Welcome, everybody, to this conference call. Good afternoon to our listeners in Europe. Good morning to those in the U.S., and a special welcome to those listeners in Asia at this very advanced time of the day. It's our pleasure to update you on the results that we have disclosed this morning. I believe we can say that this is a fantastic day for patients suffering from schizophrenia, and it's also a very good day for Newron and its shareholders. I'm here today with Ravi Anand, our Chief Medical Officer, who will take the key part of the presentation, the talk. We do not have slides today, as we do have little more results to show than those disclosed already in the press release, but have some patience with us. That will change very rapidly in the next few weeks. You will see and hear more and more about the detailed results of this study. As we have a number of listeners new to the story, let me take the opportunity and walk you through within a nutshell about Newron and what we do. Newron, for 25 years now, is developing innovative drugs for diseases of the central nervous system. We are headquartered in Milan, Italy, with a subsidiary in Morristown, New Jersey. We are listed on the Swiss Stock Exchange since 2006, and the shares can also be traded on the Frankfurt, et cetera. Our most advanced compounds have one thing in common. They are all working by a mechanism of action called voltage-gated sodium channel blockade. While most of you will know sodium channel blockers for a long time, very efficacious drugs with a number of side effects that have taken plenty of them to the graveyard, the class of compounds that we are talking about, the voltage-gated sodium channel blockers, has the advantage of the efficacy without the side effect of those sodium channel blockers. The one that is already on the market, Xadago, is an add-on treatment to levodopa in patients suffering from motor issues. This drug is already on the market in Europe since 2015, in the U.S. since 2017, and since that time, it has been approved around the world. It's licensed globally, and we have collected more than EUR 85 million of revenues, peak milestones, and royalties from that compound. For whatever it is good, take it that these drugs are safe, and we can say so not only for Xadago, this Parkinson's drug, but even more than yesterday, we can also say today on evenamide, these drugs are safe, very safe. They do work in the brain of the patients. Said that Xadago is licensed globally with a continuous revenue stream until 2029. For investors, this is not going to be any striking event. The real game changer for Newron is evenamide with a now positively completed phase III study, the first pivotal study successfully run. This drug combines the new mechanism of action, and that is what it has in common with safinamide as well, Xadago. It's a glutamatergic mechanism, and both drugs in their field are unique with that mechanism of action. Evenamide not only is acting by a glutamatergic mechanism, but it also has a unique positioning. It is the one and only drug that is currently under development in treatment-resistant schizophrenia, 30%-50% of schizophrenic patients. It is the long-looked-for alternative to those almost 70% of patients who have to switch their medication regularly because the current therapies do no longer do sufficient good. If you look at the market, it's a big indication. We are talking about 1% of the global population. As I said, 30%-50% of those are treatment-resistant with no treatment alternative but very old clozapine, massively underused. There is a number of caveats with those drugs on the market. It's more than 3 dozen drugs. Mostly, I have to say it's the massive load of side effects. We are talking about extrapyramidal symptoms, weight gain, like a U.S. pound of weight gain per week of medication, sexual dysfunction in men and women, and soon to come probably, material GI problems. So one of the key characteristics for any new drug is it should be safe. Here we come with evenamide. The second key issue with today's medications is their limited efficacy, which is fading over time. That is what I mentioned before, that more than 70%, according to the CATIE study, will ultimately have to switch their medication every 18 months looking for some alternative, in the best case, with a new mechanism of action. That's exactly where evenamide is positioned. A glutamatergic mechanism, and it could be the first add-on therapy as an add-on to any of the current antipsychotics in schizophrenia. The second indication is treatment-resistant schizophrenia. Those 30%-50% of patients who today only have clozapine. Only 5%-15%, depending on the geography of the patients, will take clozapine, though, because of the massive side effects. So for those patients suffering from TRS, what we need is a new mechanism of action, but first of all, a safe drug. Again, here comes evenamide. We are developing evenamide in both those indications. What we have reported lately in the last 18 months with a final press release in January of this year was the outcome of a one-year open label phase II study with evenamide as an add-on