris's lab, found that viral infectivity and viral load was lower, and damage to the epithelial cells was lower when treated with ColdZyme. They are the headlines, and we are going to go through some of those key findings in the next few slides. If we start with a little bit more information about the main methods of the study.
We screened almost 200 potentially eligible participants for this study, and just over 160 of those were enrolled onto the study, and they were randomized to receive a placebo, which looked, tasted, smelled, felt the same as the real product. This was double-blind, completely randomized, so that the participants could not tell whether they were having the placebo or the real product. They were monitored over a three-month period, and they recorded their, they were athletes, endurance athletes, they recorded their training, they recorded their absence, and they recorded when they thought they had symptoms of an upper respiratory infection, and they gave ratings to each of those different symptoms.
We, of course, lost a few along the way, which is always the way in real-world human studies like this, but we completed on 154 participants, and from that, we had 91 upper respiratory infection cases, and 82 of those were eligible to be included in the final analysis. Over on the right of this screen here, you can see some of the sort of key aspects of the study. The monitoring was online, so they were sent a personalized link every evening so that they could record their training, they could record their symptoms, and they could also record their use of the product. The instructions were to always use the product at the first symptoms of a suspected upper respiratory tract infection, but there was also an option for them to use it in a preventative way.
This part was not compulsory, and this was an optional part for them, so if they thought they were at increased risk, for example, traveling or when they knew they were around people who were exhibiting symptoms of these illnesses.
First of all, a very warm welcome also from my side, and thanks Eva and Glen for the introduction. I want to explain the in vitro study a bit now because to make it more, let's say, visual, what we did in our labs. We are working on two different models of the respiratory tract. One model is the so-called air-liquid interface model, which you can see here on the left-hand side of the slide, which is a very physiologic model because, as the name already says, it is in an air-liquid interface, like we also have in our respiratory tract. One side is exposed to air, the other side is exposed to liquid, to the body fluids. This is also reflected in this system.
This system consists of a really tight barrier because, as you can imagine, we are inhaling thousands of microbes and pathogens each and every day, but we rarely get sick. Therefore, this barrier has to be really very efficient, which is provided on the one hand by the cilia border, which you can see here in the moving slide. These are the ciliated cells, they are always moving, and they are moving the pathogens out of the body again. They get help from mucus-producing cells, so we also have a mucus layer, that's why it's called mucosa. This mucus-ciliated layer makes a mucociliary clearance. Therefore, normally, pathogens do not attach to the cells, and they are just thrown out of the body. During infections, the viruses or also other pathogens are able to really come into contact with the epithelia and thereby infect those tissues.
By infecting the tissues, the tissues either get destroyed or the virus somehow gets into the body, and that's how an infection starts. The second model we are using, you can see here on the right-hand side, is an organoid model that's kind of a mini-lung, let's say. This is not as physiological because it's not at an air-liquid interface. With this model, we can test lots of compounds at once because we can perform high or medium throughput analysis. Therefore, those two systems complement each other really nicely because one is really appropriate for testing compounds, the other one is highly physiological. For the ColdZyme studies, we used the air-liquid interface model because from earlier studies, we already knew which concentration to use and how to use the compound.
Here, just to show you what happens upon infection, this is just a slide with SARS-CoV-2 infected tissues. On the left-hand side, you can again see a very nice cell culture model of the respiratory tract. This is upper respiratory tract cells with the ciliated cells, mucus-producing cells in orange in between, and a very tight layer. Upon infection on the right-hand side, you see a totally different picture. As said, this is SARS-CoV-2 infection. You can see holes in the tissues. You can see those pink cells, which are virus-infected cells. In between, there are virus particles. What you can clearly see is this mucus hyperproduction and mucus plug formation. This is also something which was really seen in the very, in the first COVID-19 wave in patients. They showed mucus hypersecretion and mucus plug formation. Therefore, the system is quite physiologic.
Okay then, if we move on to the main headline results, and if you read the paper, there's lots of other results that you can look at as well. The most important outcomes we're going to summarize in the next few slides. From the in vivo human study, the primary outcome was the duration that the upper respiratory infection symptoms lasted. The left two bars that you can see on this graph here show all 82 of the episodes, and the right two bars are the 50 for whom we were able to retrieve swabs. The participants, when they were ill, were also instructed to take a swab from their throat, just like we all learned to do very well during the COVID pandemic. They were to do that on day one, three, five, and seven.
They were basically taking a swab daily for the first week so that we can look at viral load, and I'll show you that data in a moment. The separation here is you've got the full set of data on the left, and then you've got the group from whom we got the swabs on the right. It's basically showing the same thing regardless of which way you looked at it. That is that the duration of suffering with this infection was significantly shorter in the ColdZyme treated group compared to the placebo group. This is the viral load for, so we actually ran a very, very comprehensive pathogen screening panel. There are 41 different pathogens that are detected in our screening method, which is very, very comprehensive.
We were able to, therefore, in the swab, the N equals 50 swab samples, we were then able to confirm which infections were present, and we could also look at viral load over that seven-day period. What you see on these graphs on the right are the viral load, or in the case of Haemophilus influenzae, it's actually bacterial load, and it represents the whole seven-day period. It is what we call the area under the curve for that seven-day period. For rhinovirus, which we actually detected in all of those who returned samples, the viral load was basically significantly lower in the ColdZyme treatment group compared to the placebo group.
This starts to help explain why we found what we found with regards to the lower duration that the episode lasted for, but also it helps us to explain why we saw lower symptom ratings. The table on the right is a table from the paper, which shows some of these other outcome measures. If I can just show you this as a graph. This is the questionnaire that we use that we ask participants to quantify their symptoms. Those symptoms, it's called the Jackson questionnaire, and we get a total score for that. You can actually look at the different types of symptoms that make that score, and that's what's shown on this graph here.
The main message here is that for almost all of the symptoms of the eight symptoms that you can see along the bottom of that graph, the numbers were significantly lower in the ColdZyme group compared to the placebo group. The exceptions were chills and headache, but all of the other symptoms, so malaise, nasal discharge, nasal obstruction, sore throat, cough, were all significantly lower in the group that were using the ColdZyme product. Other measures, we asked them to keep a log of their training and also a log of whether they were able to continue with training as normal or whether they had to reduce or completely miss training as a result of these illnesses.
What we found there was that the days affected and the days of absence from training were also significantly lower in the ColdZyme group in comparison to the placebo group.
We found similar results in vitro, so in the cell culture, where we infected our air-liquid interface models with rhinoviruses and then looked at the viral load, as Glen already described. Also in these analyses, we found that in the rhinovirus-infected group, we saw a significantly higher load of rhinoviruses compared to the group where we pre-treated the air-liquid interface models with ColdZyme prior to rhinovirus infection, which is depicted here. This illustrates the virus secretion into the air side, so to the apical side. Other results are in the manuscript where we also monitored the basolateral side, so the side where viruses are secreted in direction of the body. This also looked similar to these data. We also performed immunofluorescence analysis.