to any second-generation antipsychotic in patients with treatment-resistant schizophrenia. What we showed in that study was that up to 12 months after the total study duration, we saw not only significant but clinically meaningful improvement on all the key endpoints, be it PANSS total, CGIS, CGIC, or level of functioning. Not only did we see that improvement, but we saw it being ever-increasing from day one till the end of the study. We saw doubling and tripling responder rates depending on the endpoint. We saw 50% of patients no longer being diagnosable as TRS at the end of the study, and we saw 25% of patients being in remission, something never seen before and reported before in TRS. So this study showed the full and ultimate potential of evenamide in a 12-month study. If you want to, and that was the two points we heard at that time, if you wanted to find anything to criticize in that study, well, it was open label. There was no placebo arm. Everybody said we cannot explain the efficacy seen by placebo, but there was some doubt in the end. The second point was that the study was mostly run in Indian sites for all a number of reasons. By today, I can say, and by the study that we have just completed and reported in patients with chronic schizophrenia, not yet treatment-resistant, those two points are put to rest. We do have a phase III placebo-controlled study, an international study run in 11 countries in multiple study centers. We have seen the same or even better results after four weeks than we saw in the four weeks of the TRS study. That all said. Before I hand over to Ravi, I think it is time for us to say thank you. I want to say a heartfelt thank you to all the patients who participated to the Study 008A that we are reporting today. The patients, the families, and the caregivers who, even if it was through COVID times, got into that study, they took a double risk, a new mechanism of action, the first add-on therapy ever. They took that risk, and they were incredibly loyal to the study and the medication. We need to thank the investigators who participated to help us make this study a success. A special thanks to Shiv Issar, the Global Head Clinical and Regulatory at CliniRx, our CRO in this study. Excellent job done, Shiv. All the other stakeholders making this study a success. Please, I ask for your forgiveness, I didn't have the chance yet, I want to say thank you to my fantastic team, starting with the directors who have supported us in the last 18 months and longer, helped us get this study done. To my team, Ravi, the Chief Medical and his people. This study was designed in a fantastic way, and it was executed flawlessly. If there's one indicator for that, I want to say that we don't know of any study in schizophrenia over the last years which has come out with any such low placebo rate. We know that placebo in schizophrenia is a major issue. That all said, it is my pleasure to hand over to Ravi to give you more detail on this study, the outcome, and the outlook. Ravi. Thank you, Stefan. After Stefan's introduction, I shall try to be brief to give you an opportunity to ask questions at the end. The most fundamental question that I have always faced when trying to explain this study and the project is what is the target indication, and between the populations you are studying, what are the differences? Let me just start by a very basic statement about schizophrenia. We know that patients with schizophrenia, they get the disease. They're usually initially treated with one antipsychotic or the other. Over the period of time, many of these patients will maintain their benefit. A segment of this patient population will not benefit tremendously or who benefit tremendously in the beginning begin to lose their effect over time. There's a third group which does not benefit at all right from the beginning or after a few years. The last group are the treatment-resistant patients. The second group, which benefits initially but then begins to lose its effect over time. These are people whom we call as inadequate responders, poor responders, and there's a belief that a very large proportion of these patients will eventually become treatment resistant. When we looked at evenamide, it looked very different from any other antipsychotic that we know of in development or on the market. First of all, uniquely, it does not interact with any monoaminergic neurotransmitter system. It does not interact with the cholinergic system. Out of the 130 plus CNS targets, it does not interact with any one of them. The only thing that it does, it inhibits sodium channel by a mechanism that we call as voltage-gated blockade. That means it is only active when it's required to be active. And this effect on the sodium channel is the mechanism by which glutamate is modulated. We know now from a lot of the work done in neuroimaging, neurochemistry, long-term follow-up studies, there's a big proportion of patients, especially those who do not respond adequately to dopamine-blocking drugs, who appear to have a normal dopaminergic function but glutamatergic dysfunction. It stands to reason that when these patients who fail