This is a really nice tool to look, on the one hand, on the integrity of the epithelia, which is shown in yellow and in green, on the viral load, which is shown in pink, and on the cell nuclei, which give an indication also how the tissue looks like. As you can easily see, in panel one, we have mock ColdZyme treated uninfected tissues, and in panel two, we have rhinovirus infected tissue. Here, when you look at the pink signal, you can see that only in rhinovirus infected tissue, you see a pink signal, while of course in uninfected, there should not be a pink signal. This is also the case. In the third panel, we pre-incubated the tissues with ColdZyme prior to rhinovirus infection, and we saw a similar picture as that in the uninfected.
We could not detect any viral signal here on the apical side.
If we just sort of sum up those key findings and the conclusions that we can draw from that, I think that the things that you can see on the slide here are the key headlines that we would like to communicate. That is that in the in vivo study, ColdZyme is effective at reducing the duration that the participants were suffering with this upper respiratory tract infection episode. It also reduced the severity of the symptom ratings, so how bad they were suffering with those symptoms when they were infected. I think both of those can be explained by the fact that viral load is reduced. The swabs that we were able to collect from the 50 cases basically give us the explanation for why we found what we found in the primary and other outcomes.
The episode is shorter and the symptoms are lower because the product is working at reducing viral load. It is that action, if you like, it is the virus infectivity which causes damage to these cells. That is one of the contributing factors to some of the symptoms that we typically report. It is logical that if we reduce this, then we are going to see a reduction in those symptoms and also a speedier resolution of the infection. That is exactly what we saw in these findings here. I think Doris's data in the in vivo studies also support this because they basically show the same thing in the in vivo model. I think we have got complementary data here which give us a real good understanding of the mechanisms that explain the findings.
Yeah, there's not so much more to add because I also think that those data complement each other really nicely. We also saw this lower viral load. We saw lower tissue damage. We saw in the immunofluorescence analysis, we did not see that much virus. Therefore, I think those two studies complement each other really nicely.
Thank you.
We want to thank you for your attention.
Thank you so much for your presentations. Now we will move on to a questions and answers session. I would like to remind those of you that are watching that you can send in questions in the upper right corner. Yes, I am a little bit curious. Could you elaborate a little bit on why you became interested in studying ColdZyme in the first place?
Yeah, I mean, I'm a sports scientist and I therefore have sort of firsthand experience of the effect that upper respiratory infections can have on athletes. I was an athlete myself to a sort of recreational and, well, fairly competitive level. I experienced firsthand how big of an impact getting ill can have on your training and your performance. That's the area of my research as a scientist. I'm always interested in interventions or products or things that can minimize that. You could tell athletes to not go out and train and not mix with people and not do all of that sort of stuff, but they won't listen to you. It's not realistic. You have to accept that.
If there are other things that can be done to allow them to suffer less or allow them to recover quickly and get back to their sport, I came across this product and it piqued my interest and I therefore wanted to explore it. That is what drew me to it. That is what made me, I guess, initiate this study.
Yeah.
In my case, it was honestly during the first COVID-19 phase. When no medications and no drugs were available, we already had the standardized cell culture model in our lab because we were working quite a long time on fungal infections, which also often affect the respiratory tract, in particular immune suppressed people. Therefore, we had the model already up and ready when COVID came in and we had a very good collaboration with the clinics. Therefore, we got the first SARS-CoV-2 samples already in April 2020. We went to the pharmacy and bought antiviral sprays and tested those. That's how we came along to product because we found that it was very effectively protecting against SARS-CoV-2, against this wild type variant or against the first variant.
Then we went on because I also really like this translational context to really investigate in our labs.
That is very interesting. Glenn, you talked a bit about symptoms and the total symptom scores were reduced. You also talked about specific symptoms. I was wondering if you could elaborate a bit on that when you compare ColdZyme and placebo, what you experience.
Yeah, I think this slide that I showed here really shows that quite nicely. The standard way to quantify these illness symptoms is with an overall Jackson score. The overall Jackson score is basically taking the sum of all of the eight symptoms that you can see along the sort of bottom of that graph there. Obviously, we can look beneath the bonnet if you like and sort of see what that total score is comprised of. You can see here there are clearly some areas where the gap is bigger between the placebo and the ColdZyme group. I think these are the symptoms and that's what people are worried about. That's how people, if you're an athlete, that's how you might decide whether or not you're going to train.
If you're a regular person, that's the thing which dictates whether or not you feel well enough to work or whether you want to go in to work or stay off. I think that, you can see here, all of the symptoms were significantly different except headache and chills. I think this aligns with what Doris has shown in the in vivo work. For example, the lower damage to the epithelial cells and tissues in the upper airways are probably, those are the things which probably contribute to things like sore throat and cough. The mucus hypersecretion is something which contributes to cough and various other symptoms. That tells us that the symptoms are affected because the underlying cause is being targeted by the intervention. I think that's probably a nice relationship between those two parts of the study, I think.
Yeah, I thought that was very interesting. On that, you have studied this in endurance athletes. Would you say that the results can be translated to the general public?
Yes, certainly. I think, I mean, that's the area that I work in is sport and endurance athletes. We know that that can be a big issue for individuals if they suffer with that. That is why I chose that as the population. Once somebody is infected, once somebody is ill, people are all the same, generally speaking, generally healthy, regular people. The way that the virus infects them, the way that the symptoms develop and all of that sort of stuff is the same. The results that we see in these people, I'm confident would be exactly the same in the wider population.
Yeah. Yes, and Doris, in the cell culture model, you used human epithelial cells from the upper respiratory tract, so övre luftvägarna på svenska. Would you say that this model represents this area as a whole or is it just specific parts?
This is really the specific part of the upper respiratory tract. In some, we have established models of the nose, of the nasal epithelium, of the upper respiratory tract, of the lower respiratory tract, and of the lungs. For these studies, it makes most sense to really take the upper respiratory tract cells because you spray ColdZyme into your mouth. Therefore, in my opinion, it makes most sense to use those cells. We also tested it on the nasal epithelial cells. Nasal and upper respiratory tract cells look pretty similar. When you go down, the epithelium becomes thinner and thinner. In nasal cells and upper respiratory tract cells, the results looked very similar.
Okay. This epithelial barrier that seems very important, could you elaborate on why it's so important for infection, for fighting infections? You mentioned it in your speech as well, but could you explain a little bit?
Yeah, of course. I mean, this is really the very first barrier before pathogens or let's say some invaders come into our body. Therefore, it's really important to have a very tight barrier. There is not only this physical barrier which the epithelium provides, but as I also said, there's also a chemical barrier due to the mucus that these cells are producing. You not only have this physical barrier, but also the chemical. In addition, you have this movement of the cilia to get really rid of most of the particles we are inhaling, 2,000 each and every day.
Yes, yeah. To keep that intact as you showed those nice pictures. Yes. Your research shows that ColdZyme reduces the viral load. Have you seen any upper limit to this effect or where the product may be less effective, or have you seen anything like that?
We have tested various concentrations, so various dilutions because in the body, we also have body fluids. We have saliva and therefore the product might also get diluted. We tested several dilutions up to a 1 to 8 dilution. Still, this dilution worked. We did not test further. If you would dilute it further, it might, of course, lose efficiency. Since a 1 to 8 dilution did not do anything, I think that might also be the same situation in the body. What we found was some limitation was when we waited too long after pre-incubation, so after pretreating the cells and waiting, for example, six hours or so. After two hours, the ColdZyme was still effective, but after six hours, you did not see that great of an effect.
Okay. The sooner, the better.
Yeah.
Yeah. Okay. If I have understood correctly, you have studied the efficacy of ColdZyme on different viruses. You have studied for variants of SARS, you mentioned that, also on influenza virus and now rhinovirus. Would you say that there are any differences in how ColdZyme efficacy is among those viruses?
I mean, you can't directly compare those three viruses because influenza as well as SARS-CoV-2 cause much more tissue harm to the tissues compared, for example, to rhinoviruses. Rhinoviruses are more superficial. They don't destroy the tissue that much, at least in our model. I mean, of course, in vivo, you have some more compounds, but as Glen has also shown, also in vivo, it's really highly relevant.
Okay. I would like to ask you, what would you say are the most important differences when you compare your cell culture models to real life?
I think, I mean, as we've hopefully shown effectively to you, there are lots of similarities. Also in terms of what's the outcome, what's, yeah, in terms of viral load and everything. Of course, such systems are not as complex as the situation in the body, but nevertheless, you get really nice results, in particular when you look at entry of pathogens, at possible treatment methods. Therefore, I think for these research questions, it's a really nice system. We can also make it more complex by incorporating immune cells or humoral immune components. That's also something we are working on.
Do you have a comment on that, Glenn, as well when you compare because you know a lot about Doris's research as well?
Yeah, absolutely. I think they're complementary. If you do either alone, I think you don't get as much of the whole picture. I think the fact that we've got these two different models, we've got the in vivo model that we used and we've got the in vitro model that Doris has done in her lab, and we get very good agreement between the overall outcome, I think shows the relevance of both models. Our model shows what happens in the real world. Doris's model helps to give us greater scientific insight into the mechanisms, what's happening at the cellular level. I think in terms of the overall outcomes, we've got very good agreement, but they're complementary because they answer different parts of the question. I think together we get a much more 360 view of not just what happens, but why that happens as well.
I agree, yeah. Yes. I think we also have some questions from the audience. I will come. Has the use of ColdZyme caused any allergic reactions? Have people allergic to fish, for example, been included in the study?
No. We do have a method and a mechanism for people to report adverse events. We haven't had any reports from any of the participants in the studies. We, of course, specifically say the potential ingredients because they might be in the placebo group, but we give a list of potential ingredients and we specify that if people had an allergy or an intolerance to any of these, then they shouldn't use it. Yeah, if people are allergic to any of the known ingredients, then yeah, we wouldn't have been able to include them in the study.
Okay.
Yeah. Which, I mean, that's the same for any product, I guess I would add.
Yes. Yes, I agree. Okay. The test was conducted on generally healthy subjects with good physical condition. Would it be even more effective for individuals with chronic illnesses, for example, people with low IgA? Maybe.
Potentially, yes. If you would ask me for a hypothesis, I would say yes. I think it would be because they are more likely to get infected. They're less likely to fight off these infections in the first place. Doris mentioned, if you remember, in her introduction of the model, we're exposed to so many things. Most of the time we don't get ill, but sometimes we do. People in that category, they will get ill more often. My hypothesis in that population would be that they would also benefit and it would help them to suffer less and maybe get rid of those infections more quickly.
Yeah. Would you like to comment on that, Doris?
No, I totally agree. I mean, we also, of course, did not test this, but I would totally agree.
Yeah. Also, some of the colds in this study seem very long. What is the reason for including? Yeah, there are two questions in one here. Some of the colds in this study seem very long. Could you explain a bit how long is a cold actually and what is it if you look at the reduction in days, for example?
Yeah. If you haven't already read the manuscript, we do talk about this in more detail in the manuscript. If you read a textbook or you speak to a general practitioner or something like that, they will tell you that a common cold normally lasts one to two weeks, okay? Seven to ten or a few more days on average, which is absolutely the case and that's what we see. That's the average. You always get a spread. You get some people for whom it's a lot shorter and some people for whom it's a lot longer. The longest case reported in the study was 44 days, which is very long.
Wow. Yeah.
There was a couple in the 30s as well, which seems very long. It is quite long, but it's not unnormal. Obviously, every person who returned a swab was positive for rhinovirus, but some of them were also positive for other pathogens. We only measured the first week. We don't know in the person, for example, who had a 44-day long episode, we don't know if they got a secondary infection later or what. Many of them were co-infected with different viruses as well. There are different, like for example, if you've got influenza, it's going to be a bit longer. If you've got pertussis, which we normally associate that with infection in children, but actually you see it in adults. That's the one that they call the 100-day cough.
Pertussis, that's whooping cough, right?
Yes.
She coughs that Swedish.
Yeah,
yeah, whooping cough, yeah. Most of them fall in the average area of one to two weeks, but it's not unusual to have longer ones. What I thought was interesting, and we do talk about this a little bit in the manuscript, is that that only happened in the placebo group. There weren't these real sort of extreme cases in the ColdZyme group. My interpretation of that is that's showing the effectiveness of the ColdZyme. If that group hadn't have had ColdZyme, I think we would have seen more up at those longer durations. I think that wide range, but nowhere in the ColdZyme group, actually gives us more support for the evidence that it's actually doing something beneficial.
Great. Okay. There is another question with this athletes and the normal public. Will you continue the study with normal people and what would you expect? Can the results be similar to the others? It is just, will you study this in normal or?
I would like to, yeah, if I can get the funding and the resources. I expect the results to be the same. Again, it's a hypothesis as scientists. We have a hypothesis, but we've got to test that hypothesis. We've got to be objective and open-minded to find whatever we find. My hypothesis would be that we would see the same. Yeah, if we do that study, come back and see the results in a few years.
Yeah. You mentioned funding. There is actually a question, how was the company Enzymatica involved in both studies?
I mean, I had to pitch my idea to them to say, would you be interested in supporting this study? It's not possible to do these studies without funding. They're very expensive. I think it's important to point out it was my idea. I conceived the study. I drafted my proposal and I sent that to the company and said, would you be interested in supporting this study? They said yes. They gave us the funding, but then they leave us alone. The study has to be independent. It's really important as scientists that we maintain our independence. It's our study. We are responsible for the conduct of it. We're responsible for the interpretation, the analysis, and all of that sort of stuff. We submit the paper and we send the report to them to see what the outcome was.
I think the important thing is that.
All the theories, how you were going to approach it, what you did and how you analysis the analysis, all of that, yes.