one antipsychotic are treated with another antipsychotic acting through the same mechanism, there would not be any benefit. Perhaps a drug which would act through glutamate modulation in the patients who have abnormal glutamate functioning may benefit. In the animal model data that we have already evaluated and are continuing to evaluate, it became very clear that this drug has some very unique properties. It has a very rapid onset in the way it gets into the brain. It appears to act when used as monotherapy, but also when used in combination with another antipsychotic, both drugs being used at doses that are ineffective. This suggests to us some degree of synergistic action in the brain. That's what led us to contemplate using evenamide as an add-on treatment. The animal data also confirmed something that we had speculated, which was that this drug, when added to clozapine even, in an animal model where pre-pulse inhibition was reduced by giving glutamate antagonists such as MK-801 or ketamine or phencyclidine, produced a benefit. Therefore, it could also be used for patients with treatment-resistant schizophrenia. That's a study which Stefan described, which is a pilot attempt, and that is the reason why we never really thought about it as a placebo-controlled study, which of course, I wish now that we had done it. That study was remarkable. It had a very high retention rate. It showed that patients who stayed on drug continued to improve over time, which almost goes against the normal teaching that patients with schizophrenia improve in about four to six weeks or eight weeks and subsequently plateau out. In that study, the proportion of patients who met criteria for response continued to increase even up to one year. What was fascinating was to see that many of the patients no longer met the operational criteria for treatment-resistant schizophrenia because they showed full response. Many of those responders met the criteria for remission, which is the ultimate goal of treatment in schizophrenia. Based upon those data, which were released in January or so, we were very, very exhilarated but also encouraged to think of the results coming from this study. The Study 008A, I think we have briefly described it in the press release, but let me just point out a few salient features. It was an extraordinarily difficult study to perform. Each and every key opinion leader, expert writes that patients with schizophrenia should be treated only with one antipsychotic. There is no benefit in combining two antipsychotics. However, when we initiated the study, asking for only patients who were not doing well on their monotherapy, we found that very few patients in the field were actually adhering to this. Second thing, what we realized also is a patient saying they're not responding is not really necessarily the only truth. Many of these patients were not compliant with their medication. When we did plasma levels for the antipsychotic the patients said they were taking, a lot of the time, we found, A, they were not taking the drug, taking inadequate amounts, taking two drugs or three drugs at the same time, taking the wrong drug compared to what they said. That is why it has taken us such a long time compared to our original projection of enrolling the patients. What we also realized is that in these patients, there's a plethora of different symptoms which requires treatment and many other medication. Because these medications are going to be taken all the time, it also requires that the drug you're adding, in this case, evenamide, be free of any drug-drug interaction. We are very happy to report, first of all, that evenamide does not induce any cytochrome P450, does not inhibit any cytochrome P450. It's not a P-gp inhibitor, therefore, it's an ideal drug. It could be added on to any antipsychotic, or any antipsychotic can be added on to this drug. In this study, we allowed patients who were on any one of eight different antipsychotics to be included in the trial. The degree to which family members, investigators are frustrated with the current treatment of patients who are not treatment resistant, but are poor responders, is illustrated by the fact that even though we had completed the enrollment in the study, one patient's family came back and requested again and again that even though the patient was late, we randomize, include the patient in the study. We actually had to change our policy and include this one patient, which cost us more than 1 to 2 months for the time to get the results. It was an effort well worth it. We have included 45 centers in 11 countries. To ensure that the same dosage ranges are being used for the drugs. To get blood samples analyzed from every patient within 21 days of their signing a consent form prior to them being randomized. To make sure the translatability of documents or procedures was a humongous effort in which I must thank the CRO and their medical monitors for having done a very meticulous job. The amazing thing that comes out first is that we had 280 of the 291 patients completing the trial. In my life, in schizophrenia research, I've very rarely ever seen such a