Yeah. I think the other important thing in that, which is really important in science, is we pre-register the study. It is double-blind. That prevents any subconscious bias in how you analyze and interpret the results. It takes away the effect of expectation. Being pre-registered is really important because there are cases in the past where people would publish studies, but they would cherry-pick the results that they like and they would bury the results that they do not like. There is something called outcome switching where they change what they pretend was really their primary outcome and this one was their secondary when it was the other way around. You cannot do that, that is why you pre-register it. It is completely transparent and objective and open. That is all documented before the study even starts recruitment.
We then have the audit trail to show we haven't changed the outcomes. We haven't cherry-picked the data. Everything we said we were going to report, we've reported.
Yes.
For our study, it was different because my group performed the first study without being funded by Enzymatica. We did it on our own during the first COVID wave. Afterwards, yeah, we got into contact with Enzymatica there. It is the same as Glen said. We are just used, so we are getting funding from third parties all the time. We are independently designing our own studies. Therefore.
Yes. I understand. Great. Thank you. How do you judge the magnitude of the effect? Could you expand a bit on using ColdZyme prophylactically?
Okay. The magnitude of the effect is, is that the full question?
Yeah.
I'll try and say what I think they're asking and then maybe they can come back on if I don't get the sort of, if I don't interpret it correctly.
Yeah,
basically the scientific interpretation of effect size is basically how big that difference is. It is the size of the effect of whatever your intervention is. You can't just look at this compared to this because there's always noise in the data. You've always got variability. You've got spread. You have to look at the size of the difference taking account of the spread around that. If two things look like they're different, but the spread is massive and they overlap a lot, that's a smaller effect, magnitude of effect than if they're very far apart and the variation doesn't overlap so much. That's a very simple sort of layperson explanation of it.
Yeah, the effect size is what we call a medium effect size. You can consider it low, small, medium, or large, or none at all. It falls into the medium category. That's what we found. That's what we found in the previous study from 2021 and in this study. That's the magnitude of the effect. In terms of what that actually means for the primary outcome, depending on whether you look at the traditional arithmetic mean as the average or the median, because the data were not normally distributed, you're looking at somewhere between two and five days difference. It's about a 40% lower duration in the treated group compared to the placebo group. What was the other part of the question?
Actually, I'm not exactly sure because it goes away when I've asked them.
All right.
Then again, going back to the symptom where we discussed the length of a cold, also there are other aspects of this, I guess, that you said that you had extremely long colds in the placebo group that you did not find in the ColdZyme. I guess on an individual level, it can also be a difference. Yeah.
The other thing to say on that actually is if you excluded those ones that were very, very long and looked at all of the others, the difference was still significant. It is not just because of those.
That's a good point.
You look at the whole dataset and it's still there.
Yes. There is a little bit of a fun question from Jens Jänkä here. Are you using ColdZyme now after these studies? Are you using ColdZyme?
Yeah, I'm using. Definitely.
Okay. Yes. There is a question, could you expand a bit on the prophylactic use?
In the in vivo? Is that?
I would suspect, yes.
This was not the primary outcome. This was a secondary outcome. The study was designed for the primary outcome mainly. A secondary outcome was whether there was a difference in incidence. Is there a prophylactic effect? This was not a compulsory part because the duration when you are ill was the primary. There was an option for participants to use it in a prophylactic way, which was basically if they thought they were at increased risk, because they were traveling or they were knowingly exposed to people who were exhibiting symptoms. Of the cases, there were about 40-ish cases where they reported that they used it in that way. There was not a difference. In this study, in the model that we have used here, using it in a prophylactic way did not reduce the symptoms. They still got ill.
It did not stop that from happening. They likely got ill for a shorter duration and they suffered symptoms less. My interpretation of that, Doris's data, and maybe you can sort of say what you think, but Doris's data in vitro showed that it was working in a prophylactic way. It was preventing infection completely. Would you agree with that?
Yeah.
I think in vivo, it's different because in vitro, it stays there. In vivo, it stays there for a bit, but then it's going to be rinsed off. You're going to swallow. You're going to have mucosal clearance, like what Doris showed in her. It's basically not going to be there 24/7. My interpretation is that in a real-world setting, you don't know when people are exposed. Even if they're using it six times a day, there's still going to be gaps. I think you can never completely stop a virus getting in in the first place. What you can do is deal with it better when it's in there if you're using the product. My theory is that's why we didn't see a prophylactic benefit and there wasn't a difference in incidence, but there was a difference in symptoms and durations.
Although the other thing that I would say is to really test that question because it was a secondary outcome. It was not necessarily the most appropriate design to answer that question. If we want to answer that question, we need a slightly different study. I would actually love to do that study. That would be a really cool study, to do a full proper quarantine prophylaxis study. Only when we do that study would we be able to know if it really could work in a prophylactic way.
Okay. Yes. You included swabs in the study. Could you elaborate a bit on why you chose to do that?
Yeah. I mean, it's quite common to just report symptoms and do the sort of questionnaires and the logs. That's what people are bothered about at the end of the day. That's one of the reasons why that's the primary outcome. The swabs are important because that helps us verify that there really is an infection there because sometimes people can report symptoms and they can give scores on those logs. It might be something else causing it. It might be acute inflammation because of an irritant or it might be an allergy like hay fever and other similar things, which can cause similar symptoms. I mean, we have criteria in the questionnaire to try and eliminate what we would call a false positive because if it's not really caused by a pathogen, then the product can't do anything against it.
The swabs are there to give an extra level of verification that it really is infection. It also allows us to look at the viral load as well because it was, I'm glad that we included it because we were able to show that the viral load was lower. That goes in line with Doris's findings and helps us explain when I said about the mechanisms, it's not just what happened. It's understanding why that happened. The swabs allow us to understand why it's happening.
Yes. To verify.
Yeah, absolutely.
A last question. I will ask this to Doris first. Was there anything that surprised you in regards to the results?
I mean, when we first tested ColdZyme in terms of SARS-CoV-2, it was really amazing how effective it was to really clear the virus in our model at least. I think it's really, really good that all tested viruses so far, because they are from totally different virus families, they were really, so the ColdZyme was really effective against all those tested viruses so far.
You, Glen?
Not massively surprised, pleasantly surprised, I think, because we have the hypothesis. And the hypothesis was that it would lower episode duration and it would lower viral load. And it did that. But your hypotheses don't always come out the way that you predict them. That's just science. I think I was pleasantly surprised that that happened, but not massively surprised because that is kind of what we predicted with the hypothesis. In relation to the primary outcome, did ColdZyme reduce duration and viral load and all of that sort of stuff? Not massively surprised there. I guess a slight tangent, one thing that did surprise me was that every single swab that was returned, or every single case, so each case was four swabs, so we could look at the seven-day area under the curve, we actually picked up rhinovirus in every single one.
Now, some people had other infections that were co-infections, and that was a bit more varied. In at least one of their swabs from the seven days, we were always picking up rhinovirus, which was higher than what you will see in some other publications. That was quite a surprise. I think the explanation is the analysis panel that we used was very broad and very comprehensive. Sometimes other researchers used a much narrower panel, which means they're probably missing things. They think that there's not an infection there, but there probably is. They just didn't screen for it. The fact that we had a very broad panel, basically there's nothing missed. That was probably the biggest surprise though, that it was everyone had rhinovirus.
Yeah. If you feel you have a cold, you have a cold probably.
I mean, that's what our data suggests is people tend to know. If it's only there for like a day and then it goes away, maybe it was something else. If it's three days and you know, okay, most people know. If you came along and said, "Oh, I've got your swab results and it says you haven't," then they'll be like, "No, you know when you're ill most of the time." So yeah.
Great. Okay. Thank you so much for your presentations and for your answers to all of these very varied questions. We will now have a break. It is a break until a quarter past two. After that, you have the opportunity to listen to a corporate update from Enzymatica. Now you can grab a coffee, relax a little bit, and be back at quarter past two. Thank you so much.
Welcome back, everyone. I hope you found this previous session insightful. I know I did. We will now move on to the second part of today's briefing, and we will shift focus to Enzymatica as a company in light of the research from Professor Davison and Professor Wilflingseder. Now we will hear what this means for business operations, strategic direction, and the general outlook. Here to provide us with insights on those topics are Enzymatica CEO, Claus Egstrand, and Chairman Bengt Baron. My name is Johanna Jansson, and I will guide you through this afternoon and/or this 45 minutes, actually. We will end with a Q&A for the audience. First, let me start off by introducing you, Klaus.
Thank you.
You have a strong background in global healthcare and consumer health markets, and you now lead Enzymatica's efforts to expand its footprint and navigate the evolving regulatory landscape. We are very keen to hear your views of the latest progress and the general outlook going forward.
Thank you.
With that, I'll leave the floor to you.
Thank you very much. Welcome, everybody. For those of you who missed the Glenn Davison and Doris Wilflingseder presentation, please watch it on our homepage. You missed something exceptional. Let me take the opportunity to thank Professor Davison, Professor Wilflingseder and their teams for an outstanding result. Congratulations. What you see on this slide is actually the title of the manuscript that they presented in great depth. We need to focus on what does it actually mean for us? What does reduced viral load actually mean? What does infection duration actually mean? We all heard earlier today, it's super important about protect airway epithelia. That's less important to the consumers and our partners because it's not a consumer proposition. Let's just focus on what it truly means for us.
What you would have heard this morning is that the latest studies indisputably confirm the efficacy of ColdZyme. Indisputably confirm the efficacy of ColdZyme. We've been through some challenging times, being questioned by government bodies and everybody else. We now have a gold standard study that proves how ColdZyme works and the effects on how it works. What I would like us all to understand is what a gold standard study means. It means that the partners with whom we would like to work are actually paying attention. Gold standard study means in consumer healthcare that the participants are more than 100 people. We had 154. It means that the study is independent, investigator-initiated studies. We've heard that before. It means it's randomized, double-blind, placebo-controlled in the in vivo study. It means that there's an airway model with a control in the in vivo model.
It's now been peer-reviewed, which means one of the most prestigious journals, the Journal of Physiology, are actually saying that the data is real. The data is real. We now have an opportunity to move forward, but I think it's important for us to understand what the data really means. There's a lot going on on this slide. Let me just explain to you what we have. We have a unique product in the self-care space that works in an entirely different way than anything else on the product on the market today. What that means is that we actually target the underlying cause of cold and other upper respiratory tract infections by reducing the viral load. What that means, if you go to the bottom left-hand corner, you see the purple line and you see the orange line. Both start on day one.
They both have first signs of infection. They both have an infection in the body. If you take ColdZyme, the infection never takes hold, i.e., this is what happens in the purple line. When we talk about 94% virus reduction, it actually means the area under the curve, there's infinitely less virus particles for the people on placebo compared to the ones on ColdZyme. What actually happens is when you're infected, ColdZyme reduces what's called propagation, which means it spreads from one cell to the next. You can, in shorthand, you can say for the first time, we've proven that we actually break the virus cycle. Because when it goes from one cell to another cell and it takes off, we get increasingly ill, which is what you see in the symptom scores, lots of light green, lots of dark green.
It basically just means the data is amazing. We have significantly shorter episode duration, and we relieve symptoms of six out of the eight symptom scores in the Jackson score, runny nose, blocked nose, sneezing, sore throat, cough, and malaise. No other product does this. This shouldn't be a surprise to us. We've known this for years. Because the consumer satisfaction on the product of the few people that have tried is very, very high. We just did a study in February and looked at about the 100 ColdZyme consumers that we asked, what do you actually think of ColdZyme? Are you happy with it? Oh my God, yes, 94%. Would you buy it again? 93%. Would you consider using it again? 91%. This data doesn't exist for any other consumer healthcare product. Full stop.
The closest one is Imodium that I used to work on a long time ago. If we look at what's the opportunity, there is lots of market data, but if you take a step back and just say, how many colds are there every year? 17.2 billion colds every year. It's an old source from 2017, but it was just recently quoted in the Journal of Allergy and Clinical Immunology in November of last year. This is the data. Imagine the good we can do. We are in the process of commissioning some health economics data that will come back and present at another time. If we actually can convert the data we have into savings for society, what would that actually mean?
We'll just kick that off briefly in agency because they need to see the data and figure out what does it actually mean in real life. Now, here's a very, very busy slide. I don't want you to remember anything of it apart from the fact, go to the bottom right-hand corner. The global healthcare market is huge. It's $15.2 billion. And this is in the ex factory dollars. If you wanted to turn it into ex pharmacy sales, you double it by two. The global consumer healthcare market is $13.4 billion if you look at Europe, Canada, U.S., Japan, and China. $13.4 billion. Now, the other thing I want you to look at and never forget is at the bottom, go to the left, one, two, three, fifth line, it says totally you.
Go to the very right and read, oh my God, Europe, but we already have a registration, is $4.3 billion. Now, why haven't we sold in Europe before? Why haven't the partners been interested? Very good question. Because the MDR classification on its own is not enough. The regulations have gotten much tougher when it comes to consumer advertising. In Germany, U.K., and France, you need to have gold standard studies to support the advertising claims. This is what the people, companies we worked with, talked to in Germany, France, and European markets have been waiting for. Now they have something they can support by advertising. They're never going to get any market share in a $4.5 billion market in Europe without consumer advertising. We've been advertising in Sweden, and we know it works.
More importantly, the companies we work with or will be working with have never seen consumer satisfaction data like the ones I shared with you. It is a very good proposition for them. Get trial, and you know that people will buy the product again. Now it is just a matter of executing against the opportunity. If we look at it in a slightly different way and just base it on X pharmacy sales in Sweden, ColdZyme, we sell SEK 63 million at the end of 2024. If we do a simple population analysis, the market opportunity, if we were running it all by ourselves, would be SEK 6.9 billion of sales. Unfortunately, we cannot do that ourselves, and we need to get some partners.