result, and this is probably the best result that I've ever seen for retention. The number of patients who dropped out for adverse events is extremely low. It's only four patients, and there's only one death, which occurred in a patient on placebo. The side effect profile is something which you can only dream about. Only about 25% of the patients reported a new adverse event. There is no difference in the proportion of patients who experience a CNS event or a psychiatric event or a GI event between evenamide and the placebo group. There are no clinically significant results indicating abnormalities in liver enzymes, kidney enzymes, et cetera, that we know about till today. Finally, we come on to the efficacy. The first thing that I was really surprised to see, is the level of placebo change. I think we have become so accustomed to seeing 12, 15, 20-point placebo changes. It was a real pleasure to see placebo group improving by only about seven points or so. The uniqueness of the data set that we have, which shows very careful attention to ratings, is illustrated by the fact that despite there being about a 10-point something reduction in the drug-treated group, we show a statistical significance in the ITT population for the primary endpoint using the treatment policy with a p-value of 0.006, which shows you how good the data are that you could get this kind of a p-value despite smaller differences between the group. The key secondary endpoint, which has been asked for by regulators, was the Clinical Global Impression of Severity, which also came out significant. One word about the level of change, which is obviously the question everybody wants to ask for. Patients who are on monotherapy in acute psychosis, hospitalized patients, they usually have a baseline score of about 90, 95, and it's fairly customary to see 30-point reduction, et cetera, in treatment groups, as well as 15, 20-point reduction in placebo groups. Patients who are inadequate responders never respond by this much because they lost the capacity to respond. Furthermore, these patients, although they were all on an antipsychotic, and they were showing all the symptoms of psychosis on this antipsychotic, despite being at a stable dose for four weeks at least, and plasma levels, which indicated it was a therapeutic dose level, they still are benefiting from that antipsychotic, though not adequately. When you add evenamide, there is an improvement. That is remarkable to see that these patients who are not doing well now begin to improve. The magnitude of the improvement will never be great because it's constrained, firstly, by the lower level of the baseline severity and secondly, because they're already taking another antipsychotic medication. Under these circumstances, to show significant superiority for both the primary endpoint as well as the key secondary endpoint in a four-week trial, tells me that this drug has a great future. If I just compare the results of this study with that of the TRS study, at four weeks, the 30 milligram dose has a better effect than the 30 milligram dose in the TRS study at six weeks. In other words, if we were to do the next study with this drug, in this patient population, a six to eight-week study, we would be having a much larger treatment difference. The second thing I think we have learned from this study is that patients will comply with the trial requirements if they believe the drug is doing well. One of the things that has always puzzled me, whether in the TRS study or in this study, why patients stayed on drug. Why did caregivers continue to come for visit after visit despite the COVID problems, et cetera? It can only be for one of two reasons. First, the drug must be well-tolerated. No patient with schizophrenia will ever accept to continue taking drug for any length of time if the drug is not well tolerated. Second, there must be some benefit. No patient would continue to take a drug if there was no benefit. I think this placebo control study has clearly demonstrated to us that there is a real benefit that patients can perceive of, which is the reason why they kept in the study and kept coming back again and again. The next question is, what does this mean for regulatory affairs? First of all, this study has met the primary and the key secondary endpoint. The significance levels are those which are required for registration. In discussions with the health authorities, we have always had the agreement that if this study were to be significantly superior to the established antipsychotics, this study would count as a pivotal study and could be used as a second study to support the TRS study, which we plan to do next. Obviously, the results of this study are going to lead to us to making some minor changes in the TRS study protocol, which we had almost got ready, had feedback from a lot of the health authorities, and we were ready to initiate, but now we're going to have to tweak that somewhat. Overall, it's a result that only a few months ago we could only have dreamed about. I can only tell you that I'm very excited that for the first time ever, a drug which acts purely by a glutamatergic mechanism