What we can do is accelerate sales in existing markets, Sweden and the U.K., which is why we hired Anna Söderlund to run Sweden. She's a pro. Now we're going to run at Sweden professionally, and we have an internal goal of increasing sales dramatically in Sweden. Now we have the data. Now let's go do it because that proof of concept will play very well with our partners. If you can't do it in your own market, why do you think we can do it in our market? In the U.K., we have a nice business. Let's figure out how we can accelerate that business. In Europe, we should just go find some partners and get going. We are in discussions with partners for Europe. That's all I can say. We are in discussion with partners in Europe.
They've been waiting for the publication of the study, which happened on Friday last week. We have got to get going because the cold season is coming. That's all I can say. In other major markets outside of Europe, we need to identify partners. We are in discussions. We can start to initiate and finalize regulatory registrations because we now have the data we need. Surprise, surprise, the regulatory authorities outside of Europe would actually like a gold standard study that proves how the product works and what the consumer benefit is. No more excuses. We have all we need, thanks to the professors and their teams. Now we have got to just get going. All that being said, forecasting is not easy.
We still feel confident that we can achieve the financial goals by the end of 2027, which is an EBIT of SEK 170 million. How are we going to get there at this very point in time? We do not know. All we know is that we now have the right cards to play. Now we are just going to play them. Thank you.
Thank you, Klaus, for an inspiring update. You showed us a few slides. I was especially intrigued by that table with lots of numbers. I like numbers. You actually see them? Exactly. A quick question for me before we move on on that. I mean, we heard about great potential, $30 billion global market, potential SEK 6.9 billion. How will you set your priorities? What order will you execute? It is all about execution.
How will you prioritize in order for Enzymatica to get the biggest slice out of that? The way we're going to break it up is let's maximize Sweden because we have something. We have to remember in the past in Sweden, we never had the opportunity to communicate at first signs. 90% of consumers take the product at first signs, not at further beyond protection. That's not how people use it. Let's get Sweden as big as we can. We need to get Europe up and running because we have the approval already. Similarly, we actually have Canada. Let's get those things going, find partners for those. Registration in the U.S. will take two years, maybe three. Just waiting for the home run, as they say in the United States, would be a very foolish thing to do. Let's just do bunt singles, whatever it takes.
The sooner we get back in black, the better it is for everybody. There is no reason for us not to get back in black quickly.
Thank you, Klaus. I'm sure there will be more questions regarding both sales and other things later on in the Q&A session. For now, to provide us with further insights and perspective from the board, I'm pleased to introduce Enzymatica's chairman, Bengt Baron. Bengt, welcome. You have an extensive leadership and experience in international businesses and consumer brands. With that, you have a crucial role in guiding Enzymatica's strategic direction. We will soon open, as I said, for the Q&A, but first a few questions from me. From a strategic point then, what does a study like the one now published in the Journal of Physiology, what does it change for Enzymatica?
It's an absolute game changer, I would say.
It gives us indisputable proof of the efficacy of the product. It is independent, it is peer reviewed, it is published in a very prestigious journal. It's no secret that we've had some questions around the efficacy of the product throughout the years that we can put to rest now. Now it's all about execution, as Klaus was saying, and moving forward, finding the right partners that have the right resources, the right engagement, willing to allocate the resources and build the business.
I also have a question on, I mean, I understand this is an important step for you. A question then on financial targets in relation to this. In July, you reiterated a quite ambitious target, although you extended it for one year until end 2027. How confident are you that Enzymatica can really scale up its business almost tenfold within that period?
The target is the target, right? It's not a promise or a given. It is a challenging target, without a doubt. However, our growth will not be a straight line. It will be lumpy. It will be bumpy. It's going to be big bumps whenever we sign up a new partner and we enter into a new market because you load up the entire pharmacy network or the store network. It's a big load going. You go from zero to 100 in no time. It's going to be lumpy and bumpy, but we feel with this study in our arsenal that we will find the right partners and that they will also be very eager to get going.
Can you
build on that for a second?
Of course.
I think it's important to understand that we have something that's not around.
When we talk scale up, we're not scaling up. We're finding people that have the resources already, that are probably in the category already. If we were doing this ourselves, there's no way we're going to do SEK 170 million in 2027. We are in discussions. The partners we're talking to can get us there. We just have to be careful how we use the word scaling up because if we did that ourselves, no way. Can we get that through partners, as Bengt said? Absolutely.
I think that is a good segue into our first question from the audience because I have something here. Hold on. Throughout 2024, the company has commented in reports that discussions are ongoing regarding launches and new partnerships in several markets such as China, Japan, North America. How does this report we've heard of today impact these discussions?
How soon can we expect new agreements? That is the first part of the question.
Let me address the first part of the question. We have ongoing discussions with existing and potential new partners that have made it very clear that the sooner you get a publication and data, the sooner we can move. The other thing that I thought I said, I tried to say earlier, is that we cannot initiate a filing with a partner in the United States until we have a double-blind placebo-controlled study because they want to actually see data that works. What we have built on MDR is very solid, but we do not have the required clinical investigation report to file in the United States. That is one piece. That does not mean we have not started discussions with FDA lawyers in terms of what could the road to market be.
Of course, we've done that. In Japan, they've been waiting for data. China, we're trying to figure out what's actually going on, like most people are in China these days. That is it. In terms of when the agreements, that was the last part of the question. In terms of when we think we'll have agreements.
Yeah, jumping in there, I think you also need to balance speed versus the correct solution. I don't think we should rush into the first possible agreement unless it is the best agreement for that market. It is also balancing between speed and also having the right results three, five, seven, ten years down the line. That is going to be interesting work for us going forward, we hope and believe.
A bit related to this, I'm going to combine two questions here from the audience, but it's also related to financial targets. With this report, does the company now feel more confident that you will achieve the target that we saw here before of at least SEK 170 million by the end of 2027? I think that's almost rhetorical.
Of course, we feel better, even better about the possibility. Again, a target is a target. The target is not something that's easily achieved or slam dunk in any way. Without this, as Klaus was alluding to, without the gold standard study, we could not run advertising in Germany. We could not run consumer advertising in the U.K., which of course would have made it more difficult. This does aid us, but we still need to build a strong partner network. Can I build on that?
Yin and yang. If you listen very closely to what Professor Davison mentioned earlier, it was basically one of the questions in the peer review was read between the lines. The data is too good to be true. Are you sure there was not any hocus pocus mistakes on the placebo versus the active? That is a big part of the manuscript that talks about why we know there is no difference. Even the journal sort of rhetorically asked, are you sure that the consumer or the participants do not know if there are active and placebo? We have lived with the data and the interim data a lot longer than most people. Our partners have not. With all due respect to Glen and Doris, it is a long manuscript. It will take some time, but we are getting there. We are in a much better shape today than on Friday.
That's all I can say.
A question on sales and potential. We have here from the online audience playing back to two years ago where you had an estimate for SEK 600 million in 2026. Now you have a lower estimate and for a year further in. Now that you have the study, why not, if you're optimistic, can you raise it? I know that's.
That's a board decision.
Yeah, but we had a target on SEK 600 million. Also what we have told is, as we are going forward, it's very possible that we will have a mixed commercial model where today we do everything. We bottle it, we get the packaging, and we sell the final product.
Down the line, as we launch in further remote markets or maybe also with bigger players, some of them might want to do the bottling and the packaging themselves, which is going to impact the relationship between sales and EBIT in a way we cannot predict today. That is why we elected at that point in time to focus much more on the EBIT target. That we are sticking to for now. As we get more clarity on what is going to happen on the commercial model and when, we are going to come back and we will update the financial targets. Now the focus is very much on the EBIT, and we will figure out how we get there with the different models. At the end of the day, cash is king. Speaking of cash, in the fourth quarter, you increased net sales by 9%, but partner sales were almost nonexistent.
Can you elaborate a bit more on what you're doing specifically to boost other markets and start fruitful partnerships?
The good news is that we're never going to have a quarter where we lap ourselves when we sold stuff. If we have no partner sales in Q1, we're comparing it to zero last year. Whatever growth we have will be positive. The other thing is the partners know that we need to get moving on orders if they want to launch for Q3, Q4 this year. My expectation is that we will get some orders if we choose to have it shipping out the door in Q3. That's to meet the core market. That's a commercial guy because that's just how it needs to work. Do I know whether we're going to get that or not? No.
Do I know that people want to launch for the next cold season? Yes. It is just logic or common sense.
A few questions on the product itself. This is also from the online audience. Do you plan to keep the product as a medical device, or will you at least for parts of the global markets make a medicinal product out of it? I guess that is sort of a regulatory question. That is a very good question.
Let me try to answer it this way without really answering the question. Every jurisdiction has a different classification of what the product does. In Canada, we registered as something called a natural health product, not a medical device. In Europe, the classification is a medical device, MDR class three. In the U.S., there are three different potential classifications we are looking into.
One of them is medical device. Every market would be different. If one of the partners outside of the EU will want a separate classification and that makes commercial sense, then we'll obviously listen to it. That's all we know. That sort of answers the question without answering the question.
We'll see. If you feel that the answer is not, or the question is not answered, please feel free to pose another one. You mentioned, Bengt, that you will be selective when selecting partners. Can you give us some more detail? How would you evaluate and select new partners to ensure Enzymatica gets the biggest slice out of this potential?
I think there are a number of parameters that you need to take into account. One is, of course, sheer power. Do they have a sales force?
Do they have an assortment, which means that they're important for the pharmacies or the retail? Another part is, of course, how eager are they? Are we just going to be something minuscule in their assortment, or are we going to be relevant in their assortment? A third area is also, at the end of the day, business is done with people. How excited are they? How much energy is it amongst the people? Another one is also, of course, the culture of the company. Do they think about things in the long term, or are they just trying stuff for six to twelve months and then decide whether they want to invest as they go, or do they withdraw? It is trying to cook all of these things down into an overall picture where we jointly with management feel, okay, this is the best bet for ColdZyme.
Another thing is also, of course, most likely in most markets, we will launch the product under an existing brand name as a new product because that way there will be a consumer franchise for that brand. The consumer will trust the brand and be faster at trying new products and believing them. Also there, we need to say, is there a good fit in that area? I could go on a little bit longer just to demonstrate that it's not as straightforward as who shows up the first at the door. It's much more complex than that if we want to maximize the value for the shareholders. Believe me, that's what we're here for.
We have a few questions on future research.
I mean, we understand that the study that we've just heard about is important for you, but if there would be future research, what could that be? We have one question here. The professor said they would like funding to extend their research. Will you finance any further studies? Asks Oliver.
At this point in time, we don't know. The reality is if it really proves something that's different and it builds to what we already have, yes. We're not going to do clinical studies that's going to ask questions as to why are you doing a similar study because you have doubts about what we already did. We are going to stay far away from that. If there's a different way of doing stuff, to Professor Davison's point, would we like to prove that it actually works prophylactically?
That is a different discussion, but we have not had any discussions around that. We have another question here related to that, maybe an idea for future research. Will you be able to show what ColdZyme does in terms of potentially reducing the effect of how an infected person using ColdZyme infects others? You have already answered the question on future research.
There are so many angles, and of course, when you have this exciting news, creativity kicks in, and everybody wants to do more. At this point in time, we want to make the most out of what we have. We can think about how we can make even more going forward, but for now, the focus is to make the most out of what we have.
Can I build on that?
Of course.
We have been through.
We were off and running and feeling awfully good in 2019, 2020, partner deals.
During the pandemic almost.
Just pre the pandemic. Unbelievable black numbers. Share price was north of SEK 20. Pandemic happened. All the partners we had launched the product as preventative because that's where they thought we had some data and where the niche was in the market. Now we need to think about this as a totally new, it's still called ColdZyme. Some of us probably worked with it for way too long, but it's a completely different product. The completely different product proposition. We couldn't talk about viral load reduction. It's completely different. I know some of the partners are looking at how do we communicate this in a new world, and that takes time. The worst thing we can do, it gets distracted about what's next. We haven't even explored what's now.
That'll be the hardest thing. Oh, we've done that. Now we're bored. Let's do something else. No. Execute on existing markets, find partners, and then we move on to the next thing.
A bit related to sales and the landscape in which you are existing, competition. Can you say something about how will Enzymatica maintain this competitive edge in this quite crowded healthcare and consumer health market?
Very good question. Thank you for every answer. The slide I showed you about how big the categories were, they're all symptom relief. They don't do anything. They basically say, "I don't feel so good. I have a runny nose." I take a nose spray on some market. I take a tablet, and it stops my nose running. It doesn't do anything to the underlying cause. Therefore, we're not shortening the duration.
We have a product, the only product that shortens the duration and relieves symptoms and multiple symptoms. We do that because we work in an entirely different way with the body and all the other ones, the pharmaceuticals that you can buy over the counter.
We also have a question from the floor, please.
All right. I hear you loud and clear. You want to stay with the product as is, even though you also went into some product life extension, bringing on the menthol. I wonder how has that worked? How is the proportion these days between the strawberry, the original, and the menthol? Would you consider bringing in other flavors?
Yes. Very good. The menthol is about, and I'm winging it a little bit, and you can correct me, but I'm winging it a little bit.
That means I'm sort of making it up on the fly. I think 80% is menthol because strawberry is like a kid's flavor. That's how it was launched. I have no idea. I don't like it personally, but I'll say 80% is menthol. Yes, we're looking at other flavors. That is coming to your theater soon.
Okay.
Thank you. You recently strengthened your cash position. I thought we should talk a bit about that too. How do you assess your financial stability going into 2025 now?
We feel very good where we are. We feel that, I mean, the shareholders have been fantastic in supporting us. We feel very grateful for that. They've been very solid. I think we're in a good position today in really having the time available to do the right things as we build up our partner network. That is not a concern today.
Can you give us, from the board's strategic perspective, can you tell us a bit more specific key steps that you are taking to enhance profitability and shareholder value?