has shown efficacy. Secondly, this is the first study ever which is adequate, well-controlled, placebo-controlled, in which patients who are inadequate responders benefit when new drug is added to their current medication. No such study has ever been done, has ever demonstrated this benefit. There are a lot of firsts for this study, and I look forward to sharing more results coming from this study in the very near future. Thank you. We are ready to take the questions, Moira. We will now begin the question and answer session. Anyone who wishes to ask a question may press star 1 on their touch-tone telephone. You will hear a tone to confirm that you've entered the queue. If you wish to remove yourself from the question queue, you may press star 2. Participants are requested to use only handsets while asking a question. Anyone who has a question may press star 1 at this time. The first question is from Bob Pooler from valuationLAB AG. Please go ahead. Thank you. Good afternoon, gentlemen. Congratulations on the positive results for Study 008A. My first question, sort of like what I had with Study 014/15, what was the most striking in these top-line results? You mentioned the placebo-like side effects, basically, also people maintaining in the trial, but also the magnitude and also the timing of the efficacy. What are your favorite sort of striking results in these top-line results? Thanks, Bob. It is a mixture of all three. I mean, to have a study with a high retention rate but without evidence of efficacy is useless. To have efficacy with a drug which is not well tolerated is also useless. We've seen that clozapine, despite being the world's most effective drug, is barely used by 14% of the population, although it's the only drug prescribed for treatment in schizophrenia. I think more than that, I think I do have a certain regret. The regret is that I chose to make this study 4 weeks. Whereas conventional wisdom always has dictated 6 weeks, 8 weeks. I think the reason why we did this was because we were driven to explore something which the FDA published, that drugs that are effective already begin to show their efficacy in 3 to 4 weeks. That's probably absolutely correct, and we thank the FDA for the analysis. What the FDA did not necessarily say is that if you do a longer study, you will not see a better treatment difference. It's a regret of mine that probably we should have done a longer study, and probably to have included another 100 patients. As you've seen now lately, every schizophrenia study has 250 to 300 patients per treatment cell. Mm-hmm. Okay. Yeah, apparently you did choose the right dosing there too. You were already extrapolating the findings of Study 014/15 there. Is this something, yeah, we could probably do. I remember when those results came out, you were very cautious in extrapolating the results to Study 008A, but do you think this could also be something that you see the increased efficacy and response rates with longer treatment duration also in these chronic schizophrenia patients who inadequately respond to current treatments? Absolutely, Bob. When I made the comment that I'd be cautious in trying to extrapolate those results, obviously I had not seen data from this study. The more we have seen the data from this study, I find remarkable similarities in the baseline demographics of the population. Even though the patients in the study, from a regulatory point of view, technical point of view, may not be called as treatment-resistant, they look like to me, they smell like, they taste like, they feel like almost treatment-resistant patients. When I look at the baseline severities and the way the change occurs, I mean, obviously we are not showing you the data. When I look at the data week by week, this study is only four weeks. Week by week, you see a benefit that is increasing. That's exactly what we saw in the TRS study. There, of course, the time frames were six weeks, six months, one year. Here we're talking about one week, two weeks, four weeks. The pattern is the same. The slopes are the same. Clearly tells me that if I were to do an eight-week study, I may not necessarily double the change that we have seen now, but definitely it will be substantially more than what we have seen now. What are the next steps with this trial? Would it be still sufficient for U.S. or EU filing, maybe an accelerated or conditional approval on the second trial? Also follow on there, have you already discussed the Study 014/15 results in TRS with the FDA or EMA? Yeah, we have submitted those to the FDA. We have also submitted a protocol I was talking about to the FDA. Obviously these results, since they are released today, we will inform the FDA. Then at the same time, as I said, we probably have to modify the protocol that we had submitted. Again, the TRS study will be a global study done probably about 13, 14 countries, because we need about 500 to 600 patients. That would be the next step. Of course, we would file for some kind of a recognition for this result, whether it's Breakthrough designation or Fast Track approval or something of that type. Mm-hmm. Because you mentioned there