It's all about scaling up from our point of view. Scaling up, as Klaus mentioned, is very much building our partner network and entering into new markets. Of course, we want to grow in Sweden and the U.K., where we control the entire value chain. It's mostly important, I think, to demonstrate what can be done and that advertising works and that the consumer loves us, as Klaus also showed, as a showcase for other markets and for partners. When it comes to improving profitability, it's all about volume. We have an incredibly scalable business model. We're incredibly asset-light. It's a volume game from now on.
The volume is going to come, as I mentioned, in chunks as we sign up new partners and as we enter into new markets. That is where the focus is. If we just execute and perform and deliver on that, everything else will take care of itself.
We're not nearly at the end of this session, but we're approaching it. Please fill in any more questions. Top right corner for you online. I have a few more left here. I'll take them in order as they come in. Two about new markets and partners. You've touched upon new markets already, but for which markets do you have go now? Is a question also from Jens.
Have go.
Have go.
I think I'm assuming we talked about registration-wise.
Registration-wise. Go for registration. We have all the markets in Europe and Canada.
In terms of partners, as soon as we can communicate something, we will do so appropriately because we are a listed company. Until then.
You can't say anything about the number of partners or?
No. No.
Okay. Another last question here, also on competition. There are several cough and cold products available on the markets, herbal and chemical ones. Even though there are different active substances, the question from the audience is, what's the specific aspect of ColdZyme unless there's a study available that compares different products?
With the benefit of having worked in the cough and cold category at J&J for 10 years, none of the other products are similar. Basically, the active ingredients are paracetamol, phenylephrine, pseudoephedrine, oxymetazoline, chlorpheniramine. They're all drugs. None of the products on the market today does anything to shorten the duration. It makes you feel better.
When it wears off, you don't feel better, and then you take something else. Nothing else is out there that's similar to it because you don't have to do a comparison.
I think going back to one of the challenges is to really make the consumer understand the difference. It's almost like if you go into a pharmacy that we would like to have a new shelf which says, "Treat the underlying cause." On that shelf, there will be one brand. It's ColdZyme. There's no other product that would be on that shelf today. In the future, we'll see. Today, there's no other product that has shown in research clinically to do what ColdZyme does.
Let me just thank you for stepping in because that made me think of something else.
One of the things that we've discussed and that people may remember, not remember, is that the FDA have actually investigated the efficacy of all the active ingredients in the existing cough and cold products. So phenylephrine, which works for sneezing, runny nose, and block nose, three of the six symptoms we have, has been deemed not to be effective in an all-dose and will come off the market in the United States. Phenylephrine is in a lot of products in the U.K. called Lebensip. In Germany, a starter product is. The starter has a protect. All of them have these active ingredients in it. It doesn't work. It's already coming into the press.
Europe for now skirted the issue by saying, "Oh, we don't really care if it's effective as long as it's safe." As soon as it comes off the market in the States, it'll spill over into Europe again. Normally, it starts in France. They say, "How can you charge French consumers to pay for stuff that doesn't work?" It will start in Europe. One active ingredient is gone. Two of the cough ingredients are being investigated. They don't have efficacy either. What is today will not be tomorrow. It will start in the States, and it'll spill over into Europe.
A question for you, Klaus, on organization and personnel. Given the recent study and now you want to execute, execute, execute, what kind of competence and personnel resources will be needed to reach the financial targets and to do this execution?
Pre-Christmas, we hired two people, one of whom we've announced. There's Anna Söderlund that sits over there. She's going to drive the hell out of Sweden. I have to worry about Sweden. We hired somebody called Charlotte Hodgkins-Byrne, an ex-Olympian who's going to drive the upside opportunity with the athlete community because they're already fans. They've been known about ColdZyme for a long time, and now they've actually proven in a clinical study that all athletes should be taking it. We're making great inroads with athletes, which I believe would be great spokespeople for normal consumers, as Glenn said. Maybe not normal, just everyday consumers. My job now is to use my network from the past to go and sign the partner agreements. It's all about who you know. It's not as good as a product.
If you start at the wrong end, it's never going to bubble up. Now we're going in at the top, and it's all bubbling down, and it goes a lot faster. Now that we've got the study done, that's where execution and execution is going to be. Whether it's Europe or international, that's my job. It may say CEO in the title, but it's Chief Commercial Officer.
You say partner agreements are key here. Could upfront payments for Enzymatica be a component when signing partners?
There's no point in speculating on how it's. I go back to it. It's going to be a fairly complex recipe once we get there. Then we'll see how the right partner wants to structure a partnership. There are so many variants that we can stand there and speculate for hours.
Let's revisit that once we have a real case in front of us.
I will take one last question from the online audience now before we wrap this up. This person, first of all, wants to thank you for answering the question so frankly. Are you prepared to have enough? This is about production capacity. Are you prepared to have enough production capacities in your facilities for increasing market demands? Is there a risk of stockouts? Rather, what's your strategy here to avoid costly stockouts?
Okay. Unfortunately, I have a chairman that must have gotten his hands burned along the way. That is the one mistake we will not make. We are actually in very good discussions with Resty Pharm, that's now owned by a company called Blue Wolf.
The way it's working now is that we will not have to cover Europe, we're fine in terms of production capacity. They can do up to 16 million units without adding extra shifts. That's a lot of units. We're fine when it comes to that. When you look at outside of Europe, does it really make sense to ship bottles and packages and containers to Canada, eventually the United States? Probably not. We will move to a different model that Bengt mentioned earlier. It's going to be a hybrid because it's going to have to be a hybrid. As Mr. Trump puts more and more import tariffs in, we probably need to make completely sure that we don't send anything that's finished to the United States.
Thank you.
I'd like to finish by asking you if you could send, we have an online audience that has been very active. We have you here on the floor here. If you could send one key message now that you have everybody's attention, what would that be here today?
Let me have a go.
Good.
I would say that Enzymatica is at an inflection point. Now we have the independent research. It is peer-reviewed. It is published. There's not a question mark around the efficacy of ColdZyme. There's no doubt about that. I have yet to meet a single person around the world who doesn't like the idea of having less symptoms and a shorter duration of the cold. I have yet to meet a single person who's never had a cold. There's no doubt that there is a potential out there.
That's what we need to go after at this point in time. That's why I think it's an extremely exciting time to be at Enzymatica. I would argue, maybe I'm slightly biased, but I would argue that Enzymatica today is the most exciting public company in Sweden. I'll stick my neck out to say that.
That's optimistic. Thank you for that optimism. It's infectious. Anyway, I think it's 3:00 P.M. With that, I'd like to conclude this briefing. On behalf of Enzymatica, I would like to remind you all that there will be a recording of both the sessions on Enzymatica's website, and that will be available shortly. With that, on behalf of Enzymatica, I'd like to thank the speakers, our audience here in Stockholm, of course, the online audience, and you.
I know Enzymatica appreciates your time and interest in this journey and look forward to keeping you informed.
May we also take the opportunity to thank you.
Okay. Thank you.
And Eva, who I think has left, but we'll pass it along. And the team that's made this happen, Pang and Anja and team, and then obviously the professors. I thank you once already.
We also have a kind thank you from the online audience. I think with that, have a great rest of your day.
Thank you.
Thank you.