might be tweaks to Study 017 there. Can you maybe shed some light on that? Can you also maintain the timeline of that trial start? I think that's Q3 this year. I think the timeline is probably not going to get affected substantially because the tweaks are going to be really in how you score something, how you do some things, whether we do one blood test during screening or we do two blood tests during screening. These are the kind of things that we would be tweaking. There's no fundamental change that I can visualize at this stage. Okay. Probably also, what impact did these positive results have on your out-license of evenamide? I think a better bargaining power there. When do you expect to sign on a partner there? Well, Bob, the news would certainly support the process. I think there's little doubt about it, and there's dynamic. Please give us the time to produce the additional results which the partners will want to see. Then we can make a better assessment of the timelines. Clearly, as you know, the pivotal study in TRS will require a partner to be on board. Our objective is to have that partner on board this year still to start the study. That is as much as we can say as today. The next question is from Samir Devani from Rx Securities. Please go ahead. Hi, guys. Congratulations on the data. I guess just got a couple of questions, mainly on the study and next steps. Ravi, could you just remind us what the baseline PANSS in Study 008A was? Have you got any information in terms of responder analysis yet? That's the first question, I guess. I guess the second question is really just you mentioned about tweaking the study. Is that mainly the timeline in terms of going beyond prior timeline that you had submitted to the FDA? Thanks very much. The baseline PANSS is around 78.2. We had basically allowed patients from 70-85, PANSS total, to be allowed into the study. This is 70-85 on an antipsychotic. That means that without an antipsychotic, you could probably add another 10 points. These patients would have been around 80-95 or so. I think since this is an outpatient study, we felt that probably was the limit we could go to without jeopardizing patient safety, and it turned out to be correct. We have no instances in which patients had to be hospitalized because of exacerbations, et cetera. The baseline PANSS is around 78.2 or 4, something like that. It is moderate to moderately severe patient population. The second question about the timeline. Obviously, if you submit new to the FDA, there will always be an impact on timeline. Whether the FDA treats it as a new submission or an amendment to an ongoing submission, those are technical questions I cannot really answer. I would definitely expect there will be an impact on that. The field impact of that probably is less, because these are really more things to do in the protocol rather than anything else. What has to happen in the field is already sort of fixed in, and those processes are ongoing. I would expect that there probably would be about a month or two months delay. That is great. Thanks very much. The next question is from Lucy Gallop from Em Partners. Please go ahead. Hi, thank you for the presentation, and congratulations on the results. I just wanted to clarify whether it was 4 patients that dropped out due to adverse events, or was it 3 patients? Because in the press release, you said 3 patients, but you said 4 in the presentation. Sorry, my mistake. In terms of the tweaking, what actually needs to be done for the tweaking of the trial? Sorry? Yeah. Sorry. Lucy, you're right. Absolutely. I think I misspoke. Probably it's 3 patients. The tweaking of the trial basically is to do more with how we manage the ratings of the patients. In other words, what are the monitoring criteria? That's the first thing. The training of the investigators, we probably need to change slightly how we did it. How we were planning to do it in the new study compared to what we did in this study. We probably may add an extra efficacy measure, which we did not have in this study. Those are the kind of things that would be the fundamental changes. Of course, probably we have learned some lessons on statistics from this trial, which we want to make use of in adapting the statistical analysis plan. As you probably do know that the FDA, as well as the EMA, any other health authority now, absolutely insist on having the primary analysis in the intent-to-treat population. Previously, we were all very happy to report efficacy analysis in what we call the full analysis set, which was in modified intent-to-treat. Now it's going to be the intent-to-treat population. These are minor changes, but with every minor change, there's a sort of a litany of smaller changes that have to be made elsewhere. As I said, we probably will add an efficacy measure, and most of this will probably take another 1 to 2 months, depending upon FDA and European authority review times. Great. Thank you. For any further questions, please press star and one. Once again, for any further questions, please press star and one. There are no more questions from the phone. Thank you so much, Moira. We can complete